TY - JOUR
T1 - Kappa Opioid receptor ligands regulate angiogenesis in development and in tumours
AN - 1837294725; 21214314
AB - Opioid systems mainly regulate physiological functions such as pain, emotional tone and reward circuitry in neural tissues (brain and spinal cord). These systems are also found in extraneural tissues (ganglia, gut, spleen, stomach, lung, pancreas, liver, heart, blood and blood vessels), and recent studies have elucidated their roles in various organs. The current review focuses on the roles of opioid systems in blood vessels, especially angiogenesis, during development and tumour malignancy. The balance between endogenous activators and inhibitors of angiogenesis delicately maintains a normally quiescent vasculature to sustain homeostasis. Disturbance of this balance causes pathogenic angiogenesis and, especially in tumours, several activators such as VEGF are highly expressed in the tumour microenvironment and strongly induce tumour angiogenesis, the so-called angiogenic switch. Recently, we demonstrated that Kappa opioid receptor agonists function as anti-angiogenic factors, which impede the angiogenic switch, in vascular development and tumour angiogenesis by inhibiting the expression of receptors for VEGF. In clinical medicine, angiogenesis inhibitors that target VEGF signalling such as bevacizumab are used as anti-cancer drugs. Although therapies that inhibit tumour angiogenesis have been highly successful for tumour therapy, most patients eventually develop resistance to this anti-angiogenic therapy. Thus, we must identify novel targets for anti-angiogenic agents to sustain inhibition of angiogenesis for tumour therapy. The regulation of responses to Kappa opioid receptor ligands could be useful for controlling vascular formation under physiological conditions and in cancers, and thus could offer therapeutic benefits beyond the relief of pain. Linked Articles This article is part of a themed section on Opioids: New Pathways to Functional Selectivity. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2015.172.issue-2
JF - British Journal of Pharmacology
AU - Yamamizu, Kohei
AU - Hamada, Yusuke
AU - Narita, Minoru
AD - Laboratory of Genetics, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Y1 - 2015/01//
PY - 2015
DA - January 2015
SP - 268
EP - 276
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 172
IS - 2
SN - 0007-1188, 0007-1188
KW - Toxicology Abstracts
KW - Vascular endothelial growth factor
KW - Opioid receptors
KW - Heart
KW - Receptor mechanisms
KW - Spinal cord
KW - Pancreas
KW - angiogenesis inhibitors
KW - Angiogenesis
KW - Spleen
KW - Pain
KW - Tumors
KW - Homeostasis
KW - Bevacizumab
KW - Digestive tract
KW - Blood vessels
KW - Lung
KW - Reinforcement
KW - Ganglia
KW - Signal transduction
KW - X 24380:Social Poisons & Drug Abuse
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1837294725?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+Journal+of+Pharmacology&rft.atitle=Kappa+Opioid+receptor+ligands+regulate+angiogenesis+in+development+and+in+tumours&rft.au=Yamamizu%2C+Kohei%3BHamada%2C+Yusuke%3BNarita%2C+Minoru&rft.aulast=Yamamizu&rft.aufirst=Kohei&rft.date=2015-01-01&rft.volume=172&rft.issue=2&rft.spage=268&rft.isbn=&rft.btitle=&rft.title=British+Journal+of+Pharmacology&rft.issn=00071188&rft_id=info:doi/10.1111%2Fbph.12573
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2016-11-01
N1 - Last updated - 2016-12-22
N1 - SubjectsTermNotLitGenreText - Heart; Opioid receptors; Vascular endothelial growth factor; Receptor mechanisms; Spinal cord; angiogenesis inhibitors; Pancreas; Angiogenesis; Spleen; Pain; Bevacizumab; Homeostasis; Tumors; Digestive tract; Blood vessels; Lung; Reinforcement; Ganglia; Signal transduction
DO - http://dx.doi.org/10.1111/bph.12573
ER -
TY - JOUR
T1 - Expression signature of microRNA-155 in hepatitis C virus genotype 4 infection.
AN - 1826606642; 25469255
AB - Hepatits C virus (HCV) genotype 4 (GT4) shows low treatment response rates and discrepancies when compared to other genotypes. However, the reason underlying these discrepancies remains unclear due to the limited number of studies on GT4. microRNA-155 (miR-155) is a noteworthy example of a discrepancy in GT4, as it was found to be upregulated in genotypes 1, 2 and 3 HCV infection, but downregulated in GT4-HCV-infected peripheral blood mononuclear cells (PBMCs). The present study aimed to investigate the expression of miR-155 in PBMCs, serum and liver tissues of GT4-HCV-infected patients. miR-155 expression was assessed using reverse transcription-quantitative polymerase chain reaction in GT4-HCV-infected PBMCs, serum and liver tissues, as well as GT2- and GT4-infected Huh7 cells, and compared to the healthy controls. There was no difference in miR-155 expression observed between naïve GT4-HCV patients and healthy controls in the PBMCs and serum. In HCV-infected liver tissues, however, a significant downregulation was observed. The unique miR-155 expression pattern during GT4 infection was confirmed in the infected Huh7 cell lines when compared to GT2 infection. Clinical data showed a positive correlation between liver transaminases and serum miR-155 expression. In addition, serum miR-155 expression was significantly lower in naïve non-responders (NRs) than naïve sustained virological responders (SVRs), and in post-treatment NRs compared to post-treatment SVRs. In conclusion, miR-155 was not only proven to be a genotype-specific microRNA that is not induced during GT4-HCV infection, but also a good prognostic factor and predictor of response to treatment enabling a non-invasive differentiation between NRs and SVRs during GT4-HCV infection.
JF - Biomedical reports
AU - Riad, Sarah Ehab
AU - El-Ekiaby, Nada
AU - Mekky, Radwa Yehia
AU - Ahmed, Rasha
AU - El Din, Mohammad Ahmed Mohey
AU - El-Sayed, Mohammad
AU - Abouelkhair, Mahmoud Mohammad
AU - Salah, Ayman
AU - Zekri, Abdel Rahman
AU - Esmat, Gamal
AU - Abdelaziz, Ahmed Ihab
AD - The Molecular Pathology Research Group, Department of Pharmacology and Toxicology, German University in Cairo, New Cairo 11835, Egypt. ; Departments of Endemic Medicine and Hepatology and Egypt. ; Departments of Surgery, Cairo University, Cairo 11562, Egypt. ; Virology and Immunology Unit, Cancer Biology Department, National Cancer Institute, Cairo University, Cairo 11976, Egypt.
Y1 - 2015/01//
PY - 2015
DA - January 2015
SP - 93
EP - 97
VL - 3
IS - 1
SN - 2049-9434, 2049-9434
KW - microRNA-155
KW - genotype 4
KW - treatment response
KW - hepatitis C virus
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1826606642?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biomedical+reports&rft.atitle=Expression+signature+of+microRNA-155+in+hepatitis+C+virus+genotype+4+infection.&rft.au=Riad%2C+Sarah+Ehab%3BEl-Ekiaby%2C+Nada%3BMekky%2C+Radwa+Yehia%3BAhmed%2C+Rasha%3BEl+Din%2C+Mohammad+Ahmed+Mohey%3BEl-Sayed%2C+Mohammad%3BAbouelkhair%2C+Mahmoud+Mohammad%3BSalah%2C+Ayman%3BZekri%2C+Abdel+Rahman%3BEsmat%2C+Gamal%3BAbdelaziz%2C+Ahmed+Ihab&rft.aulast=Riad&rft.aufirst=Sarah&rft.date=2015-01-01&rft.volume=3&rft.issue=1&rft.spage=93&rft.isbn=&rft.btitle=&rft.title=Biomedical+reports&rft.issn=20499434&rft_id=info:doi/
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date created - 2014-12-03
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
ER -
TY - JOUR
T1 - Short food safety videos promote peer networking and behavior change
AN - 1815692745; PQ0003313174
AB - Purpose - The purpose of this paper is to create a series of 30-60-second short videos to promote improved food safety behaviors of middle school youth, determine the feasibility of disseminating the videos through peer networks, and measure their effects on food safety attitudes, perceived social norms, and behaviors of youth. Design/methodology/approach - Food safety content specialists, learning experts, programmers, illustrators, project managers, instructional designers, scriptwriters, and stakeholders were involved in creation of the Don't Be Gross short videos before evaluation by middle school youth (sixth to eighth grades). The experimental group ( n =220) completed the following activities at about one-week intervals: pre-test, viewed videos, post-test, and follow-up test. The control group ( n =112) completed the same activities at similar intervals but did not have access to the videos until after the follow-up test. Findings - Controlling for grade and gender, linear mixed-effects models revealed significant time by group effects for participants' perceived susceptibility to foodborne illness; intentions to perform recommended food safety behaviors approached significance. Additionally, compared to the pre-test, the experimental group perceived their friends as being significantly more confident in performing food safety behaviors at post- and follow-up tests. Google Analytics data revealed that the bounce rate from the home page of the videos was low (38 percent) suggesting that the videos were engaging. Originality/value - The Don't Be Gross videos were liked by youth and shared among their peers and may have the potential to promote positive food safety behaviors and intentions among youth.
JF - British Food Journal
AU - Quick, Virginia
AU - Corda, Kirsten W
AU - Martin-Biggers, Jennifer
AU - Chamberlin, Barbara
AU - Schaffner, Donald W
AU - Byrd-Bredbenner, Carol
AD - Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development/ National Institutes of Health, Bethesda, Maryland, USA
Y1 - 2015///0,
PY - 2015
DA - 0, 2015
SP - 78
EP - 93
PB - Emerald Group Publishing Limited, 60-62 Toller Lane Bradford West Yorkshire BD8 9BY United Kingdom
VL - 117
IS - 1
SN - 0007-070X, 0007-070X
KW - Biotechnology and Bioengineering Abstracts
KW - Food safety
KW - Youth
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1815692745?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+Food+Journal&rft.atitle=Short+food+safety+videos+promote+peer+networking+and+behavior+change&rft.au=Quick%2C+Virginia%3BCorda%2C+Kirsten+W%3BMartin-Biggers%2C+Jennifer%3BChamberlin%2C+Barbara%3BSchaffner%2C+Donald+W%3BByrd-Bredbenner%2C+Carol&rft.aulast=Quick&rft.aufirst=Virginia&rft.date=2015-01-01&rft.volume=117&rft.issue=1&rft.spage=78&rft.isbn=&rft.btitle=&rft.title=British+Food+Journal&rft.issn=0007070X&rft_id=info:doi/
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2016-08-01
N1 - Number of references - 55
N1 - Last updated - 2016-09-01
ER -
TY - JOUR
T1 - Endothelial Expression of Scavenger Receptor Class B, Type I Protects against Development of Atherosclerosis in Mice
AN - 1758247233; PQ0002448370
AB - The role of scavenger receptor class B, type I (SR-BI) in endothelial cells (EC) was examined in several novel transgenic mouse models expressing SR-BI in endothelium of mice with normal C57Bl6/N, apoE-KO, or Scarb1 -KO backgrounds. Mice were also created expressing SR-BI exclusively in endothelium and liver. Endothelial expression of the Tie2-Scarb1 transgene had no significant effect on plasma lipoprotein levels in mice on a normal chow diet but on an atherogenic diet, significantly decreased plasma cholesterol levels, increased plasma HDL cholesterol (HDL-C) levels, and protected mice against atherosclerosis. In 8-month-old apoE-KO mice fed a normal chow diet, the Tie2-Scarb1 transgene decreased aortic lesions by 24%. Mice expressing SR-BI only in EC and liver had a 1.5 plus or minus 0.1-fold increase in plasma cholesterol compared to mice synthesizing SR-BI only in liver. This elevation was due mostly to increased HDL-C. In EC culture studies, SR-BI was found to be present in both basolateral and apical membranes but greater cellular uptake of cholesterol from HDL was found in the basolateral compartment. In summary, enhanced expression of SR-BI in EC resulted in a less atherogenic lipoprotein profile and decreased atherosclerosis, suggesting a possible role for endothelial SR-BI in the flux of cholesterol across EC.
JF - BioMed Research International
AU - Vaisman, Boris L
AU - Vishnyakova, Tatyana G
AU - Freeman, Lita A
AU - Amar, Marcelo J
AU - Demosky, Stephen J
AU - Liu, Chengyu
AU - Stonik, John A
AU - Sampson, Maureen L
AU - Pryor, Milton
AU - Bocharov, Alexander V
AU - Eggerman, Thomas L
AU - Patterson, Amy P
AU - Remaley, Alan T
AD - Lipoprotein Metabolism Section, Cardiovascular-Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA, borisv@mail.nih.gov
Y1 - 2015/01//
PY - 2015
DA - January 2015
PB - Hindawi Publishing Corporation, P.O. Box 3079 Cuyahoga Falls OH 44223 United States
VL - 2015
SN - 2314-6133, 2314-6133
KW - Biotechnology and Bioengineering Abstracts
KW - Diets
KW - Atherogenic diet
KW - Aorta
KW - Transgenes
KW - Lipoproteins (high density)
KW - Animal models
KW - Cell culture
KW - Arteriosclerosis
KW - Cholesterol
KW - Transgenic mice
KW - Endothelial cells
KW - Endothelium
KW - Lipoproteins
KW - Liver
KW - scavenger receptors
KW - W 30925:Genetic Engineering
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1758247233?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BioMed+Research+International&rft.atitle=Endothelial+Expression+of+Scavenger+Receptor+Class+B%2C+Type+I+Protects+against+Development+of+Atherosclerosis+in+Mice&rft.au=Vaisman%2C+Boris+L%3BVishnyakova%2C+Tatyana+G%3BFreeman%2C+Lita+A%3BAmar%2C+Marcelo+J%3BDemosky%2C+Stephen+J%3BLiu%2C+Chengyu%3BStonik%2C+John+A%3BSampson%2C+Maureen+L%3BPryor%2C+Milton%3BBocharov%2C+Alexander+V%3BEggerman%2C+Thomas+L%3BPatterson%2C+Amy+P%3BRemaley%2C+Alan+T&rft.aulast=Vaisman&rft.aufirst=Boris&rft.date=2015-01-01&rft.volume=2015&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=BioMed+Research+International&rft.issn=23146133&rft_id=info:doi/10.1155%2F2015%2F607120
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2016-01-01
N1 - Number of references - 1
N1 - Last updated - 2016-05-13
N1 - SubjectsTermNotLitGenreText - Diets; Atherogenic diet; Aorta; Lipoproteins (high density); Transgenes; Animal models; Cell culture; Cholesterol; Arteriosclerosis; Transgenic mice; Endothelial cells; Lipoproteins; Endothelium; Liver; scavenger receptors
DO - http://dx.doi.org/10.1155/2015/607120
ER -
TY - JOUR
T1 - Acceptable Approaches to Enrolling Adults Who Cannot Consent in More Than Minimal Risk Research
AN - 1753465623; PQ0002370724
JF - American Journal of Bioethics
AU - Danis, Marion
AU - Wendler, David
AU - Kim, Scott
AD - National Institutes of Health Clinical Center
PY - 2015
SP - 70
EP - 71
PB - Taylor & Francis Group Ltd., 2 Park Square Oxford OX14 4RN United Kingdom
VL - 15
IS - 10
SN - 1526-5161, 1526-5161
KW - Environment Abstracts
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1753465623?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aenvabstractsmodule&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Bioethics&rft.atitle=Acceptable+Approaches+to+Enrolling+Adults+Who+Cannot+Consent+in+More+Than+Minimal+Risk+Research&rft.au=Danis%2C+Marion%3BWendler%2C+David%3BKim%2C+Scott&rft.aulast=Danis&rft.aufirst=Marion&rft.date=2015-01-01&rft.volume=15&rft.issue=10&rft.spage=70&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Bioethics&rft.issn=15265161&rft_id=info:doi/10.1080%2F15265161.2015.1075806
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2016-01-01
N1 - Last updated - 2016-01-06
DO - http://dx.doi.org/10.1080/15265161.2015.1075806
ER -
TY - JOUR
T1 - Prospective study on nanoparticle albumin-bound paclitaxel in advanced breast cancer: clinical results and biological observations in taxane-pretreated patients
AN - 1753464302; PQ0002418717
AB - There is a deep need to improve the care of metastatic breast cancer (MBC) patients, since even today it remains an incurable disease. Taxanes are considered the most effective cytotoxic drugs for the treatment of MBC, both in monotherapy and in combined schedules, but the need for synthetic solvents contributes to the severe toxicities and may have a negative impact on the efficacy. Nanoparticle albumin-bound paclitaxel (Nab-paclitaxel) is a colloidal suspension of paclitaxel and human serum albumin initially developed to avoid the toxicities associated with conventional taxanes. The aim of this prospective, single-center open-label, noncomparative study was to evaluate the efficacy and safety of nab-paclitaxel in MBC patients pretreated with taxanes. The patients were treated with nab-paclitaxel as a single agent, 260 mg/m2 on day 1 of each 3-week cycle or 125 mg/m2 weekly. The primary endpoint was the overall response rate (ORR). Secondary objectives were duration of response, clinical benefit rate, progression-free survival (PFS), overall survival, and safety. A total of 42 patients (median age 48 years, median Eastern Cooperative Oncology Group performance status 0, triple-negative MBC 19%, all pretreated with a taxane-based therapy, mainly in advanced disease) were enrolled in the study. The ORR was 23.8%, including one complete response (2.4%) and nine partial responses (21.4%); the disease control rate was 50%. The median duration of response was 7.2 months. After a median follow-up of 9 months, the median PFS was 4.6 months. ORR and PFS were similar irrespective of the previous chemotherapy lines, metastatic sites, and biomolecular expression. Nab-paclitaxel was well tolerated, and the most frequent treatment-related toxicities were mild to moderate (grades 1-2). This real-life study shows that nab-paclitaxel has a significant antitumor activity and a manageable safety profile in patients pretreated with taxanes and experiencing a treatment failure after at least one line of chemotherapy.
JF - Drug Design, Development and Therapy
AU - Fabi, Alessandra
AU - Giannarelli, Diana
AU - Malaguti, Paola
AU - Ferretti, Gianluigi
AU - Vari, Sabrina
AU - Papaldo, Paola
AU - Nistico, Cecilia
AU - Caterino, Mauro
AU - De Vita, Roy
AU - Mottolese, Marcella
AU - Iacorossi, Laura
AU - Cognetti, Francesco
AD - Department of Medical Oncology, Regina Elena National Cancer Institute, Rome, Italy
PY - 2015
SP - 6177
EP - 6183
PB - Dove Medical Press Ltd, Beechfield House Macclesfield SK11 0JL United Kingdom
VL - 9
KW - Biotechnology and Bioengineering Abstracts
KW - nab-paclitaxel
KW - metastatic breast cancer
KW - anthracyclines
KW - Age
KW - Chemotherapy
KW - Disease control
KW - Solvents
KW - Survival
KW - taxanes
KW - human serum albumin
KW - Drug development
KW - Oncology
KW - Toxicity
KW - Metastases
KW - Cytotoxicity
KW - Paclitaxel
KW - Breast cancer
KW - nanoparticles
KW - Antitumor activity
KW - W 30915:Pharmaceuticals & Vaccines
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1753464302?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Drug+Design%2C+Development+and+Therapy&rft.atitle=Prospective+study+on+nanoparticle+albumin-bound+paclitaxel+in+advanced+breast+cancer%3A+clinical+results+and+biological+observations+in+taxane-pretreated+patients&rft.au=Fabi%2C+Alessandra%3BGiannarelli%2C+Diana%3BMalaguti%2C+Paola%3BFerretti%2C+Gianluigi%3BVari%2C+Sabrina%3BPapaldo%2C+Paola%3BNistico%2C+Cecilia%3BCaterino%2C+Mauro%3BDe+Vita%2C+Roy%3BMottolese%2C+Marcella%3BIacorossi%2C+Laura%3BCognetti%2C+Francesco&rft.aulast=Fabi&rft.aufirst=Alessandra&rft.date=2015-01-01&rft.volume=9&rft.issue=&rft.spage=6177&rft.isbn=&rft.btitle=&rft.title=Drug+Design%2C+Development+and+Therapy&rft.issn=1177-8881&rft_id=info:doi/10.2147%2FDDDT.S89575
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2016-01-01
N1 - Last updated - 2016-01-21
N1 - SubjectsTermNotLitGenreText - Age; Chemotherapy; Solvents; Disease control; human serum albumin; taxanes; Survival; Oncology; Drug development; Toxicity; Metastases; Cytotoxicity; Paclitaxel; Breast cancer; nanoparticles; Antitumor activity
DO - http://dx.doi.org/10.2147/DDDT.S89575
ER -
TY - JOUR
T1 - Quantitative assessment of myocardial fibrosis in an age-related rat model by ex vivo late gadolinium enhancement magnetic resonance imaging with histopathological correlation
AN - 1751214996; PQ0002336595
AB - Late gadolinium enhanced (LGE) cardiac magnetic resonance (CMR) imaging can detect the presence of myocardial infarction from ischemic cardiomyopathies (ICM). However, it is more challenging to detect diffuse myocardial fibrosis from non-ischemic cardiomyopathy (NICM) with this technique due to more subtle and heterogeneous enhancement of the myocardium. This study investigates whether high-resolution LGE CMR can detect age-related myocardial fibrosis using quantitative texture analysis with histological validation. LGE CMR of twenty-four rat hearts (twelve 6-week-old and twelve 2-year-old) was performed using a 7T MRI scanner. Picrosirius red was used as the histopathology reference for collagen staining. Fibrosis in the myocardium was quantified with standard deviation (SD) threshold methods from the LGE CMR images and 3D contrast texture maps that were computed from gray level co-occurrence matrix of the CMR images. There was a significant increase of collagen fibers in the aged compared to the young rat histology slices (2.60 plus or minus 0.27 %LV vs. 1.24 plus or minus 0.29 %LV, p<0.01). Both LGE CMR and texture images showed a significant increase of myocardial fibrosis in the elderly compared to the young rats. Fibrosis in the LGE CMR images correlated strongly with histology with the 3 SD threshold (r=0.84, y=0.99x+0.00). Similarly, fibrosis in the contrast texture maps correlated with the histology using the 4 SD threshold (r=0.89, y=1.01x+0.00). High resolution ex-vivo LGE CMR can detect the presence of diffuse fibrosis that naturally developed in elderly rat hearts. Our results suggest that texture analysis may improve the assessment of myocardial fibrosis in LGE CMR images.
JF - Computers in Biology and Medicine
AU - Beliveau, Pascale
AU - Cheriet, Farida
AU - Anderson, Stasia A
AU - Taylor, Joni L
AU - Arai, Andrew E
AU - Hsu, Li-Yueh
AD - National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA
PY - 2015
SP - 103
EP - 113
PB - Elsevier B.V., P.O. Box 800 Kidlington Oxford OX5 1DX United Kingdom
VL - 65
SN - 0010-4825, 0010-4825
KW - Biotechnology and Bioengineering Abstracts
KW - CMR cardiac magnetic resonance
KW - DTI diffusion tensor imaging
KW - DTPA diethylenetriamine pentaacetic acid
KW - ECV extracellular volume fraction
KW - Gd gadolinium
KW - GLCM gray level co-occurrence matrix
KW - HSV hue-saturation-value
KW - ICM ischemic cardiomyopathies
KW - LGE late gadolinium enhancement
KW - LV left ventricular
KW - NICM non-ischemic cardiomyopathy
KW - NS not statically significant
KW - ROI region of interest
KW - SA short-axis
KW - SI signal intensity
KW - SD standard deviation
KW - Diffuse myocardial fibrosis
KW - Gadolinium
KW - Magnetic resonance imaging
KW - Texture analysis
KW - Computer quantification
KW - Aging
KW - Heart
KW - Age
KW - Fibrosis
KW - Ischemia
KW - Maps
KW - Computer applications
KW - Myocardial infarction
KW - Collagen
KW - Cardiomyopathy
KW - Fibers
KW - Standard deviation
KW - Geriatrics
KW - Myocardium
KW - W 30960:Bioinformatics & Computer Applications
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1751214996?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Computers+in+Biology+and+Medicine&rft.atitle=Quantitative+assessment+of+myocardial+fibrosis+in+an+age-related+rat+model+by+ex+vivo+late+gadolinium+enhancement+magnetic+resonance+imaging+with+histopathological+correlation&rft.au=Beliveau%2C+Pascale%3BCheriet%2C+Farida%3BAnderson%2C+Stasia+A%3BTaylor%2C+Joni+L%3BArai%2C+Andrew+E%3BHsu%2C+Li-Yueh&rft.aulast=Beliveau&rft.aufirst=Pascale&rft.date=2015-01-01&rft.volume=65&rft.issue=&rft.spage=103&rft.isbn=&rft.btitle=&rft.title=Computers+in+Biology+and+Medicine&rft.issn=00104825&rft_id=info:doi/10.1016%2Fj.compbiomed.2015.07.027
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-12-01
N1 - Number of references - 48
N1 - Last updated - 2016-01-21
N1 - SubjectsTermNotLitGenreText - Heart; Age; Fibrosis; Magnetic resonance imaging; Gadolinium; Ischemia; Computer applications; Maps; Myocardial infarction; Collagen; Fibers; Cardiomyopathy; Standard deviation; Geriatrics; Myocardium
DO - http://dx.doi.org/10.1016/j.compbiomed.2015.07.027
ER -
TY - JOUR
T1 - Structure of RC1339/APRc from Rickettsia conorii, a retropepsin-like aspartic protease
AN - 1746874544; PQ0002167264
AB - The crystal structures of two constructs of RC1339/APRc from Rickettsia conorii, consisting of either residues 105-231 or 110-231 followed by a His tag, have been determined in three different crystal forms. As predicted, the fold of a monomer of APRc resembles one-half of the mandatory homodimer of retroviral pepsin-like aspartic proteases (retropepsins), but the quaternary structure of the dimer of APRc differs from that of the canonical retropepsins. The observed dimer is most likely an artifact of the expression and/or crystallization conditions since it cannot support the previously reported enzymatic activity of this bacterial aspartic protease. However, the fold of the core of each monomer is very closely related to the fold of retropepsins from a variety of retroviruses and to a single domain of pepsin-like eukaryotic enzymes, and may represent a putative common ancestor of monomeric and dimeric aspartic proteases.
JF - Acta Crystallographica Section D
AU - Li, Mi
AU - Gustchina, Alla
AU - Cruz, Rui
AU - Simoes, Marisa
AU - Curto, Pedro
AU - Martinez, Juan
AU - Faro, Carlos
AU - Simoes, Isaura
AU - Wlodawer, Alexander
AD - Protein Structure Section, Macromolecular Crystallography Laboratory, National Cancer Institute, Frederick, MD 21702, USA.
PY - 2015
SP - 2109
EP - 2118
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 71
IS - 10
SN - 1399-0047, 1399-0047
KW - Microbiology Abstracts B: Bacteriology
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1746874544?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Acta+Crystallographica+Section+D&rft.atitle=Structure+of+RC1339%2FAPRc+from+Rickettsia+conorii%2C+a+retropepsin-like+aspartic+protease&rft.au=Li%2C+Mi%3BGustchina%2C+Alla%3BCruz%2C+Rui%3BSimoes%2C+Marisa%3BCurto%2C+Pedro%3BMartinez%2C+Juan%3BFaro%2C+Carlos%3BSimoes%2C+Isaura%3BWlodawer%2C+Alexander&rft.aulast=Li&rft.aufirst=Mi&rft.date=2015-01-01&rft.volume=71&rft.issue=10&rft.spage=2109&rft.isbn=&rft.btitle=&rft.title=Acta+Crystallographica+Section+D&rft.issn=13990047&rft_id=info:doi/10.1107%2FS1399004715013905
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-12-01
N1 - Last updated - 2015-12-09
DO - http://dx.doi.org/10.1107/S1399004715013905
ER -
TY - JOUR
T1 - Does focal incidental super(18)F-FDG PET/CT uptake in the prostate have significance?
AN - 1735922376; PQ0002271374
AB - super(18)F-FDG PET/CT is used to characterize many malignancies, but is not recommended for localized prostate cancer. This study explores the value of multi-parametric MRI (mpMRI) in characterizing incidental prostate super(18)F-FDG uptake. Thirty-one patients who underwent super(18)F-FDG PET/CT for reasons unrelated to prostate cancer and prostate mpMRI were eligible for this retrospective study. The mpMRI included T2-weighted (T2W), dynamic contrast enhancement (DCE), apparent diffusion coefficient (ADC), and MR spectroscopy (MRS) sequences. Fourteen patients were excluded (n = 8 insufficient histopathology, n = 6 radical prostatectomy before PET), and final analysis included 17 patients. A nuclear medicine physician, blinded to clinicopathologic findings, identified suspicious areas and maximum standardized uptake values (SUVmax) on super(18)F-FDG PET/CT. Sector-based imaging findings were correlated with annotated histopathology from whole-mount or MRI/transrectal ultrasound fusion biopsy samples. Positive predictive values (PPVs) were estimated using generalized estimating equations with logit link. Results were evaluated with Kruskal-Wallis and Dunn's multiple comparisons tests. The PPV of super(18)F-FDG PET alone in detecting prostate cancer was 0.65. Combining super(18)F-FDG PET as a base parameter with mpMRI (T2W, DCE, ADC, and MRS) increased the PPV to 0.82, 0.83, 0.83, and 0.94, respectively. All benign lesions had SUVmax 6. Using mpMRI to further evaluate incidental super(18)F-FDG uptake aids the diagnosis of prostate cancer.
JF - Abdominal Imaging
AU - Brown, Anna M
AU - Lindenberg, Maria L
AU - Sankineni, Sandeep
AU - Shih, Joanna H
AU - Johnson, Linda M
AU - Pruthy, Suneha
AU - Kurdziel, Karen A
AU - Merino, Maria J
AU - Wood, Bradford J
AU - Pinto, Peter A
AU - Choyke, Peter L
AU - Turkbey, Baris
AD - Molecular Imaging Program, National Cancer Institute, NIH, 10 Center Drive, Room B3B85, Bethesda, MD, 20892, USA, turkbeyi@mail.nih.gov
PY - 2015
SP - 3222
EP - 3229
PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL - 40
IS - 8
SN - 0942-8925, 0942-8925
KW - Biotechnology and Bioengineering Abstracts
KW - Mathematical models
KW - Magnetic resonance imaging
KW - Biopsy
KW - Malignancy
KW - Prostate cancer
KW - Magnetic resonance spectroscopy
KW - Computed tomography
KW - Positron emission tomography
KW - Nuclear medicine
KW - Diffusion coefficient
KW - Ultrasound
KW - Benign
KW - W 30910:Imaging
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2016-05-23
N1 - Date created - 2015-10-31
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1517/13543784.2015.1096344
ER -
TY - JOUR
T1 - Transgenic mice and metabolomics for study of hepatic xenobiotic metabolism and toxicity
AN - 1727673452; PQ0002136369
AB - Introduction: The study of xenobiotic metabolism and toxicity has been greatly aided by the use of genetically modified mouse models and metabolomics. Areas covered: Gene knockout mice can be used to determine the enzymes responsible for the metabolism of xenobiotics in vivo and to examine the mechanisms of xenobiotic-induced toxicity. Humanized mouse models are especially important because there exist marked species differences in the xenobiotic-metabolizing enzymes and the nuclear receptors that regulate these enzymes. Humanized mice expressing CYPs and nuclear receptors including the pregnane X receptor, the major regulator of xenobiotic metabolism and transport were produced. With genetically modified mouse models, metabolomics can determine the metabolic map of many xenobiotics with a level of sensitivity that allows the discovery of even minor metabolites. This technology can be used for determining the mechanism of xenobiotic toxicity and to find early biomarkers for toxicity. Expert opinion: Metabolomics and genetically modified mouse models can be used for the study of xenobiotic metabolism and toxicity by: i) comparison of the metabolomics profiles between wild-type and genetically modified mice, and searching for genotype-dependent endogenous metabolites; ii) searching for and elucidating metabolites derived from xenobiotics; and iii) discovery of specific alterations of endogenous compounds induced by xenobiotics-induced toxicity.
JF - Expert Opinion on Drug Metabolism and Toxicology
AU - Gonzalez, Frank J
AU - Fang, Zhong-Ze
AU - Ma, Xiaochao
AD - National Institutes of Health, National Cancer Institute, Center for Cancer Research, Laboratory of Metabolism, Bethesda, MD 20892, USA
Y1 - 2015///0,
PY - 2015
DA - 0, 2015
SP - 869
EP - 881
PB - Informa Healthcare
VL - 11
IS - 6
SN - 1742-5255, 1742-5255
KW - Genetics Abstracts; Biotechnology and Bioengineering Abstracts; Toxicology Abstracts
KW - CYP
KW - CYP3A4
KW - genetically modified mice
KW - metabolomics
KW - pregnane X receptor
KW - UPLC-ESI-QTOFMS
KW - xenobiotics
KW - Protein transport
KW - Nuclear receptors
KW - Animal models
KW - Enzymes
KW - Metabolites
KW - Toxicity
KW - pregnane X receptors
KW - Transgenic mice
KW - biomarkers
KW - X 24310:Pharmaceuticals
KW - G 07870:Mammals
KW - W 30960:Bioinformatics & Computer Applications
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-10-01
N1 - Last updated - 2016-02-18
N1 - SubjectsTermNotLitGenreText - Protein transport; Nuclear receptors; Animal models; Enzymes; Metabolites; pregnane X receptors; Toxicity; Transgenic mice; biomarkers; metabolomics
DO - http://dx.doi.org/10.1517/17425255.2015.1032245
ER -
TY - JOUR
T1 - GNormPlus: An Integrative Approach for Tagging Genes, Gene Families, and Protein Domains
AN - 1722175691; PQ0002026600
AB - The automatic recognition of gene names and their associated database identifiers from biomedical text has been widely studied in recent years, as these tasks play an important role in many downstream text-mining applications. Despite significant previous research, only a small number of tools are publicly available and these tools are typically restricted to detecting only mention level gene names or only document level gene identifiers. In this work, we report GNormPlus: an end-to-end and open source system that handles both gene mention and identifier detection. We created a new corpus of 694 PubMed articles to support our development of GNormPlus, containing manual annotations for not only gene names and their identifiers, but also closely related concepts useful for gene name disambiguation, such as gene families and protein domains. GNormPlus integrates several advanced text-mining techniques, including SimConcept for resolving composite gene names. As a result, GNormPlus compares favorably to other state-of-the-art methods when evaluated on two widely used public benchmarking datasets, achieving 86.7% F1-score on the BioCreative II Gene Normalization task dataset and 50.1% F1-score on the BioCreative III Gene Normalization task dataset. The GNormPlus source code and its annotated corpus are freely available, and the results of applying GNormPlus to the entire PubMed are freely accessible through our web-based tool PubTator.
JF - BioMed Research International
AU - Wei, Chih-Hsuan
AU - Kao, Hung-Yu
AU - Lu, Zhiyong
AD - National Center for Biotechnology Information (NCBI), 8600 Rockville Pike, Bethesda, MD 20894, USA, zhiyong.lu@nih.gov
Y1 - 2015/01//
PY - 2015
DA - January 2015
PB - Hindawi Publishing Corporation, P.O. Box 3079 Cuyahoga Falls OH 44223 United States
VL - 2015
SN - 2314-6133, 2314-6133
KW - Genetics Abstracts; Biotechnology and Bioengineering Abstracts
KW - Databases
KW - G 07730:Development & Cell Cycle
KW - W 30960:Bioinformatics & Computer Applications
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1722175691?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BioMed+Research+International&rft.atitle=GNormPlus%3A+An+Integrative+Approach+for+Tagging+Genes%2C+Gene+Families%2C+and+Protein+Domains&rft.au=Wei%2C+Chih-Hsuan%3BKao%2C+Hung-Yu%3BLu%2C+Zhiyong&rft.aulast=Wei&rft.aufirst=Chih-Hsuan&rft.date=2015-01-01&rft.volume=2015&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=BioMed+Research+International&rft.issn=23146133&rft_id=info:doi/10.1155%2F2015%2F918710
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-10-01
N1 - Number of references - 10
N1 - Last updated - 2016-05-13
N1 - SubjectsTermNotLitGenreText - Databases
DO - http://dx.doi.org/10.1155/2015/918710
ER -
TY - JOUR
T1 - Hierarchical decision making: resource distribution exhibits stronger effect on crayfish dominance relationships and shelter occupation than prior social experience and resource ownership
AN - 1722169703; PQ0002040446
AB - The outcome of agonistic interactions is critical to the acquisition of vital resources. These behaviours can be influenced by several intrinsic and extrinsic factors, and multi-faceted studies are necessary for ecologically relevant studies. The aim of this study was to combine the effects of past social experience, resource ownership, and the distribution of shelter resources to examine the combination of these effects on various measures of agonism in crayfish (Orconectes rusticus). Crayfish were assigned to one of three social conditioning treatments (naive, subordinate, dominant) and then introduced to an arena where they were assigned to a resident or intruder treatment. An intruder shelter was then positioned 20, 60 or 120 cm from the resident shelter. We found that resource distribution (shelter distance) played a larger role in influencing agonistic behaviour than did past social experience or current social status.
JF - Behaviour
AU - Chibucos, K
AU - Wofford, S J
AU - Moore, P A
AD - Program for Genomics Differentiation, Eunice K. Shiver Institute for Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA, pmoore@bgsu.edu
Y1 - 2015///0,
PY - 2015
DA - 0, 2015
SP - 1063
EP - 1082
PB - Brill Academic Publishers, P.O. Box 9000 Leiden PA 2300 Netherlands
VL - 152
SN - 0005-7959, 0005-7959
KW - Ecology Abstracts; ASFA 1: Biological Sciences & Living Resources; Animal Behavior Abstracts
KW - crayfish
KW - dominance
KW - prior residence
KW - resource ownership
KW - shelter
KW - social status
KW - status reversal
KW - Predation
KW - Cambaridae
KW - Shelter
KW - Freshwater
KW - Agonistic behaviour
KW - Orconectes rusticus
KW - Dominance hierarchies
KW - Social interactions
KW - Dominance
KW - Decision making
KW - Intruder
KW - Freshwater crustaceans
KW - Shelters
KW - Property rights
KW - Territoriality
KW - D 04040:Ecosystem and Ecology Studies
KW - Q1 08604:Stock assessment and management
KW - Y 25070:Learning, Memory, Reinforcement, and Motivation
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1722169703?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aecology&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Behaviour&rft.atitle=Hierarchical+decision+making%3A+resource+distribution+exhibits+stronger+effect+on+crayfish+dominance+relationships+and+shelter+occupation+than+prior+social+experience+and+resource+ownership&rft.au=Chibucos%2C+K%3BWofford%2C+S+J%3BMoore%2C+P+A&rft.aulast=Chibucos&rft.aufirst=K&rft.date=2015-01-01&rft.volume=152&rft.issue=&rft.spage=1063&rft.isbn=&rft.btitle=&rft.title=Behaviour&rft.issn=00057959&rft_id=info:doi/10.1163%2F1568539X-00003292
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-10-01
N1 - Last updated - 2016-12-22
N1 - SubjectsTermNotLitGenreText - Predation; Freshwater crustaceans; Property rights; Shelters; Territoriality; Agonistic behaviour; Dominance hierarchies; Decision making; Intruder; Shelter; Dominance; Social interactions; Cambaridae; Orconectes rusticus; Freshwater
DO - http://dx.doi.org/10.1163/1568539X-00003292
ER -
TY - JOUR
T1 - Genetic and Phenotypic Properties of Vero Cell-Adapted Japanese Encephalitis Virus SA14-14-2 Vaccine Strain Variants and a Recombinant Clone, Which Demonstrates Attenuation and Immunogenicity in Mice
AN - 1722168082; PQ0002059450
AB - The live-attenuated Japanese encephalitis virus CEV) SA14-14-2 vaccine, produced in primary hamster kidney cells, is safe and effective. Past attempts to adapt this virus to replicate in cells that are more favorable for vaccine production resulted in mutations that significantly reduced immunogenicity. In this study, 10 genetically distinct Vero cell-adapted JEV SA14-14-2 variants were isolated and a recombinant wild-type JEV clone, modified to contain the JEV SA14-14-2 polyprotein amino acid sequence, was recovered in Vero cells. A single capsid protein mutation (S66L) was important for Vero cell-adaptation. Mutations were also identified that modulated virus sensitivity to type I interferon-stimulation in Vero cells. A subset of JEV SA14-14-2 variants and the recombinant clone were evaluated in vivo and exhibited levels of attenuation that varied significantly in suckling mice, but were avirulent and highly immunogenic in weanling mice and are promising candidates for the development of a second-generation, recombinant vaccine.
JF - American Journal of Tropical Medicine and Hygiene
AU - Gromowski, Gregory D
AU - Firestone, Cai-Yen
AU - Bustos-Arriaga, Jose
AU - Whitehead, Stephen S
AD - Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, gromowskig@niaid.nih.gov
Y1 - 2015/01//
PY - 2015
DA - January 2015
SP - 98
EP - 107
PB - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States
VL - 92
IS - 1
SN - 0002-9637, 0002-9637
KW - Genetics Abstracts; CSA Neurosciences Abstracts; Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts B: Bacteriology; Immunology Abstracts; Virology & AIDS Abstracts; ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality
KW - Clones
KW - polyproteins
KW - Vero cells
KW - Mutations
KW - Disease control
KW - Suckling behavior
KW - Attenuation
KW - Kidneys
KW - Phenotypes
KW - Encephalitis
KW - Recombinants
KW - Immunogenicity
KW - Kidney
KW - Japanese encephalitis virus
KW - Vaccines
KW - Hygiene
KW - Mutation
KW - Capsid protein
KW - Amino acid sequence
KW - K 03410:Animal Diseases
KW - Q5 08503:Characteristics, behavior and fate
KW - N3 11029:Neurophysiology & biophysics
KW - F 06905:Vaccines
KW - V 22350:Immunology
KW - J 02350:Immunology
KW - Q1 08485:Species interactions: pests and control
KW - G 07730:Development & Cell Cycle
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1722168082?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.atitle=Genetic+and+Phenotypic+Properties+of+Vero+Cell-Adapted+Japanese+Encephalitis+Virus+SA14-14-2+Vaccine+Strain+Variants+and+a+Recombinant+Clone%2C+Which+Demonstrates+Attenuation+and+Immunogenicity+in+Mice&rft.au=Gromowski%2C+Gregory+D%3BFirestone%2C+Cai-Yen%3BBustos-Arriaga%2C+Jose%3BWhitehead%2C+Stephen+S&rft.aulast=Gromowski&rft.aufirst=Gregory&rft.date=2015-01-01&rft.volume=92&rft.issue=1&rft.spage=98&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.14-0427
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-10-01
N1 - Last updated - 2016-10-12
N1 - SubjectsTermNotLitGenreText - Clones; Recombinants; Mutations; Disease control; Attenuation; Kidneys; Vaccines; Hygiene; Phenotypes; polyproteins; Vero cells; Immunogenicity; Kidney; Suckling behavior; Mutation; Encephalitis; Amino acid sequence; Capsid protein; Japanese encephalitis virus
DO - http://dx.doi.org/10.4269/ajtmh.14-0427
ER -
TY - JOUR
T1 - Chondroitin sulfate proteoglycan 4 as a target for chimeric antigen receptor-based T-cell immunotherapy of solid tumors.
AN - 1713527622; 26190756
AB - Proteoglycans are critical molecules involved in multiple physiological cell functions, but also key players in cancer development and progression. In particular, chondroitin sulfate proteoglycan 4 (CSPG4) is recognized as an attractive target for antibody-based approaches because of its high expression on cancer cells in several types of human malignancies and its restricted distribution in normal tissues.
Adoptive transfer of genetically modified T cells is emerging as a powerful therapeutic approach in cancer patients. In this regard, the selection of the appropriate antigen to be targeted in solid tumors becomes a critical aspect in promoting potent antitumor effects while preventing toxicities. This review summarizes the authors' current knowledge on the expression and function of CSPG4 in normal tissues and malignant tumors, with a particular focus on the potential use of CSPG4 as a target for antigen-specificity redirected T cells. T cells expressing a CSPG4-specific chimeric antigen receptor (CAR) offer the possibility to target a broad spectrum of solid tumors for which no curative treatment is currently available. In addition, since CSPG4 is also selectively up-regulated on tumor-associated pericytes, targeting this antigen may also contribute to tumor regression via inhibition of neoangiogenesis. Preclinical experiments to date justify the clinical translation of CSPG4-specific CAR-T cells.
JF - Expert opinion on therapeutic targets
AU - Wang, Yangyang
AU - Geldres, Claudia
AU - Ferrone, Soldano
AU - Dotti, Gianpietro
AD - a 1 Massachusetts General Hospital, Harvard Medical School, Department of Surgery , 55 Fruit Street, Boston, MA 02114, USA Sferrone@MGH.Harvard.edu. ; b 2 National Cancer Institute, Experimental Transplantation and Immunology Branch , Bethesda, MD 20892, USA. ; c 3 University of North Carolina, Lineberger Comprehensive Cancer Center , Chapel Hill, NC, USA gdotti@med.unc.edu.
Y1 - 2015
PY - 2015
DA - 2015
SP - 1339
EP - 1350
VL - 19
IS - 10
KW - Antigens
KW - 0
KW - Proteoglycans
KW - Receptors, Antigen, T-Cell
KW - chondroitin sulfate proteoglycan 4
KW - Index Medicus
KW - T-cell therapies
KW - solid tumors
KW - chimeric antigen receptor
KW - CSPG4
KW - Animals
KW - Humans
KW - Molecular Targeted Therapy
KW - Receptors, Antigen, T-Cell -- immunology
KW - T-Lymphocytes -- immunology
KW - Neoplasms -- pathology
KW - Neoplasms -- therapy
KW - Antigens -- immunology
KW - Proteoglycans -- immunology
KW - Neoplasms -- immunology
KW - Immunotherapy -- methods
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1713527622?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Expert+opinion+on+therapeutic+targets&rft.atitle=Chondroitin+sulfate+proteoglycan+4+as+a+target+for+chimeric+antigen+receptor-based+T-cell+immunotherapy+of+solid+tumors.&rft.au=Wang%2C+Yangyang%3BGeldres%2C+Claudia%3BFerrone%2C+Soldano%3BDotti%2C+Gianpietro&rft.aulast=Wang&rft.aufirst=Yangyang&rft.date=2015-01-01&rft.volume=19&rft.issue=10&rft.spage=1339&rft.isbn=&rft.btitle=&rft.title=Expert+opinion+on+therapeutic+targets&rft.issn=1744-7631&rft_id=info:doi/10.1517%2F14728222.2015.1068759
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2016-05-05
N1 - Date created - 2015-09-16
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1517/14728222.2015.1068759
ER -
TY - JOUR
T1 - The Implementation Road: Engaging Community Partnerships in Evidence-Based Cancer Control Interventions
AN - 1708526700; 2011-842022
AB - Southern rural and underserved counties have high proportions of individuals with increased mortality for cervical and breast cancers. To improve the integration of behavioral research into practice, the dissemination and implementation of efficacious interventions to encourage the use of screening have increased in recent years. This study addressed gaps in the dissemination and implementation of evidence-based interventions with a pilot called Team Up. Qualitative interviews with 24 key individuals in six state-level partnerships explored partnership characteristics that influenced selection and use of evidence-based interventions among low-income, rarely or never screened women. Guided by diffusion of innovations theory and the Lasker and Weiss partnership functioning model, interviews about the intervention centered on (a) knowledge surrounding evidence base; (b) identification, selection, and adoption; (c) planning and adaptation; (d) implementation; and (e) partnership reflections and impact. Using grounded theory and content analysis, data revealed that lack of communication and high partner turnover hindered adoption and adaptation, whereas failure of partnership leaders to engage local stakeholders and lack of sufficient funds hampered implementation. Delivery of evidence-based interventions was more effective when partnerships included local partners in early decision making and when coaches were introduced to facilitate strategic thinking about translating evidence-based interventions into practice. A challenge for public health partnerships was the translation of interventions into successful programs, such that underserved communities benefited from early detection intervention research. [Reprinted by permission of Sage Publications Inc., copyright holder.]
JF - Health Promotion Practice
AU - Breslau, Erica S
AU - Weiss, Elisa S
AU - Williams, Abigail
AU - Burness, Allison
AU - Kepka, Deanna
AD - National Cancer Institute, Bethesda, MD, USA
Y1 - 2015/01//
PY - 2015
DA - January 2015
SP - 46
EP - 54
PB - Sage Publications, Thousand Oaks CA
VL - 16
IS - 1
SN - 1524-8399, 1524-8399
KW - Business and service sector - Business organization and administration
KW - Health conditions and policy - Health and health policy
KW - Population groups, population policy, and demographics - Women
KW - Population groups, population policy, and demographics - Demography and census
KW - Health conditions and policy - Diseases and disorders
KW - Science and technology policy - Technology and technology policy
KW - Social conditions and policy - Communication
KW - cancer prevention and control health disparities health education health promotion partnerships/coalitions program planning and evaluation women's health
KW - Mortality
KW - Partnership
KW - Women
KW - Communication
KW - Diffusion of innovations
KW - Breast cancer
KW - Health policy
KW - Cancer
KW - Public health
KW - article
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1708526700?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Apais&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Health+Promotion+Practice&rft.atitle=The+Implementation+Road%3A+Engaging+Community+Partnerships+in+Evidence-Based+Cancer+Control+Interventions&rft.au=Breslau%2C+Erica+S%3BWeiss%2C+Elisa+S%3BWilliams%2C+Abigail%3BBurness%2C+Allison%3BKepka%2C+Deanna&rft.aulast=Breslau&rft.aufirst=Erica&rft.date=2015-01-01&rft.volume=16&rft.issue=1&rft.spage=46&rft.isbn=&rft.btitle=&rft.title=Health+Promotion+Practice&rft.issn=15248399&rft_id=info:doi/10.1177%2F1524839914528705
LA - English
DB - PAIS Index
N1 - Date revised - 2015-09-01
N1 - Last updated - 2016-09-28
N1 - SubjectsTermNotLitGenreText - Partnership; Public health; Women; Mortality; Breast cancer; Diffusion of innovations; Cancer; Health policy; Communication
DO - http://dx.doi.org/10.1177/1524839914528705
ER -
TY - JOUR
T1 - Combined Analysis of SNP Array Data Identifies Novel CNV Candidates and Pathways in Ependymoma and Mesothelioma
AN - 1701500771; PQ0001772704
AB - Copy number variation is a class of structural genomic modifications that includes the gain and loss of a specific genomic region, which may include an entire gene. Many studies have used low-resolution techniques to identify regions that are frequently lost or amplified in cancer. Usually, researchers choose to use proprietary or non-open-source software to detect these regions because the graphical interface tends to be easier to use. In this study, we combined two different open-source packages into an innovative strategy to identify novel copy number variations and pathways associated with cancer. We used a mesothelioma and ependymoma published datasets to assess our tool. We detected previously described and novel copy number variations that are associated with cancer chemotherapy resistance. We also identified altered pathways associated with these diseases, like cell adhesion in patients with mesothelioma and negative regulation of glutamatergic synaptic transmission in ependymoma patients. In conclusion, we present a novel strategy using open-source software to identify copy number variations and altered pathways associated with cancer.
JF - BioMed Research International
AU - Wajnberg, Gabriel
AU - Carvalho, Benilton S
AU - Ferreira, Carlos G
AU - Passetti, Fabio
AD - Bioinformatics Unit, Clinical Research Coordination, National Cancer Institute of Brazil (INCA), 20231-050 Rio de Janeiro, RJ, Brazil, passetti@fiocruz.br
Y1 - 2015/01//
PY - 2015
DA - Jan 2015
PB - Hindawi Publishing Corporation, P.O. Box 3079 Cuyahoga Falls OH 44223 United States
VL - 2015
SN - 2314-6133, 2314-6133
KW - Biotechnology and Bioengineering Abstracts
KW - Data processing
KW - Chemotherapy
KW - Cancer
KW - copy number
KW - Cell adhesion
KW - Computer programs
KW - software
KW - Glutamatergic transmission
KW - Single-nucleotide polymorphism
KW - mesothelioma
KW - genomics
KW - Synaptic transmission
KW - W 30960:Bioinformatics & Computer Applications
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1701500771?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=Lipid+exhange+at+contact+sites&rft.au=Prinz%2C+Will&rft.aulast=Prinz&rft.aufirst=Will&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-08-01
N1 - Last updated - 2015-11-16
N1 - SubjectsTermNotLitGenreText - Computer programs; Glutamatergic transmission; software; Data processing; Single-nucleotide polymorphism; Chemotherapy; mesothelioma; Synaptic transmission; genomics; Cancer; Cell adhesion; copy number
DO - http://dx.doi.org/10.1155/2015/902419
ER -
TY - JOUR
T1 - The Implementation Road: Engaging Community Partnerships in Evidence-Based Cancer Control Interventions
AN - 1683509130
AB - Southern rural and underserved counties have high proportions of individuals with increased mortality for cervical and breast cancers. To improve the integration of behavioral research into practice, the dissemination and implementation of efficacious interventions to encourage the use of screening have increased in recent years. This study addressed gaps in the dissemination and implementation of evidence-based interventions with a pilot called Team Up. Qualitative interviews with 24 key individuals in six state-level partnerships explored partnership characteristics that influenced selection and use of evidence-based interventions among low-income, rarely or never screened women. Guided by diffusion of innovations theory and the Lasker and Weiss partnership functioning model, interviews about the intervention centered on (a) knowledge surrounding evidence base; (b) identification, selection, and adoption; (c) planning and adaptation; (d) implementation; and (e) partnership reflections and impact. Using grounded theory and content analysis, data revealed that lack of communication and high partner turnover hindered adoption and adaptation, whereas failure of partnership leaders to engage local stakeholders and lack of sufficient funds hampered implementation. Delivery of evidence-based interventions was more effective when partnerships included local partners in early decision making and when coaches were introduced to facilitate strategic thinking about translating evidence-based interventions into practice. A challenge for public health partnerships was the translation of interventions into successful programs, such that underserved communities benefited from early detection intervention research.
JF - Health Promotion Practice
AU - Breslau, Erica S
AU - Weiss, Elisa S
AU - Williams, Abigail
AU - Burness, Allison
AU - Kepka, Deanna
AD - National Cancer Institute, Bethesda, MD, USA ; The Leukemia & Lymphoma Society, White Plains, NY, USA ; Mayor’s Office to Combat Domestic Violence, The City of New York, New York, NY, USA ; National Cancer Institute, Bethesda, MD, USA, MedStar Washington Hospital Center, Washington, DC, USA ; National Cancer Institute, Bethesda, MD, USA, University of Utah, Salt Lake City, UT, USA ; National Cancer Institute, Bethesda, MD, USA
Y1 - 2015/01//
PY - 2015
DA - Jan 2015
SP - 46
EP - 54
CY - Thousand Oaks
PB - SAGE PUBLICATIONS, INC.
VL - 16
IS - 1
SN - 1524-8399
KW - Public Health And Safety
KW - cancer prevention and control
KW - health disparities
KW - health education
KW - health promotion
KW - partnerships/coalitions
KW - program planning and evaluation
KW - women’s health
KW - Adaptation
KW - Breast cancer
KW - Cervical cancer
KW - Early warnings
KW - Evidence based
KW - Evidence based medicine
KW - Funds
KW - Grounded theory
KW - Health education
KW - Identification
KW - Innovations
KW - Interventions
KW - Low income people
KW - Low income women
KW - Mortality
KW - Partnerships
KW - Public health
KW - Public health policy
KW - Rural communities
KW - Screening
KW - Behaviour
KW - Cancer
KW - Coalitions
KW - Communication
KW - Content analysis
KW - Decision making
KW - Detection
KW - Dissemination
KW - Early intervention programmes
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1683509130?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=Imaging+the+molecular+architecture+of+the+plasma+membrane+with+correlative+3D+super+resolution+light+and+electron+microscopy&rft.au=Taraska%2C+Justin&rft.aulast=Taraska&rft.aufirst=Justin&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Date revised - 2015-05-14
N1 - Last updated - 2016-05-13
DO - http://dx.doi.org/10.1177/1524839914528705
ER -
TY - JOUR
T1 - Novel dosing strategies increase exposures of the potent antituberculosis drug rifapentine but are poorly tolerated in healthy volunteers.
AN - 1681266550; 25824215
AB - Rifapentine is a potent antituberculosis drug currently in phase III trials. Bioavailability decreases with increasing dose, yet high daily exposures are likely needed to improve efficacy and shorten the tuberculosis treatment duration. Further, the limits of tolerability are poorly defined. The phase I multicenter trial in healthy adults described here investigated two strategies to increase rifapentine exposures: dividing the dose or giving the drug with a high-fat meal. In arm 1, rifapentine was administered at 10 mg/kg of body weight twice daily and 20 mg/kg once daily, each for 14 days, separated by a 28-day washout; the dosing sequence was randomized. In arm 2, 15 mg/kg rifapentine once daily was given with a high-fat versus a low-fat breakfast. Sampling for pharmacokinetic analysis was performed on days 1 and 14. Population pharmacokinetic analyses were performed. This trial was stopped early for poor tolerability and because of safety concerns. Of 44 subjects, 20 discontinued prematurely; 11 of these discontinued for protocol-defined toxicity (a grade 3 or higher adverse event or grade 2 or higher rifamycin hypersensitivity). Taking rifapentine with a high-fat meal increased the median steady-state area under the concentration-time curve from time zero to 24 h (AUC0-24ss) by 31% (relative standard error, 6%) compared to that obtained when the drug was taken with a low-fat breakfast. Dividing the dose increased exposures substantially (e.g., 38% with 1,500 mg/day). AUC0-24ss was uniformly higher in our study than in recent tuberculosis treatment trials, in which toxicity was rare. In conclusion, two strategies to increase rifapentine exposures, dividing the dose or giving it with a high-fat breakfast, successfully increased exposures, but toxicity was common in healthy adults. The limits of tolerability in patients with tuberculosis remain to be defined. (AIDS Clinical Trials Group study A5311 has been registered at ClinicalTrials.gov under registration no. NCT01574638.).
Copyright © 2015, American Society for Microbiology. All Rights Reserved.
JF - Antimicrobial agents and chemotherapy
AU - Dooley, Kelly E
AU - Savic, Radojka M
AU - Park, Jeong-Gun
AU - Cramer, Yoninah
AU - Hafner, Richard
AU - Hogg, Evelyn
AU - Janik, Jennifer
AU - Marzinke, Mark A
AU - Patterson, Kristine
AU - Benson, Constance A
AU - Hovind, Laura
AU - Dorman, Susan E
AU - Haas, David W
AU - ACTG A5311 Study Team
AD - Johns Hopkins University School of Medicine, Baltimore, Maryland, USA kdooley1@jhmi.edu. ; University of California, San Francisco, California, USA. ; Center for Biostatistics in AIDS Research, Harvard School of Public Health, Boston, Massachusetts, USA. ; Division of AIDS, National Institutes of Health, Bethesda, Maryland, USA. ; Social & Scientific Systems, Inc., Silver Spring, Maryland, USA. ; Frontier Science Foundation, Amherst, New York, USA. ; Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. ; University of North Carolina, Chapel Hill, North Carolina, USA. ; University of California, San Diego, California, USA. ; Vanderbilt University School of Medicine, Nashville, Tennessee, USA. ; ACTG A5311 Study Team
Y1 - 2015
PY - 2015
DA - 2015
SP - 3399
EP - 3405
VL - 59
IS - 6
KW - Antitubercular Agents
KW - 0
KW - Rifampin
KW - VJT6J7R4TR
KW - rifapentine
KW - XJM390A33U
KW - Index Medicus
KW - Young Adult
KW - Drug Administration Schedule
KW - Humans
KW - Adult
KW - Aged
KW - Middle Aged
KW - Healthy Volunteers
KW - Adolescent
KW - Male
KW - Female
KW - Antitubercular Agents -- pharmacokinetics
KW - Rifampin -- analogs & derivatives
KW - Rifampin -- adverse effects
KW - Antitubercular Agents -- administration & dosage
KW - Rifampin -- pharmacokinetics
KW - Rifampin -- administration & dosage
KW - Antitubercular Agents -- adverse effects
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1681266550?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Antimicrobial+agents+and+chemotherapy&rft.atitle=Novel+dosing+strategies+increase+exposures+of+the+potent+antituberculosis+drug+rifapentine+but+are+poorly+tolerated+in+healthy+volunteers.&rft.au=Dooley%2C+Kelly+E%3BSavic%2C+Radojka+M%3BPark%2C+Jeong-Gun%3BCramer%2C+Yoninah%3BHafner%2C+Richard%3BHogg%2C+Evelyn%3BJanik%2C+Jennifer%3BMarzinke%2C+Mark+A%3BPatterson%2C+Kristine%3BBenson%2C+Constance+A%3BHovind%2C+Laura%3BDorman%2C+Susan+E%3BHaas%2C+David+W%3BACTG+A5311+Study+Team&rft.aulast=Dooley&rft.aufirst=Kelly&rft.date=2015-01-01&rft.volume=59&rft.issue=6&rft.spage=3399&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+agents+and+chemotherapy&rft.issn=1098-6596&rft_id=info:doi/10.1128%2FAAC.05128-14
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2016-02-16
N1 - Date created - 2015-05-15
N1 - Date revised - 2017-01-14
N1 - Genetic sequence - NCT01574638; ClinicalTrials.gov
N1 - SuppNotes - Cited By:
Medicine (Baltimore). 1999 Nov;78(6):361-9 [10575418]
Antimicrob Agents Chemother. 2012 Aug;56(8):4331-40 [22664964]
MMWR Morb Mortal Wkly Rep. 2003 Aug 8;52(31):735-9 [12904741]
Rev Infect Dis. 1983 Jul-Aug;5 Suppl 3:S440-50 [6356277]
Clin Pharmacol Ther. 2005 Oct;78(4):342-50 [16198653]
Antimicrob Agents Chemother. 2007 Aug;51(8):2994-6 [17517849]
PLoS Med. 2007 Dec;4(12):e344 [18092886]
Antimicrob Agents Chemother. 2010 Aug;54(8):3390-4 [20516273]
Am J Respir Crit Care Med. 2011 May 1;183(9):1254-61 [21330452]
Int J Tuberc Lung Dis. 2011 Aug;15(8):1133 [21740683]
Antimicrob Agents Chemother. 2011 Sep;55(9):4122-7 [21709081]
J Infect Dis. 2012 Oct 1;206(7):1030-40 [22850121]
Lancet Infect Dis. 2013 Jan;13(1):27-35 [23103177]
Int J Tuberc Lung Dis. 2013 May;17(5):590-6 [23575322]
Antimicrob Agents Chemother. 2014 Jun;58(6):3035-42 [24614383]
Antimicrob Agents Chemother. 2003 Jul;47(7):2118-24 [12821456]
N Engl J Med. 2011 Dec 8;365(23):2155-66 [22150035]
Clin Pharmacol Ther. 2012 May;91(5):881-8 [22472995]
Am J Respir Crit Care Med. 2015 Feb 1;191(3):333-43 [25489785]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1128/AAC.05128-14
ER -
TY - JOUR
T1 - Inositol pyrophosphates: Why so many phosphates?
AN - 1680451541; PQ0001535628
AB - The inositol pyrophosphates (PP-InsPs) are a specialized group of "energetic" signaling molecules found in yeasts, plants and animals. PP-InsPs boast the most crowded three dimensional phosphate arrays found in Nature; multiple phosphates and diphosphates are crammed around the six-carbon, inositol ring. Yet, phosphate esters are also a major energy currency in cells. So the synthesis of PP-InsPs, and the maintenance of their levels in the face of a high rate of ongoing turnover, all requires significant bioenergetic input. What are the particular properties of PP-InsPs that repay this investment of cellular energy? Potential answers to that question are discussed here, against the backdrop of a recent hypothesis that signaling by PP-InsPs is evolutionarily ancient. The latter idea is extended herein, with the proposal that the primordial origins of PP-InsPs is reflected in the apparent lack of isomeric specificity of certain of their actions. Nevertheless, there are other aspects of signaling by these polyphosphates that are more selective for a particular PP-InsP isomer. Consideration of the nature of both specific and non-specific effects of PP-InsPs can help rationalize why such molecules possess so many phosphates.
JF - Advances in Biological Regulation
AU - Shears, Stephen B
AD - Inositol Signaling Group, Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, NIH, DHHS, PO Box 12233, Research Triangle Park, NC 27709, USA, Shears@niehs.nih.gov
Y1 - 2015
PY - 2015
DA - 2015
SP - 203
EP - 216
PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom
VL - 57
SN - 2212-4926, 2212-4926
KW - Biotechnology and Bioengineering Abstracts
KW - Inositol pyrophosphates
KW - Structure
KW - Analogs
KW - Diphosphoinositol polyphosphates
KW - Cell-signaling
KW - Kinase
KW - Phosphorylation
KW - Phosphate
KW - Bioenergetics
KW - Energy
KW - Inositol
KW - polyphosphates
KW - Esters
KW - pyrophosphates
KW - Evolution
KW - Isomers
KW - W 30910:Imaging
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1680451541?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Advances+in+Biological+Regulation&rft.atitle=Inositol+pyrophosphates%3A+Why+so+many+phosphates%3F&rft.au=Shears%2C+Stephen+B&rft.aulast=Shears&rft.aufirst=Stephen&rft.date=2015-01-01&rft.volume=57&rft.issue=&rft.spage=203&rft.isbn=&rft.btitle=&rft.title=Advances+in+Biological+Regulation&rft.issn=22124926&rft_id=info:doi/10.1016%2Fj.jbior.2014.09.015
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-05-01
N1 - Last updated - 2015-11-16
N1 - SubjectsTermNotLitGenreText - Phosphate; Bioenergetics; Energy; polyphosphates; Inositol; Esters; Evolution; pyrophosphates; Isomers
DO - http://dx.doi.org/10.1016/j.jbior.2014.09.015
ER -
TY - JOUR
T1 - Molecular mechanism behind the synergistic activity of diphenylmethyl selenocyanate and Cisplatin against murine tumor model.
AN - 1677894407; 25584690
AB - Various preclinical, clinical and epidemiological studies have already well established the cancer chemopreventive and chemoprotective potential of selenium compounds. In addition to its protective efficacy, recent studies have also proved the abilities of selenium compounds to induce cell death specifically in malignant cells. Therefore, our intention is to improve the therapeutic efficacy of an alkylating agent, cisplatin, by the adjuvant use of an organoselenium compound, diphenylmethyl selenocyanate (DMSE). It was observed that combined treatment decreased the tumor burden significantly through reactive oxygen species generation and modulation of antioxidant and detoxifying enzyme system in tumor cells. These activities ultimately led to significant DNA damage and apoptosis in tumor cells. Study of the molecular pathway disclosed that the adjuvant treatment caused induction of p53, Bax and suppressed Bcl-2 followed by the activation of caspase cascade. Furthermore, a concomitant decrease in cisplatin-induced nephrotoxicity and hematopoietic toxicity by DMSE might also have enhanced the efficacy of cisplatin and provided survival advantage to the host. Results suggested that the combination treatment with DMSE and cisplatin may offer potential therapeutic benefit, and utilization of cisplatin in cancer chemotherapy exempt of its limitations.
JF - Anti-cancer agents in medicinal chemistry
AU - Chakraborty, Pramita
AU - Roy, Somnath Singha
AU - Bhattacharya, Sudin
AD - Department of Cancer Chemoprevention, Chittaranjan National Cancer Institute, 37- S. P. Mukherjee Road, Kolkata-700026, India. sudinb19572004@yahoo.co.in.
Y1 - 2015
PY - 2015
DA - 2015
SP - 501
EP - 510
VL - 15
IS - 4
KW - Antineoplastic Agents
KW - 0
KW - Organoselenium Compounds
KW - Proto-Oncogene Proteins c-bcl-2
KW - Reactive Oxygen Species
KW - Tumor Suppressor Protein p53
KW - diphenylmethyl selenocyanate
KW - Caspases
KW - EC 3.4.22.-
KW - Cisplatin
KW - Q20Q21Q62J
KW - Index Medicus
KW - Reactive Oxygen Species -- metabolism
KW - Animals
KW - Apoptosis
KW - Enzyme Activation
KW - DNA Damage
KW - Proto-Oncogene Proteins c-bcl-2 -- metabolism
KW - Tumor Burden
KW - Mice
KW - Drug Synergism
KW - Tumor Suppressor Protein p53 -- metabolism
KW - Male
KW - Caspases -- metabolism
KW - Organoselenium Compounds -- pharmacology
KW - Cisplatin -- therapeutic use
KW - Organoselenium Compounds -- therapeutic use
KW - Carcinoma, Ehrlich Tumor -- pathology
KW - Carcinoma, Ehrlich Tumor -- drug therapy
KW - Cisplatin -- pharmacology
KW - Antineoplastic Agents -- therapeutic use
KW - Antineoplastic Agents -- pharmacology
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1677894407?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Anti-cancer+agents+in+medicinal+chemistry&rft.atitle=Molecular+mechanism+behind+the+synergistic+activity+of+diphenylmethyl+selenocyanate+and+Cisplatin+against+murine+tumor+model.&rft.au=Chakraborty%2C+Pramita%3BRoy%2C+Somnath+Singha%3BBhattacharya%2C+Sudin&rft.aulast=Chakraborty&rft.aufirst=Pramita&rft.date=2015-01-01&rft.volume=15&rft.issue=4&rft.spage=501&rft.isbn=&rft.btitle=&rft.title=Anti-cancer+agents+in+medicinal+chemistry&rft.issn=1875-5992&rft_id=info:doi/
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-12-21
N1 - Date created - 2015-05-01
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
ER -
TY - JOUR
T1 - Targeting the HIV RNA genome: high-hanging fruit only needs a longer ladder.
AN - 1675876016; 25735922
AB - Small molecules targeting the enzymes responsible for human immunodeficiency virus (HIV) maturation, DNA synthesis and its subsequent chromosomal integration as ribonucleotide-free double-stranded DNA remain the mainstay of combination antiretroviral therapy. For infected individuals harboring drug-susceptible virus, this approach has afforded complete or near-complete viral suppression. However, in the absence of a curative strategy, the predictable emergence of drug-resistant variants requires continued development of improved antiviral strategies, inherent to which is the necessity of identifying novel targets. Regulatory elementsRegulatory elements that mediate transcription, translation, nucleocytoplasmic transport, dimerization, packaging and reverse transcription of the (+) strand RNA genomeRNA genome should now be considered viable targets for small molecule, peptide- and oligonucleotide-based therapeuticsTherapeutics . Where target specificity and cellular penetration and toxicity have been the primary obstacle to successful "macromolecule therapeutics", this chapter summarizes (a) novel approaches targeting RNA motifs whose three-dimensional structure is critical for biological function and consequently may be less prone to resistance-conferring mutations and (b) improved methods for deliveryDelivery .
JF - Current topics in microbiology and immunology
AU - Le Grice, Stuart F J
AD - RT Biochemistry Section, Basic Research Laboratory, National Cancer Institute, Frederick, MD, 21702, USA, legrices@mail.nih.gov.
Y1 - 2015
PY - 2015
DA - 2015
SP - 147
EP - 169
VL - 389
SN - 0070-217X, 0070-217X
KW - Anti-HIV Agents
KW - 0
KW - DNA, Viral
KW - RNA, Viral
KW - Viral Proteins
KW - Index Medicus
KW - Virus Assembly
KW - HIV Long Terminal Repeat
KW - DNA, Viral -- biosynthesis
KW - Virus Replication -- drug effects
KW - Active Transport, Cell Nucleus -- drug effects
KW - Humans
KW - Viral Proteins -- biosynthesis
KW - Reverse Transcription -- drug effects
KW - Genome, Viral -- drug effects
KW - Anti-HIV Agents -- pharmacology
KW - RNA, Viral -- drug effects
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Current+topics+in+microbiology+and+immunology&rft.atitle=Targeting+the+HIV+RNA+genome%3A+high-hanging+fruit+only+needs+a+longer+ladder.&rft.au=Le+Grice%2C+Stuart+F+J&rft.aulast=Le+Grice&rft.aufirst=Stuart+F&rft.date=2015-01-01&rft.volume=389&rft.issue=&rft.spage=147&rft.isbn=&rft.btitle=&rft.title=Current+topics+in+microbiology+and+immunology&rft.issn=0070217X&rft_id=info:doi/10.1007%2F82_2015_434
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-07-09
N1 - Date created - 2015-04-23
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1007/82_2015_434
ER -
TY - JOUR
T1 - Is Visual Registration Equivalent to Semiautomated Registration in Prostate Biopsy?
AN - 1668253471; PQ0001292482
AB - In magnetic resonance iimaging- (MRI-) ultrasound (US) guided biopsy, suspicious lesions are identified on MRI, registered on US, and targeted during biopsy. The registration can be performed either by a human operator (visual registration) or by fusion software. Previous studies showed that software registration is fairly accurate in locating suspicious lesions and helps to improve the cancer detection rate. Here, the performance of visual registration was examined for ability to locate suspicious lesions defined on MRI. This study consists of 45 patients. Two operators with differing levels of experience (<1 and 18 years) performed visual registration. The overall spatial difference by the two operators in 72 measurements was 10.6 plus or minus 6.0 mm. Each operator showed a spatial difference of 9.4 plus or minus 5.1 mm (experienced; 39 lesions) and 12.1 plus or minus 6.6 mm (inexperienced; 33 lesions), respectively. In a head-to-head comparison of the same 16 lesions from 12 patients, the spatial differences were 9.7 mm plus or minus 4.9 mm (experienced) and 13.4 mm plus or minus 7.4 mm (inexperienced). There were significant differences between the two operators (unpaired, P value = 0.042; paired, P value = 0.044). The substantial differences by the two operators suggest that visual registration could improperly and inaccurately target many tumors, thereby potentially leading to missed diagnosis or false characterization on pathology.
JF - BioMed Research International
AU - Kwak, Jin Tae
AU - Hong, Cheng William
AU - Pinto, Peter A
AU - Williams, Molly
AU - Xu, Sheng
AU - Kruecker, Jochen
AU - Yan, Pingkun
AU - Turkbey, Baris
AU - Choyke, Peter L
AU - Wood, Bradford J
AD - Center for Interventional Oncology, National Institutes of Health Clinical Center, Bethesda, MD 20892, USA, bwood@cc.nih.gov
Y1 - 2015/01//
PY - 2015
DA - Jan 2015
PB - Hindawi Publishing Corporation, P.O. Box 3079 Cuyahoga Falls OH 44223 United States
VL - 2015
SN - 2314-6133, 2314-6133
KW - Biotechnology and Bioengineering Abstracts
KW - Computer programs
KW - software
KW - Magnetic resonance imaging
KW - Biopsy
KW - N.M.R.
KW - Tumors
KW - Ultrasound
KW - Prostate
KW - Cancer
KW - W 30910:Imaging
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1668253471?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BioMed+Research+International&rft.atitle=Is+Visual+Registration+Equivalent+to+Semiautomated+Registration+in+Prostate+Biopsy%3F&rft.au=Kwak%2C+Jin+Tae%3BHong%2C+Cheng+William%3BPinto%2C+Peter+A%3BWilliams%2C+Molly%3BXu%2C+Sheng%3BKruecker%2C+Jochen%3BYan%2C+Pingkun%3BTurkbey%2C+Baris%3BChoyke%2C+Peter+L%3BWood%2C+Bradford+J&rft.aulast=Kwak&rft.aufirst=Jin&rft.date=2015-01-01&rft.volume=2015&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=BioMed+Research+International&rft.issn=23146133&rft_id=info:doi/10.1155%2F2015%2F394742
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-03-01
N1 - Last updated - 2015-11-16
N1 - SubjectsTermNotLitGenreText - Computer programs; software; Magnetic resonance imaging; N.M.R.; Biopsy; Tumors; Prostate; Ultrasound; Cancer
DO - http://dx.doi.org/10.1155/2015/394742
ER -
TY - JOUR
T1 - Measuring Outcome Expectancy Value of Leisure-Time Physical Activity for African Americans
AN - 1665150732
AB - A scale was adapted from existing scales to measure the outcome expectancy value (EV) as one of contributory factors to leisure-time physical activity (LTPA) and was administered to 649 African American adults. The eligible participants (N = 569) for the analysis were split into three subsamples (rate = 0.5 : 0.25 : 0.25) respectively for Exploratory Factor Analysis (N = 285) and cross-validation (N = 142 for the calibration group and N = 142 for the validation group) to evaluate the psychometric properties of the scale. Item analysis of the scale provided adequate psychometric properties. The 2-factor solution with positive and negative outcome EV subscales was supported based on the exploratory factor analysis and the multiple-group confirmatory factor analysis for both the calibration and validation samples. The results support the factorial construct validity and criterion validity of the outcome EV scale applied to assess LTPA in a sample of church-going African Americans.
JF - Behavioral Medicine
AU - Li, Kaigang
AU - Seo, Dong-Chul
AU - Torabi, Mohammad R
AD - National Institute of Child Health and Human Development, Ewha Womans University, College of Health Sciences, Indiana University School of Public Health-Bloomington ; National Institute of Child Health and Human Development; Ewha Womans University, College of Health Sciences; Indiana University School of Public Health-Bloomington
Y1 - 2015/01//
PY - 2015
DA - Jan 2015
SP - 33
EP - 39
CY - Washington
PB - Taylor & Francis Ltd.
VL - 41
IS - 1
SN - 0896-4289
KW - Psychology
KW - American people
KW - Analysis
KW - Leisure activities
KW - Time use
KW - Black American people
KW - Confirmatory factor analysis
KW - Construct validity
KW - Exploratory factor analysis
KW - Factor analysis
KW - Leisure
KW - Physical activity
KW - Psychometric properties
KW - Validation
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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:
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Curr Hematol Malig Rep. 2012 Sep;7(3):241-7 [22833351]
Clin Cancer Res. 2012 Nov 1;18(21):5845-9 [22962441]
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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:
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Comment In:
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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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1002/em.21892
ER -
TY - JOUR
T1 - Withdrawal from long-term methamphetamine self-administration 'normalizes' neurometabolites in rhesus monkeys: a super(1)H MR spectroscopy study
AN - 1647024729; 21213421
AB - super(1)H magnetic resonance spectroscopy has demonstrated alterations in several neurometabolites in methamphetamine (METH)-dependent individuals in brain regions implicated in addiction. Yet, it is unclear whether these neurochemicals return to homeostatic levels after an individual abstains from drug use, a difficult question to address due to high recidivism and poor study retention in human subjects. We thus utilized a non-human primate model of addiction to explore the effects of long-term drug exposure and withdrawal on brain neurochemistry. Ten rhesus macaque monkeys on an active METH self-administration protocol (average use 4.6 plus or minus 0.8 years, average daily intake between 0.4 and 1.2mg/kg) and 10 age- and sex-matched drug-naive controls (CONT) served as subjects. Concentrations of several neurochemicals were evaluated at several timepoints following withdrawal from drug availability (10 monkeys at 1 week and 1 and 3 months, and 6 monkeys at 6 and 12 months; CONT examined at one timepoint). At 1 week following METH withdrawal, we found increases in myo-inositol in anterior cingulate cortex in the METH group relative to CONT. These alterations showed a linear pattern of decreased levels ('normalization') by 1 year of abstinence. We also found decreases in glutamine and Glx (composed mainly of glutamate and glutamine) in the caudate-putamen of the same animals at early withdrawal that showed a similar linear pattern of increasing concentration by 1 year. These results demonstrate that despite protracted, long-term use, neurochemical changes seen following long-term drug administration do not persist following prolonged abstinence, suggesting therapeutic effects of long-term withdrawal from drug use.
JF - Addiction Biology
AU - Yang, Shaolin
AU - Belcher, Annabelle M
AU - Chefer, Svetlana
AU - Vaupel, DBruce
AU - Schindler, Charles W
AU - Stein, Elliot A
AU - Yang, Yihong
AD - Neuroimaging Research Branch, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD, USA.
Y1 - 2015/01//
PY - 2015
DA - Jan 2015
SP - 69
EP - 79
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 20
IS - 1
SN - 1355-6215, 1355-6215
KW - Toxicology Abstracts; CSA Neurosciences Abstracts
KW - Glutamine
KW - Caudate-putamen
KW - Withdrawal
KW - Brain
KW - Neurochemistry
KW - Drug abuse
KW - Primates
KW - Cortex (cingulate)
KW - Methamphetamine
KW - Magnetic resonance spectroscopy
KW - Self-administration
KW - Macaca mulatta
KW - Addiction
KW - Glutamic acid
KW - X 24380:Social Poisons & Drug Abuse
KW - N3 11001:Behavioral and Cognitive Neuroscience
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647024729?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Addiction+Biology&rft.atitle=Withdrawal+from+long-term+methamphetamine+self-administration+%27normalizes%27+neurometabolites+in+rhesus+monkeys%3A+a+super%281%29H+MR+spectroscopy+study&rft.au=Yang%2C+Shaolin%3BBelcher%2C+Annabelle+M%3BChefer%2C+Svetlana%3BVaupel%2C+DBruce%3BSchindler%2C+Charles+W%3BStein%2C+Elliot+A%3BYang%2C+Yihong&rft.aulast=Yang&rft.aufirst=Shaolin&rft.date=2015-01-01&rft.volume=20&rft.issue=1&rft.spage=69&rft.isbn=&rft.btitle=&rft.title=Addiction+Biology&rft.issn=13556215&rft_id=info:doi/10.1111%2Fadb.12078
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-01-01
N1 - Last updated - 2015-11-16
N1 - SubjectsTermNotLitGenreText - Methamphetamine; Glutamine; Caudate-putamen; Magnetic resonance spectroscopy; Withdrawal; Brain; Self-administration; Neurochemistry; Glutamic acid; Addiction; Drug abuse; Cortex (cingulate); Macaca mulatta; Primates
DO - http://dx.doi.org/10.1111/adb.12078
ER -
TY - JOUR
T1 - OdoCapsule: Next-Generation Wireless Capsule Endoscopy With Accurate Lesion Localization and Video Stabilization Capabilities
AN - 1647020562; 21210091
AB - In this paper, we propose a platform to achieve accurate localization of small-bowel lesions and endoscopic video stabilization in wireless capsule endoscopy. Current research modules rely on the use of external magnetic fields and triangulation methods to calculate the position vector of the capsule, leading to considerable error margins. Our platform, entitled OdoCapsule (a synthesis of the words Odometer and Capsule), provides real-time distance information from the point of duodenal entry to the point of exit from the small bowel. To achieve this, OdoCapsule is equipped with three miniature legs. Each leg carries a soft rubber wheel, which is made with human-compliant material. These legs are extendable and retractable thanks to a micromotor and three custom-made torsion springs. The wheels are specifically designed to function as microodometers: each rotation they perform is registered. Hence, the covered distance is measured accurately in real time. Furthermore, with its legs fully extended, OdoCapsule can stabilize itself inside the small-bowel lumen thus offering smoother video capture and better image processing. Recent ex vivo testing of this concept, using porcine small bowel and a commercially available (custom-modified) capsule endoscope, has proved its viability.
JF - IEEE Transactions on Biomedical Engineering
AU - Karargyris, Alexandros
AU - Koulaouzidis, Anastastios
AD - , National Library of Medicine National Institutes of Health, Bethesda, MD, USA
Y1 - 2015/01//
PY - 2015
DA - Jan 2015
SP - 352
EP - 360
PB - Institute of Electrical and Electronics Engineers, Inc., 345 E. 47th St. NY NY 10017-2394 United States
VL - 62
IS - 1
SN - 0018-9294, 0018-9294
KW - Biotechnology and Bioengineering Abstracts
KW - Leg
KW - Magnetic fields
KW - Intestine
KW - Rubber
KW - Image processing
KW - Endoscopes
KW - Endoscopy
KW - W 30905:Medical Applications
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647020562?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=IEEE+Transactions+on+Biomedical+Engineering&rft.atitle=OdoCapsule%3A+Next-Generation+Wireless+Capsule+Endoscopy+With+Accurate+Lesion+Localization+and+Video+Stabilization+Capabilities&rft.au=Karargyris%2C+Alexandros%3BKoulaouzidis%2C+Anastastios&rft.aulast=Karargyris&rft.aufirst=Alexandros&rft.date=2015-01-01&rft.volume=62&rft.issue=1&rft.spage=352&rft.isbn=&rft.btitle=&rft.title=IEEE+Transactions+on+Biomedical+Engineering&rft.issn=00189294&rft_id=info:doi/10.1109%2FTBME.2014.2352493
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-01-01
N1 - Last updated - 2015-11-16
N1 - SubjectsTermNotLitGenreText - Leg; Magnetic fields; Intestine; Image processing; Rubber; Endoscopes; Endoscopy
DO - http://dx.doi.org/10.1109/TBME.2014.2352493
ER -
TY - JOUR
T1 - Insecticide Residues in Soil, Water, and Eggplant Fruits and Farmers' Health Effects Due to Exposure to Pesticides
AN - 1647008143; 21314194
AB - Objectives: Eggplant (Solanum melongena L.) is an important vegetable crop that is widely cultivated in the tropical and subtropical areas in Asia. Globally, the top three eggplant producers are China, India, and Egypt. The Philippines has been one of the top 10 eggplant-producing countries based on area planted and crop productivity. This study aims to describe the insecticide residues found in soil, water, and eggplant fruits in eggplant farms in Sta. Maria, Pangasinan. Methods: The study design is a cross sectional of randomly selected eggplant farms in Sta. Maria, Pangasinan. Soil, water, and eggplant fruits were collected and subjected to gas chromatography (Shimadzu) analysis for multi-pesticide residues. Results: Farmers from Sta. Maria, Pangasinan were found to be applying a broad spectrum of insecticides on their eggplant crop. Soil samples from 11 (about 42 %) out of the 26 farms tested positive for insecticide residues, six of which from four farms exceeded the acceptable maximum residue limit. These residues were profenofos, triazophos, chlorpyrifos, cypermethrin, and malathion. No insecticide residues were detected from water samples taken from the 26 farms. Cypermethrin and chlorpyrifos were the insecticide residues detected in eggplant fruit samples. A maximum of 20 % of the eggplant samples tested positive for insecticide residues. In the eggplant fruit study, all farmers have been using Prevathon super( registered ) for 24 years at a rate of 10 ml/application, and Malathion super( registered ) for 25 years at about 16.5 ml/application, respectively equivalent to 0.24 liter-years and 0.413 liter-years of exposure. Similarly, to the findings in the soil and water study, although Brodan super( registered ) and Magnum super( registered ) were not prevalently applied, the farmers' liter-years of exposure to these insecticides, and their active ingredients, were highest at about 18.92 and 10.0, respectively. The farmers and farm workers in the soil and water study reported experiencing itchiness of the skin (63.8 %), redness of the eyes (29.3 %), muscle pains (27.6 %), and headaches (27.6 %), as being related to their pesticide exposure. Conclusion: In summary, a maximum of 20 % of the eggplant samples tested positive for insecticide residues at any one stage of sampling done. The farmers and farm workers also reported of pesticide-related illnesses but none of them sought any medical attention. Intervention to reduce the farmers' pesticide exposure can focus on the risk factors identified, primarily the toxicity of pesticides used, the unsafe application practices, and the adverse health effects of pesticide exposure.
JF - Environmental Health and Preventive Medicine
AU - Del Prado-Lu, Jinky Leilanie
AD - Institute of Health Policy and Development Studies, National Institutes of Health, University of the Philippines Manila, NIH Bldg, P. Gil St., UP Manila, Taft Avenue, 1100, Manila, Philippines, jinky_lu@yahoo.com
Y1 - 2015/01//
PY - 2015
DA - January 2015
SP - 53
EP - 62
PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL - 20
IS - 1
SN - 1342-078X, 1342-078X
KW - Toxicology Abstracts; Risk Abstracts; Pollution Abstracts; Health & Safety Science Abstracts
KW - Philippines
KW - Fruits
KW - Egypt, Arab Rep.
KW - Vegetables
KW - Farms
KW - Water sampling
KW - Intervention
KW - Solanum melongena
KW - Crops
KW - Malathion
KW - India
KW - Soil
KW - Workers
KW - triazophos
KW - Insecticides
KW - Gas chromatography
KW - Risk factors
KW - Headache
KW - Sampling
KW - Occupational exposure
KW - Residues
KW - Cypermethrin
KW - Muscles
KW - Insecticide residues
KW - Toxicity
KW - Chlorpyrifos
KW - Pesticides
KW - China, People's Rep.
KW - H 5000:Pesticides
KW - P 2000:FRESHWATER POLLUTION
KW - R2 23060:Medical and environmental health
KW - X 24330:Agrochemicals
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=Neurogenetic+insights+into+organelle+biogenesis&rft.au=Blackstone%2C+Craig&rft.aulast=Blackstone&rft.aufirst=Craig&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-01-01
N1 - Number of references - 44
N1 - Last updated - 2016-08-03
N1 - SubjectsTermNotLitGenreText - Fruits; Vegetables; Farms; Cypermethrin; Muscles; Toxicity; Malathion; Crops; Soil; Chlorpyrifos; Workers; triazophos; Insecticides; Gas chromatography; Risk factors; Pesticides; Headache; Sampling; Occupational exposure; Water sampling; Residues; Intervention; Insecticide residues; Solanum melongena; Philippines; Egypt, Arab Rep.; China, People's Rep.; India
DO - http://dx.doi.org/10.1007/s12199-014-0425-3
ER -
TY - JOUR
T1 - Design of self-assembling peptide hydrogelators amenable to bacterial expression
AN - 1647006236; 21286534
AB - Hydrogels formed from self-assembling peptides are finding use in tissue engineering and drug delivery applications. Given the notorious difficulties associated with producing self-assembling peptides by recombinant expression, most are typically prepared by chemical synthesis. Herein, we report the design of a family of self-assembling beta -hairpin peptides amenable to efficient production using an optimized bacterial expression system. Expressing peptides, EX1, EX2 and EX3 contain identical eight-residue amphiphilic beta -strands connected by varying turn sequences that are responsible for ensuring chain reversal and the proper intramolecular folding and consequent self-assembly of the peptide into a hydrogel network under physiological conditions. EX1 was initially used to establish and optimize the bacterial expression system by which all the peptides could be eventually individually expressed. Expression clones were designed to allow exploration of possible fusion partners and investigate both enzymatic and chemical cleavage as means to liberate the target peptide. A systematic analysis of possible expression systems followed by fermentation optimization lead to a system in which all three peptides could be expressed as fusions with BAD-BH3, the BH3 domain of the proapoptotic BAD (Bcl-2 Associated Death) Protein. CNBr cleavage followed by purification afforded 50, 31, and 15 mg/L yields of pure EX1, EX2 and EX3, respectively. CD spectroscopy, TEM, and rheological analysis indicate that these peptides fold and assembled into well-defined fibrils that constitute hydrogels having shear-thin/recovery properties.
JF - Biomaterials
AU - Sonmez, Cem
AU - Nagy, Katelyn J
AU - Schneider, Joel P
AD - National Cancer Institute, Center for Cancer Research, Frederick, MD 21701, United States
Y1 - 2015/01//
PY - 2015
DA - Jan 2015
SP - 62
EP - 72
PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom
VL - 37
SN - 0142-9612, 0142-9612
KW - Microbiology Abstracts B: Bacteriology; Biotechnology and Bioengineering Abstracts
KW - Hydrogel
KW - Peptide
KW - Assembly
KW - Expression
KW - Injectable
KW - Bacteria
KW - Drug delivery
KW - Apoptosis
KW - hydrogels
KW - Fermentation
KW - Self-assembly
KW - Bcl-2 protein
KW - Tissue engineering
KW - Spectroscopy
KW - Fibrils
KW - J 02310:Genetics & Taxonomy
KW - W 30920:Tissue Engineering
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biomaterials&rft.atitle=Design+of+self-assembling+peptide+hydrogelators+amenable+to+bacterial+expression&rft.au=Sonmez%2C+Cem%3BNagy%2C+Katelyn+J%3BSchneider%2C+Joel+P&rft.aulast=Sonmez&rft.aufirst=Cem&rft.date=2015-01-01&rft.volume=37&rft.issue=&rft.spage=62&rft.isbn=&rft.btitle=&rft.title=Biomaterials&rft.issn=01429612&rft_id=info:doi/10.1016%2Fj.biomaterials.2014.10.011
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-01-01
N1 - Last updated - 2015-11-16
N1 - SubjectsTermNotLitGenreText - Drug delivery; Apoptosis; hydrogels; Fermentation; Self-assembly; Bcl-2 protein; Spectroscopy; Tissue engineering; Fibrils; Bacteria
DO - http://dx.doi.org/10.1016/j.biomaterials.2014.10.011
ER -
TY - JOUR
T1 - The design of covalent allosteric drugs.
AN - 1643407497; 25149918
AB - A key issue in drug discovery is how to reduce drug dosage and increase specificity while retaining or increasing efficacy, as high dosage is often linked to toxicity. There are two types of drugs on the market: orthosteric and allosteric. Orthosteric drugs can be noncovalent or covalent. The latter are advantageous because they may be prescribed in lower doses, but their potential off-target toxicity is a primary concern. The chief advantages of allosteric drugs are their higher specificity and their consequently lower chance of toxic side effects. Covalent allosteric drugs combine the pharmacological merits of covalent drugs with the additional benefit of the higher specificity of allosteric drugs. In a recent promising step in therapeutic drug development, allosteric, disulfide-tethered fragments successfully modulated the activity of a protein kinase and K-Ras.
JF - Annual review of pharmacology and toxicology
AU - Nussinov, Ruth
AU - Tsai, Chung-Jung
AD - Cancer and Inflammation Program, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, National Cancer Institute, Frederick, Maryland 21702; email: NussinoR@helix.nih.gov.
Y1 - 2015
PY - 2015
DA - 2015
SP - 249
EP - 267
VL - 55
KW - Enzyme Activators
KW - 0
KW - Enzyme Inhibitors
KW - Index Medicus
KW - allosteric drug discovery
KW - toxicity
KW - antagonist
KW - allosteric modulator
KW - agonist
KW - pharmacology
KW - Molecular Structure
KW - Animals
KW - Models, Molecular
KW - Humans
KW - Drug-Related Side Effects and Adverse Reactions -- etiology
KW - Protein Binding
KW - Structure-Activity Relationship
KW - Binding Sites
KW - Kinetics
KW - Signal Transduction -- drug effects
KW - Allosteric Regulation
KW - Computer-Aided Design
KW - Drug-Related Side Effects and Adverse Reactions -- prevention & control
KW - Protein Conformation
KW - Enzyme Inhibitors -- adverse effects
KW - Enzyme Activators -- chemistry
KW - Enzyme Inhibitors -- chemistry
KW - Enzyme Inhibitors -- pharmacology
KW - Enzyme Activators -- adverse effects
KW - Enzyme Activators -- pharmacology
KW - Drug Design
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-09-09
N1 - Date created - 2015-01-07
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1146/annurev-pharmtox-010814-124401
ER -
TY - JOUR
T1 - Free radical generation from an aniline derivative in HepG2 cells: a possible captodative effect.
AN - 1641016976; 25450331
AB - Xenobiotic metabolism can induce the generation of protein radicals, which are believed to play an important role in the toxicity of chemicals and drugs. It is therefore important to identify chemical structures capable of inducing macromolecular free radical formation in living cells. In this study, we evaluated the ability of four structurally related environmental chemicals, aniline, nitrosobenzene, N,N-dimethylaniline, and N,N-dimethyl-4-nitrosoaniline (DMNA), to induce free radicals and cellular damage in the hepatoma cell line HepG2. Cytotoxicity was assessed using lactate dehydrogenase assays, and morphological changes were observed using phase contrast microscopy. Protein free radicals were detected by immuno-spin trapping using in-cell western experiments and confocal microscopy to determine the subcellular locale of free radical generation. DMNA induced free radical generation, lactate dehydrogenase release, and morphological changes in HepG2 cells, whereas aniline, nitrosobenzene, N,N-dimethylaniline did not. Confocal microscopy showed that DMNA induced free radical generation mainly in the cytosol. Preincubation of HepG2 cells with N-acetylcysteine and 2,2'-dipyridyl significantly prevented free radical generation on subsequent incubation with DMNA, whereas preincubation with apocynin and dimethyl sulfoxide had no effect. These results suggest that DMNA is metabolized to reactive free radicals capable of generating protein radicals which may play a critical role in DMNA toxicity. We propose that the captodative effect, the combined action of the electron-releasing dimethylamine substituent, and the electron-withdrawing nitroso substituent, leads to a thermodynamically stabilized radical, facilitating enhanced protein radical formation by DMNA. Copyright © 2014 Elsevier Inc. All rights reserved.
JF - Free radical biology & medicine
AU - Horinouchi, Yuya
AU - Summers, Fiona A
AU - Ehrenshaft, Marilyn
AU - Mason, Ronald P
AD - Free Radical Metabolism Group, Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. Electronic address: yuya.h@basic.med.tokushima-u.ac.jp. ; Free Radical Metabolism Group, Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. Electronic address: summersfa@niehs.nih.gov. ; Free Radical Metabolism Group, Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. Electronic address: ehrensh1@niehs.nih.gov. ; Free Radical Metabolism Group, Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. Electronic address: mason4@niehs.nih.gov.
Y1 - 2015/01//
PY - 2015
DA - January 2015
SP - 111
EP - 117
VL - 78
KW - Aniline Compounds
KW - 0
KW - Carcinogens
KW - Free Radical Scavengers
KW - Free Radicals
KW - Nitroso Compounds
KW - 4-nitrosodimethylaniline
KW - 138-89-6
KW - N,N-dimethylaniline
KW - 7426719369
KW - L-Lactate Dehydrogenase
KW - EC 1.1.1.27
KW - aniline
KW - SIR7XX2F1K
KW - nitrosobenzene
KW - ZI9W9E8G2Z
KW - Index Medicus
KW - Cytotoxicity
KW - Immuno-spin trapping
KW - Confocal microscopy
KW - In-cell western
KW - Environmental chemicals
KW - Captodative effect
KW - Microscopy, Confocal
KW - Carcinogens -- pharmacology
KW - Blotting, Western
KW - Spin Trapping
KW - Hep G2 Cells
KW - Humans
KW - Electron Spin Resonance Spectroscopy
KW - L-Lactate Dehydrogenase -- metabolism
KW - Cell Proliferation -- drug effects
KW - Aniline Compounds -- pharmacology
KW - Nitroso Compounds -- pharmacology
KW - Free Radicals -- metabolism
KW - Free Radical Scavengers -- pharmacology
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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:
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BMC Biotechnol. 2012;12:59 [22953695]
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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]
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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
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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
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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
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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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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]
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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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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]
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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]
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Nature. 1993 Nov 25;366(6453):324-7 [8247126]
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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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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:
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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
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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
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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
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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
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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:
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CA Cancer J Clin. 2011 Mar-Apr;61(2):69-90 [21296855]
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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
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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
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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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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:
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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]
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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]
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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]
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MAbs. 2009 Mar-Apr;1(2):163-71 [20061826]
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Blood. 2010 Nov 11;116(19):3705-14 [20610811]
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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]
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Curr Opin Chem Biol. 2009 Jun;13(3):235-44 [19414278]
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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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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]
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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
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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]
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Brain Res Brain Res Protoc. 2000 Feb;5(1):109-14 [10719272]
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Exp Neurol. 1976 Feb;50(2):330-6 [1248554]
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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]
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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
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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
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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]
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Cancer Res. 2001 Feb 1;61(3):1013-21 [11221827]
Cancer Res. 2004 Aug 15;64(16):5760-6 [15313917]
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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
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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
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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
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T1 - Myosin II pulls the nucleus forward to increase intracellular pressure and drive 3D cell movement
T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB)
AN - 1647638818; 6328120
JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB)
AU - Petrie, R
AU - Koo, H
AU - Yamada, K
Y1 - 2014/12/06/
PY - 2014
DA - 2014 Dec 06
KW - Myosin
KW - Cell migration
KW - Pressure
KW - Nuclei
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T1 - Biomedical PhD career development trends: implications for workforce development and diversity
T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB)
AN - 1647638813; 6327718
JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB)
AU - Gibbs Jr, Kenneth
Y1 - 2014/12/06/
PY - 2014
DA - 2014 Dec 06
KW - Species diversity
KW - Careers
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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
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T1 - Cytoskeletal dynamics, adhesion, and imaging
T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB)
AN - 1647638801; 6327888
JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB)
AU - Waterman, Clare
Y1 - 2014/12/06/
PY - 2014
DA - 2014 Dec 06
KW - Cytoskeleton
KW - Adhesion
KW - Imaging techniques
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T1 - Your career: strategy or luck of the draw
T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB)
AN - 1647638778; 6327992
JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB)
AU - Misteli, Tom
Y1 - 2014/12/06/
PY - 2014
DA - 2014 Dec 06
KW - Careers
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T1 - PINK1 is a ubiquitin kinase
T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB)
AN - 1647638763; 6328137
JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB)
AU - Kane, L
AU - Lazarou, M
AU - Fogel, A
AU - Li, Y.
AU - Yamano, K
AU - Sarraf, S
AU - Banerjee, S
AU - Youle, R
Y1 - 2014/12/06/
PY - 2014
DA - 2014 Dec 06
KW - PTEN-induced putative kinase
KW - Ubiquitin
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N1 - Date revised - 2014-12-31
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T1 - Transcriptional regulation by noncoding RNA dissected with single-molecule observation in living cells
T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB)
AN - 1647638711; 6327809
JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB)
AU - Larson, Daniel
Y1 - 2014/12/06/
PY - 2014
DA - 2014 Dec 06
KW - RNA
KW - Gene regulation
KW - Transcription
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N1 - Date revised - 2014-12-31
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T1 - Organelle biogenesis: insights from the hereditary spastic paraplegias
T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB)
AN - 1647638686; 6328069
JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB)
AU - Blackstone, Craig
Y1 - 2014/12/06/
PY - 2014
DA - 2014 Dec 06
KW - Hereditary spastic paraplegia
KW - Biogenesis
KW - Organelles
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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
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N1 - Date revised - 2014-12-31
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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
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N1 - Date revised - 2014-12-31
N1 - Last updated - 2015-01-23
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T1 - iPALM and FRET reveal the mechanism of vinculin activation and nano-scale spatial organization in focal adhesions
T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB)
AN - 1647638521; 6328016
JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB)
AU - Case, L
AU - Baird, M
AU - Shtengel, G
AU - Campbell, S
AU - Hess, H
AU - Davidson, M
AU - Waterman, C
Y1 - 2014/12/06/
PY - 2014
DA - 2014 Dec 06
KW - vinculin
KW - fluorescence resonance energy transfer
KW - Adhesion
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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
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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
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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
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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
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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
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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
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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
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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
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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
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N1 - Date revised - 2014-12-31
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T1 - A mitochondria-specific isoform of the actin nucleating Spire protein regulates mitochondrial dynamics
T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB)
AN - 1647635546; 6327733
JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB)
AU - Manor, Uri
Y1 - 2014/12/06/
PY - 2014
DA - 2014 Dec 06
KW - Mitochondria
KW - Actin
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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
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N1 - Date revised - 2014-12-31
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T1 - Imaging the molecular architecture of the plasma membrane with correlative 3D super resolution light and electron microscopy
T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB)
AN - 1647635478; 6327816
JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB)
AU - Taraska, Justin
Y1 - 2014/12/06/
PY - 2014
DA - 2014 Dec 06
KW - Plasma membranes
KW - Imaging techniques
KW - Electron microscopy
KW - Light effects
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N1 - Date revised - 2014-12-31
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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
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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
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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
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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
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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
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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
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N1 - Date revised - 2014-12-31
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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
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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
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N1 - Date revised - 2014-12-31
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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
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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
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DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-12-31
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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
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DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-12-31
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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
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DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-12-31
N1 - Last updated - 2015-01-23
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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
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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
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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
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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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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:
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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
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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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Research&rft.atitle=CD47+in+the+Tumor+Microenvironment+Limits+Cooperation+between+Antitumor+T-cell+Immunity+and+Radiotherapy&rft.au=Soto-Pantoja%2C+David+R%3BTerabe%2C+Masaki%3BGhosh%2C+Arunima%3BRidnour%2C+Lisa+A%3BDeGraff%2C+William+G%3BWink%2C+David+A%3BBerzofsky%2C+Jay+A%3BRoberts%2C+David+D&rft.aulast=Soto-Pantoja&rft.aufirst=David&rft.date=2014-12-01&rft.volume=74&rft.issue=23&rft.spage=6771&rft.isbn=&rft.btitle=&rft.title=Cancer+Research&rft.issn=00085472&rft_id=info:doi/10.1158%2F0008-5472.CAN-14-0037-T
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2016-08-01
N1 - Last updated - 2016-10-26
N1 - SubjectsTermNotLitGenreText - Fibrosarcoma; Radiotherapy; CD8 antigen; Tumors; Toxicity; Tumor cells; Cancer; Effector cells; Melanoma; Metastases; granzyme B; Cytotoxicity; Radiation; Immunosurveillance; Radioprotection; Adoptive transfer; Lymphocytes T; Microenvironments; Radiosensitivity
DO - http://dx.doi.org/10.1158/0008-5472.CAN-14-0037-T
ER -
TY - JOUR
T1 - Phase II Clinical Trial of Amatuximab, a Chimeric Antimesothelin Antibody with Pemetrexed and Cisplatin in Advanced Unresectable Pleural Mesothelioma
AN - 1808642784; PQ0003457449
AB - Purpose: Amatuximab is a chimeric monoclonal antibody to mesothelin, a cell surface glycoprotein highly expressed in malignant pleural mesothelioma (MPM). On the basis of its synergy with chemotherapy in preclinical studies, we evaluated the antitumor activity of amatuximab plus pemetrexed and cisplatin in patients with unresectable MPM.Experimental Design: In a single-arm phase II study, amatuximab (5 mg/kg) was administered on days 1 and 8 with pemetrexed (500 mg/m2) and cisplatin (75 mg/m2) on day 1 of 21-day cycles for up to six cycles. Patients with response or stable disease received amatuximab maintenance until disease progression. Primary endpoint was progression-free survival (PFS) at 6 months. Secondary endpoints were overall survival (OS), response rate, and safety.Results: Eighty-nine patients were enrolled at 26 centers. Median of five cycles (range, 1-6) of combination treatment was administered, and 56 (63%) patients received amatuximab maintenance. Combination therapy resulted in no overlapping toxicities. Eleven patients (12.4%) had amatuximab-related hypersensitivity reactions. Responses included partial responses in 33 (40%) and stable disease in 42 (51%). Six-month PFS rate was 51% [95% confidence interval (CI), 39.1-62.3)], median PFS was 6.1 months (95% CI, 5.8-6.4), and median OS was 14.8 months (95% CI, 12.4-18.5) with 29 patients alive at data cut-off.Conclusions: Amatuximab with pemetrexed and cisplatin was well tolerated with objective tumor response or stable disease rate of 90% by independent radiologic review. Although PFS was not significantly different from historical controls, the median OS was 14.8 months with a third of patients alive and 5 continuing to receive amatuximab at the time of analysis. Clin Cancer Res; 20(23); 5927-36. copyright 2014 AACR.
JF - Clinical Cancer Research
AU - Hassan, Raffit
AU - Kindler, Hedy L
AU - Jahan, Thierry
AU - Bazhenova, Lyudmila
AU - Reck, Martin
AU - Thomas, Anish
AU - Pastan, Ira
AU - Parno, Jeff
AU - O'Shannessy, Daniel J
AU - Fatato, Penny
AU - Maltzman, Julia D
AU - Wallin, Bruce A
AD - Thoracic and GI Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, hassanr@mail.nih.gov
Y1 - 2014/12/01/
PY - 2014
DA - 2014 Dec 01
SP - 5927
EP - 5936
PB - American Association for Cancer Research, 615 Chestnut St., 17th Floor Philadelphia PA 19106-4404 United States
VL - 20
IS - 23
SN - 1078-0432, 1078-0432
KW - Biotechnology and Bioengineering Abstracts
KW - Cell surface
KW - Data processing
KW - Monoclonal antibodies
KW - Chemotherapy
KW - Survival
KW - Tumors
KW - Toxicity
KW - Clinical trials
KW - Cancer
KW - Hypersensitivity
KW - Cisplatin
KW - mesothelioma
KW - Glycoproteins
KW - Antitumor activity
KW - W 30915:Pharmaceuticals & Vaccines
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808642784?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+Cancer+Research&rft.atitle=Phase+II+Clinical+Trial+of+Amatuximab%2C+a+Chimeric+Antimesothelin+Antibody+with+Pemetrexed+and+Cisplatin+in+Advanced+Unresectable+Pleural+Mesothelioma&rft.au=Hassan%2C+Raffit%3BKindler%2C+Hedy+L%3BJahan%2C+Thierry%3BBazhenova%2C+Lyudmila%3BReck%2C+Martin%3BThomas%2C+Anish%3BPastan%2C+Ira%3BParno%2C+Jeff%3BO%27Shannessy%2C+Daniel+J%3BFatato%2C+Penny%3BMaltzman%2C+Julia+D%3BWallin%2C+Bruce+A&rft.aulast=Hassan&rft.aufirst=Raffit&rft.date=2014-12-01&rft.volume=20&rft.issue=23&rft.spage=5927&rft.isbn=&rft.btitle=&rft.title=Clinical+Cancer+Research&rft.issn=10780432&rft_id=info:doi/10.1158%2F1078-0432.CCR-14-0804
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2016-07-01
N1 - Last updated - 2016-08-17
N1 - SubjectsTermNotLitGenreText - Cell surface; Data processing; Monoclonal antibodies; Chemotherapy; Survival; Toxicity; Tumors; Clinical trials; Cancer; Hypersensitivity; Cisplatin; mesothelioma; Glycoproteins; Antitumor activity
DO - http://dx.doi.org/10.1158/1078-0432.CCR-14-0804
ER -
TY - JOUR
T1 - Perceptions of cancer as a death sentence: Prevalence and consequences
AN - 1683509645
AB - Research suggests that perceiving cancer as a death sentence is a critical determinant of health care–seeking behaviors. However, there is limited information regarding the prevalence of this perception in the US population. Cross-sectional analysis of data (n = 7674 adults) from the 2007-2008 administration of the nationally representative Health Information National Trends Survey (HINTS 3) was performed. A majority (61.6%) of respondents perceived cancer as death sentence, and more than one-third (36%) of respondents reported that they avoid seeing their physicians. In the adult US population, perceiving cancer as a death sentence is common and is associated with education level and avoidance of physicians.
JF - Journal of Health Psychology
AU - Moser, Richard P
AU - Arndt, Jamie
AU - Han, Paul K
AU - Waters, Erika A
AU - Amsellem, Marni
AU - Hesse, Bradford W
AD - National Cancer Institute, USA ; University of Missouri, USA ; Maine Medical Center, USA ; Washington University School of Medicine, USA ; National Cancer Institute, SAIC-Frederick, USA ; National Cancer Institute, USA
Y1 - 2014/12//
PY - 2014
DA - Dec 2014
SP - 1518
EP - 1524
CY - London
PB - SAGE PUBLICATIONS, INC.
VL - 19
IS - 12
SN - 1359-1053
KW - Psychology
KW - cancer
KW - health behavior
KW - health psychology
KW - perception
KW - public health psychology
KW - Avoidance
KW - Mental health services
KW - Cancer
KW - Death
KW - Doctors
KW - Health behaviour
KW - Health care
KW - Health information
KW - Health psychology
KW - Perceptions
KW - United States--US
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1683509645?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Health+Psychology&rft.atitle=Perceptions+of+cancer+as+a+death+sentence%3A+Prevalence+and+consequences&rft.au=Moser%2C+Richard+P%3BArndt%2C+Jamie%3BHan%2C+Paul+K%3BWaters%2C+Erika+A%3BAmsellem%2C+Marni%3BHesse%2C+Bradford+W&rft.aulast=Moser&rft.aufirst=Richard&rft.date=2014-12-01&rft.volume=19&rft.issue=12&rft.spage=1518&rft.isbn=&rft.btitle=&rft.title=Journal+of+Health+Psychology&rft.issn=13591053&rft_id=info:doi/10.1177%2F1359105313494924
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Date revised - 2015-05-19
N1 - Last updated - 2016-05-13
N1 - SubjectsTermNotLitGenreText - United States--US
DO - http://dx.doi.org/10.1177/1359105313494924
ER -
TY - JOUR
T1 - NAG-1/GDF-15 prevents obesity by increasing thermogenesis, lipolysis and oxidative metabolism
AN - 1680442107; PQ0001187868
AB - Objective: Obesity is a major health problem associated with high morbidity and mortality. NSAID-activated gene (NAG-1) is a TGF- beta superfamily member reported to alter adipose tissue levels in mice. We investigated whether hNAG-1 acts as a regulator of adiposity and energy metabolism.Design/Subjects:hNAG-1 mice, ubiquitously expressing hNAG-1, were placed on a control or high-fat diet for 12 weeks. hNAG-1-expressing B16/F10 melanoma cells were used in a xenograft model to deliver hNAG-1 to obese C57BL/6 mice. Results: As compared with wild-type littermates, transgenic hNAG-1 mice have less white fat and brown fat despite equivalent food intake, improved glucose tolerance, lower insulin levels and are resistant to dietary- and genetic-induced obesity. hNAG-1 mice are more metabolically active with higher energy expenditure. Obese C57BL/6 mice treated with hNAG-1-expressing xenografts show decreases in adipose tissue and serum insulin levels. hNAG-1 mice and obese mice treated with hNAG-1-expressing xenografts show increased thermogenic gene expression (UCP1, PGC1 alpha , ECH1, Cox8b, Dio2, Cyc1, PGC1 beta , PPAR alpha , Elvol3) in brown adipose tissue (BAT) and increased expression of lipolytic genes (Adrb3, ATGL, HSL) in both white adipose tissue (WAT) and BAT, consistent with higher energy metabolism. Conclusion: hNAG-1 modulates metabolic activity by increasing the expression of key thermogenic and lipolytic genes in BAT and WAT. hNAG-1 appears to be a novel therapeutic target in preventing and treating obesity and insulin resistance.
JF - International Journal of Obesity
AU - Chrysovergis, K
AU - Wang, X
AU - Kosak, J
AU - Lee, S-H
AU - Kim, J S
AU - Foley, J F
AU - Travlos, G
AU - Singh, S
AU - Baek, S J
AU - Eling, T E
AD - Laboratory of Molecular Carcinogenesis, NIEHS, NIH, Research Triangle Park, NC, USA
Y1 - 2014/12//
PY - 2014
DA - Dec 2014
SP - 1555
EP - 1564
PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL - 38
IS - 12
SN - 0307-0565, 0307-0565
KW - Physical Education Index
KW - Obesity
KW - Animal subjects
KW - Objectives
KW - Fats
KW - Football (American)
KW - Diet
KW - Hormones
KW - Metabolism
KW - Professional sports
KW - PE 030:Exercise, Health & Physical Fitness
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1680442107?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aphysicaleducation&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Obesity&rft.atitle=NAG-1%2FGDF-15+prevents+obesity+by+increasing+thermogenesis%2C+lipolysis+and+oxidative+metabolism&rft.au=Chrysovergis%2C+K%3BWang%2C+X%3BKosak%2C+J%3BLee%2C+S-H%3BKim%2C+J+S%3BFoley%2C+J+F%3BTravlos%2C+G%3BSingh%2C+S%3BBaek%2C+S+J%3BEling%2C+T+E&rft.aulast=Chrysovergis&rft.aufirst=K&rft.date=2014-12-01&rft.volume=38&rft.issue=12&rft.spage=1555&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Obesity&rft.issn=03070565&rft_id=info:doi/10.1038%2Fijo.2014.27
LA - English
DB - Physical Education Index
N1 - Date revised - 2015-05-01
N1 - Last updated - 2015-11-16
N1 - SubjectsTermNotLitGenreText - Obesity; Objectives; Animal subjects; Football (American); Fats; Diet; Hormones; Professional sports; Metabolism
DO - http://dx.doi.org/10.1038/ijo.2014.27
ER -
TY - JOUR
T1 - Regulatory Forum Opinion Piece*: New Testing Paradigms for Reproductive and Developmental Toxicity-The NTP Modified One Generation Study and OECD 443
AN - 1680437041; PQ0001532683
AB - The National Toxicology Program (NTP) has developed a new flexible study design, termed the modified one generation (MOG) reproduction study. The MOG study will encompass measurements of developmental and reproductive toxicity parameters as well as enable the setting of appropriate dose levels for a cancer bioassay through evaluation of target organ toxicity that is based on test article exposure that starts during gestation. This study design is compared and contrasted with the new Organization for Economic Co-operation and Development (OECD) 443 test guideline, the extended one generation reproduction study. The MOG study has a number of advantages, with a focus on F1 animals, the generation of adequately powered, robust data sets that include both pre and postnatal developmental toxicity information, and the measurement of effects on reproductive structure and function in the same animals. This new study design does not employ the use of internal triggers in the design structure for the use of animals already on test and is also consistent with the principles of the 3R's.
JF - Toxicologic Pathology
AU - Foster, Paul MD
AD - Division of the National Toxicology Program, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA, foster2@niehs.nih.gov
Y1 - 2014/12//
PY - 2014
DA - December 2014
SP - 1165
EP - 1167
PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom
VL - 42
IS - 8
SN - 0192-6233, 0192-6233
KW - Toxicology Abstracts
KW - developmental pathology
KW - endocrine disrupters
KW - female reproduction
KW - male reproduction
KW - reproductive system
KW - safety assessment.
KW - Data processing
KW - Structure-function relationships
KW - Economics
KW - Gestation
KW - Oligodendrocyte-myelin glycoprotein
KW - Reproduction
KW - Toxicity
KW - Cancer
KW - X 24300:Methods
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1680437041?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+Pathology&rft.atitle=Regulatory+Forum+Opinion+Piece*%3A+New+Testing+Paradigms+for+Reproductive+and+Developmental+Toxicity-The+NTP+Modified+One+Generation+Study+and+OECD+443&rft.au=Foster%2C+Paul+MD&rft.aulast=Foster&rft.aufirst=Paul&rft.date=2014-12-01&rft.volume=42&rft.issue=8&rft.spage=1165&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F0192623314534920
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-05-01
N1 - Number of references - 6
N1 - Last updated - 2016-08-03
N1 - SubjectsTermNotLitGenreText - Data processing; Structure-function relationships; Gestation; Economics; Reproduction; Oligodendrocyte-myelin glycoprotein; Toxicity; Cancer
DO - http://dx.doi.org/10.1177/0192623314534920
ER -
TY - JOUR
T1 - Comparative Uterotrophic Effects of Endoxifen and Tamoxifen in Ovariectomized Sprague-Dawley Rats
AN - 1680436314; PQ0001532676
AB - Endoxifen (4-hydroxy-N-desmethyl-tamoxifen), one of the major active metabolites of tamoxifen, has substantially greater estrogen antagonist properties and antiproliferative effects in breast tumor cells than tamoxifen, a mixed estrogen agonist/antagonist. An associated risk of endometrial cancer and hyperplasia has been linked to the estrogen agonist properties of tamoxifen. We evaluated endoxifen using a classic uterotrophic effects method. Rats were given endoxifen or tamoxifen orally for 3 days. Estradiol was the positive control. Endoxifen and tamoxifen plasma levels exceeded those previously observed clinically. Uterine weight was 3-fold higher in the estradiol group than in the tamoxifen or endoxifen groups, which did not differ from vehicle controls. Tamoxifen and endoxifen caused a greater increase in luminal epithelial cell height than estradiol. Both tamoxifen and endoxifen produced an increase in the stromal BrdU labeling index (LI) that was less than or equal to estradiol and inversely related to dose, but did not affect luminal epithelial cell BrdU LI. As expected, estradiol increased luminal epithelial cell proliferation. These results indicate that endoxifen induces uterotrophic effects, but is less potent than estradiol in eliciting these effects. Given prior preclinical observations that endoxifen has superior antitumor activity than tamoxifen, the observations of similar uterine effects suggest that the endoxifen risk/benefit ratio may be superior to tamoxifen.
JF - Toxicologic Pathology
AU - Schweikart, Karen M
AU - Eldridge, Sandy R
AU - Safgren, Stephanie L
AU - Parman, Toufan
AU - Reid, Joel M
AU - Ames, Matthew M
AU - Goetz, Matthew P
AU - Davis, Myrtle A
AD - Developmental Therapeutics Program, National Cancer Institute, Bethesda, Maryland, USA, schweikk@mail.nih.gov
Y1 - 2014/12//
PY - 2014
DA - December 2014
SP - 1188
EP - 1196
PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom
VL - 42
IS - 8
SN - 0192-6233, 0192-6233
KW - Toxicology Abstracts
KW - endoxifen
KW - tamoxifen
KW - endometrial cell proliferation.
KW - Epithelial cells
KW - Endometrium
KW - Uterus
KW - Estrogens
KW - Metabolites
KW - Tumor cells
KW - Tamoxifen
KW - Cancer
KW - Estradiol
KW - Plasma levels
KW - Hyperplasia
KW - Ovariectomy
KW - Menopause
KW - Antitumor activity
KW - X 24310:Pharmaceuticals
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1680436314?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+Pathology&rft.atitle=Comparative+Uterotrophic+Effects+of+Endoxifen+and+Tamoxifen+in+Ovariectomized+Sprague-Dawley+Rats&rft.au=Schweikart%2C+Karen+M%3BEldridge%2C+Sandy+R%3BSafgren%2C+Stephanie+L%3BParman%2C+Toufan%3BReid%2C+Joel+M%3BAmes%2C+Matthew+M%3BGoetz%2C+Matthew+P%3BDavis%2C+Myrtle+A&rft.aulast=Schweikart&rft.aufirst=Karen&rft.date=2014-12-01&rft.volume=42&rft.issue=8&rft.spage=1188&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F0192623314525688
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-05-01
N1 - Number of references - 38
N1 - Last updated - 2016-02-04
N1 - SubjectsTermNotLitGenreText - Epithelial cells; Estrogens; Uterus; Endometrium; Metabolites; Tamoxifen; Tumor cells; Estradiol; Cancer; Hyperplasia; Plasma levels; Ovariectomy; Menopause; Antitumor activity
DO - http://dx.doi.org/10.1177/0192623314525688
ER -
TY - JOUR
T1 - Cognitive problems among breast cancer survivors: loneliness enhances risk
AN - 1665162336
AB - Background Cancer survivors often experience cognitive difficulties after treatment completion. Although chemotherapy enhances risk for cognitive problems, it is likely only one piece of a complex puzzle that explains survivorsʼ cognitive functioning. Loneliness may be one psychosocial risk factor. The current studies included both subjective and objective cognitive measures and tested whether lonelier breast cancer survivors would have more concentration and memory complaints and experience more concentration difficulties than their less lonely counterparts. Methods The relationship between loneliness and cognitive function was tested among three samples of breast cancer survivors. Study 1 was a sample of breast cancer survivors ( n=200) who reported their concentration and memory problems. Study 2a was a sample of breast cancer survivors ( n=185) and noncancer controls ( n=93) who reported their concentration and memory problems. Study 2b was a subsample of Study 2a breast cancer survivors ( n=22) and noncancer controls ( n=21) who completed a standardized neuropsychological test assessing concentration. Results Studies 1 and 2a revealed that lonelier women reported more concentration and memory problems than less lonely women. Study 2b utilized a standardized neuropsychological continuous performance test and demonstrated that lonelier women experienced more concentration problems than their less lonely counterparts. Conclusions These studies demonstrated that loneliness is linked to concentration and memory complaints and the experience of concentration problems among breast cancer survivors. The results were also highly consistent across three samples of breast cancer survivors. These data suggest that loneliness may be a risk factor for cognitive difficulties among cancer survivors. Copyright © 2014 John Wiley & Sons, Ltd.
JF - Psycho-Oncology
AU - Jaremka, Lisa M
AU - Peng, Juan
AU - Bornstein, Robert
AU - Alfano, Catherine M
AU - Andridge, Rebecca R
AU - Povoski, Stephen P
AU - Lipari, Adele M
AU - Agnese, Doreen M
AU - Farrar, William B
AU - Yee, Lisa D
AU - Carson, William E
AU - Kiecolt-Glaser, Janice K
AD - Institute for Behavioral Medicine Research, The Ohio State University College of Medicine, Columbus, OH, USA. ; Institute for Behavioral Medicine Research, The Ohio State University College of Medicine, Columbus, OH, USA., College of Public Health, The Ohio State University College of Medicine, Columbus, OH, USA. ; Department of Psychiatry, The Ohio State University College of Medicine, Columbus, OH, USA. ; National Cancer Institute, Bethesda, MD, USA. ; College of Public Health, The Ohio State University College of Medicine, Columbus, OH, USA. ; Comprehensive Cancer Center, The Ohio State University College of Medicine, Columbus, OH, USA., Department of Surgery, The Ohio State University College of Medicine, Columbus, OH, USA. ; Institute for Behavioral Medicine Research, The Ohio State University College of Medicine, Columbus, OH, USA., Department of Psychiatry, The Ohio State University College of Medicine, Columbus, OH, USA., Comprehensive Cancer Center, The Ohio State University College of Medicine, Columbus, OH, USA. ; Institute for Behavioral Medicine Research, The Ohio State University College of Medicine, Columbus, OH, USA.
Y1 - 2014/12//
PY - 2014
DA - Dec 2014
SP - 1356
EP - 1364
CY - Chichester
PB - Wiley Subscription Services, Inc.
VL - 23
IS - 12
SN - 1057-9249
KW - Medical Sciences--Psychiatry And Neurology
KW - Breast cancer
KW - Cancer
KW - Chemotherapy
KW - Clinical outcomes
KW - Cognitive functioning
KW - Complaints
KW - Concentration
KW - Continuous performance tasks
KW - Loneliness
KW - Memory
KW - Psychosocial factors
KW - Survivors
KW - Women
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665162336?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Psycho-Oncology&rft.atitle=Cognitive+problems+among+breast+cancer+survivors%3A+loneliness+enhances+risk&rft.au=Jaremka%2C+Lisa+M%3BPeng%2C+Juan%3BBornstein%2C+Robert%3BAlfano%2C+Catherine+M%3BAndridge%2C+Rebecca+R%3BPovoski%2C+Stephen+P%3BLipari%2C+Adele+M%3BAgnese%2C+Doreen+M%3BFarrar%2C+William+B%3BYee%2C+Lisa+D%3BCarson%2C+William+E%3BKiecolt-Glaser%2C+Janice+K&rft.aulast=Jaremka&rft.aufirst=Lisa&rft.date=2014-12-01&rft.volume=23&rft.issue=12&rft.spage=1356&rft.isbn=&rft.btitle=&rft.title=Psycho-Oncology&rft.issn=10579249&rft_id=info:doi/10.1002%2Fpon.3544
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Date revised - 2015-01-09
N1 - Last updated - 2016-08-16
DO - http://dx.doi.org/10.1002/pon.3544
ER -
TY - JOUR
T1 - Disparities in Health Care Access and Receipt of Preventive Services by Disability Type: Analysis of the Medical Expenditure Panel Survey
AN - 1665151201
AB - OBJECTIVE: To examine differences in access to health care and receipt of clinical preventive services by type of disability among working-age adults with disabilities. DATA SOURCE: Secondary analysis of Medical Expenditure Panel Survey (MEPS) data from 2002 to 2008. STUDY DESIGN: We conducted cross-sectional logistic regression analyses comparing people with different types of disabilities on health insurance status and type; presence of a usual source of health care; delayed or forgone care; and receipt of dental checkups and cancer screening. DATA COLLECTION: We pooled annualized MEPS data files across years. Our analytic sample consisted of adults (18-64 years) with physical, sensory, or cognitive disabilities and nonmissing data for all variables of interest. PRINCIPAL FINDINGS: Individuals with hearing impairment had better health care access and receipt than people with other disability types. People with multiple types of limitations were especially likely to have health care access problems and unmet health care needs. CONCLUSIONS: There are differences in health care access and receipt of preventive care depending on what type of disability people have. More in-depth research is needed to identify specific causes of these disparities and assess interventions to address health care barriers for particular disability groups.
JF - Health Services Research
AU - Horner‐Johnson, Willi
AU - Dobbertin, Konrad
AU - Lee, Jae Chul
AU - Andresen, Elena M
AD - Institute on Development and Disability. Oregon Health and Science University ; Rehabilitation Medicine Department, Clinical Research Center. National Institutes of Health ; Institute on Development and Disability. Oregon Health and Science University
Y1 - 2014/12//
PY - 2014
DA - Dec 2014
SP - 1980
EP - 1999
CY - Chicago
PB - Wiley Subscription Services, Inc.
VL - 49
IS - 6
SN - 0017-9124
KW - Medical Sciences
KW - Disability
KW - Analysis
KW - Cancer
KW - Delayed
KW - Health costs
KW - Health insurance
KW - Health status
KW - Hearing
KW - Hearing impairment
KW - Insurance
KW - Interventions
KW - Learning disabled people
KW - Screening
KW - Service provision
KW - Unmet needs
KW - Expenditure
KW - Health care
KW - Health inequalities
KW - Preventive health care
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665151201?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Health+Services+Research&rft.atitle=Disparities+in+Health+Care+Access+and+Receipt+of+Preventive+Services+by+Disability+Type%3A+Analysis+of+the+Medical+Expenditure+Panel+Survey&rft.au=Horner%E2%80%90Johnson%2C+Willi%3BDobbertin%2C+Konrad%3BLee%2C+Jae+Chul%3BAndresen%2C+Elena+M&rft.aulast=Horner%E2%80%90Johnson&rft.aufirst=Willi&rft.date=2014-12-01&rft.volume=49&rft.issue=6&rft.spage=1980&rft.isbn=&rft.btitle=&rft.title=Health+Services+Research&rft.issn=00179124&rft_id=info:doi/10.1111%2F1475-6773.12195
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Date revised - 2015-01-09
N1 - Last updated - 2016-05-25
DO - http://dx.doi.org/10.1111/1475-6773.12195
ER -
TY - JOUR
T1 - Characterizing the Factor Structure of Parent Reported Executive Function in Autism Spectrum Disorders: The Impact of Cognitive Inflexibility
AN - 1665151191
AB - Parents of children with autism spectrum disorders (ASD) consistently report executive functioning (EF) deficits. This study investigates the factor structure of the Behavior Rating Inventory of Executive Function (BRIEF) as reported by parents of children with ASD and typically developing children (TDC). BRIEFs for 411 children with ASD and 467 TDC were examined. Confirmatory factor analysis of a nine-factor model met thresholds for goodness-of-fit in TDC, but not in the ASD sample. We found globally elevated EF problems in the ASD sample, especially on the Shift scale. These findings confirm that children with ASD exhibit significant EF deficits. Further investigation is needed to understand the pervasive nature of cognitive inflexibility in children with ASD.
JF - Journal of Autism and Developmental Disorders
AU - Granader, Yael
AU - Wallace, Gregory L
AU - Hardy, Kristina K
AU - Yerys, Benjamin E
AU - Lawson, Rachel A
AU - Rosenthal, Michael
AU - Wills, Meagan C
AU - Dixon, Eunice
AU - Pandey, Juhi
AU - Penna, Rebecca
AU - Schultz, Robert T
AU - Kenworthy, Lauren
AD - Children’s National Medical Center, 15245 Shady Grove Road, Suite 350, Rockville, MD, 20850, USA ygranade@childrensnational.org ygranade@childrensnational.org ygranade@childrensnational.org ygranade@childrensnational.org ygranade@childrensnational.org; Laboratory of Brain and Cognition, National Institute of Mental Health, Bethesda, MD, USA, Department of Speech and Hearing Sciences, George Washington University, Washington, DC, USA ; Center for Autism Research, Children’s Hospital of Philadelphia and the University of Pennsylvania, Philadelphia, PA, USA ; Children’s National Medical Center, 15245 Shady Grove Road, Suite 350, Rockville, MD, 20850, USA, Loyola University Maryland, Baltimore, MD, USA ; Laboratory of Brain and Cognition, National Institute of Mental Health, Bethesda, MD, USA ; Children’s National Medical Center, 15245 Shady Grove Road, Suite 350, Rockville, MD, 20850, USA
Y1 - 2014/12//
PY - 2014
DA - Dec 2014
SP - 3056
EP - 3062
CY - New York
PB - Springer Science & Business Media
VL - 44
IS - 12
SN - 0162-3257
KW - Children And Youth - About
KW - Autism
KW - Autistic children
KW - Autistic spectrum disorders
KW - Children
KW - Confirmatory factor analysis
KW - Executive function
KW - Factor analysis
KW - Parents
KW - Thresholds
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665151191?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Autism+and+Developmental+Disorders&rft.atitle=Characterizing+the+Factor+Structure+of+Parent+Reported+Executive+Function+in+Autism+Spectrum+Disorders%3A+The+Impact+of+Cognitive+Inflexibility&rft.au=Granader%2C+Yael%3BWallace%2C+Gregory+L%3BHardy%2C+Kristina+K%3BYerys%2C+Benjamin+E%3BLawson%2C+Rachel+A%3BRosenthal%2C+Michael%3BWills%2C+Meagan+C%3BDixon%2C+Eunice%3BPandey%2C+Juhi%3BPenna%2C+Rebecca%3BSchultz%2C+Robert+T%3BKenworthy%2C+Lauren&rft.aulast=Granader&rft.aufirst=Yael&rft.date=2014-12-01&rft.volume=44&rft.issue=12&rft.spage=3056&rft.isbn=&rft.btitle=&rft.title=Journal+of+Autism+and+Developmental+Disorders&rft.issn=01623257&rft_id=info:doi/10.1007%2Fs10803-014-2169-8
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Date revised - 2015-01-09
N1 - Last updated - 2016-05-12
DO - http://dx.doi.org/10.1007/s10803-014-2169-8
ER -
TY - JOUR
T1 - Pathways between acculturation and health behaviors among residents of low-income housing: the mediating role of social and contextual factors
AN - 1660032497; 4650083
AB - Acculturation may influence health behaviors, yet mechanisms underlying its effect are not well understood. In this study, we describe relationships between acculturation and health behaviors among low-income housing residents, and examine whether these relationships are mediated by social and contextual factors. Residents of 20 low-income housing sites in the Boston metropolitan area completed surveys that assessed acculturative characteristics, social/contextual factors, and health behaviors. A composite acculturation scale was developed using latent class analysis, resulting in four distinct acculturative groups. Path analysis was used to examine interrelationships between acculturation, health behaviors, and social/contextual factors, specifically self-reported social ties, social support, stress, material hardship, and discrimination. Of the 828 respondents, 69% were born outside of the U.S. Less acculturated groups exhibited healthier dietary practices and were less likely to smoke than more acculturated groups. Acculturation had a direct effect on diet and smoking, but not physical activity. Acculturation also showed an indirect effect on diet through its relationship with material hardship. Our finding that material hardship mediated the relationship between acculturation and diet suggests the need to explicate the significant role of financial resources in interventions seeking to promote healthy diets among low-income immigrant groups. Future research should examine these social and contextual mediators using larger, population-based samples, preferably with longitudinal data. All rights reserved, Elsevier
JF - Social science and medicine
AU - Stoddard, Anne M
AU - Tamers, Sara
AU - Tucker-Seeley, Reginald D
AU - Sorensen, Glorian C
AU - Allen, Jennifer Dacey
AU - Caspi, Caitlin
AU - Yang, May
AU - Leyva, Bryan
AD - DanaFarber Cancer Institute ; University of Minnesota ; New England Research Institutes ; National Cancer Institute
Y1 - 2014/12//
PY - 2014
DA - Dec 2014
SP - 26
EP - 36
VL - 123
SN - 0277-9536, 0277-9536
KW - Sociology
KW - Smoking
KW - Acculturation
KW - Social support
KW - Immigrants
KW - Social housing
KW - U.S.A.
KW - Low income
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660032497?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Social+science+and+medicine&rft.atitle=Pathways+between+acculturation+and+health+behaviors+among+residents+of+low-income+housing%3A+the+mediating+role+of+social+and+contextual+factors&rft.au=Stoddard%2C+Anne+M%3BTamers%2C+Sara%3BTucker-Seeley%2C+Reginald+D%3BSorensen%2C+Glorian+C%3BAllen%2C+Jennifer+Dacey%3BCaspi%2C+Caitlin%3BYang%2C+May%3BLeyva%2C+Bryan&rft.aulast=Stoddard&rft.aufirst=Anne&rft.date=2014-12-01&rft.volume=123&rft.issue=&rft.spage=26&rft.isbn=&rft.btitle=&rft.title=Social+science+and+medicine&rft.issn=02779536&rft_id=info:doi/10.1016%2Fj.socscimed.2014.10.034
LA - English
DB - International Bibliography of the Social Sciences (IBSS)
N1 - Date revised - 2015-03-02
N1 - Last updated - 2015-03-03
N1 - SubjectsTermNotLitGenreText - 539 3105 3198; 6232 8037; 11847 6045 5706; 11755 5707 6071 1542 11325; 7553 6271; 11938 11949 13521; 433 293 14
DO - http://dx.doi.org/10.1016/j.socscimed.2014.10.034
ER -
TY - JOUR
T1 - Beyond cry and laugh: Toward a multilevel model of language production
AN - 1660012673; 201501622
AB - Language production is a multilevel phenomenon, and human capacities to communicate vocally progress from early forms, based on projections of motor cortex to brainstem nuclei, to complex elaborations, mediated by high-order cognition and fostered by socially mediated feedback. Adapted from the source document
JF - Behavioral and Brain Sciences
AU - Bornstein, Marc H
AU - Esposito, Gianluca
AD - Child and Family Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Rockledge I, Bethesda, MD 20892-7971, USA. Marc_H_Bornstein@nih.gov
Y1 - 2014/12//
PY - 2014
DA - December 2014
SP - 548
EP - 549
VL - 37
IS - 6
SN - 0140-525X, 0140-525X
KW - Cognitive Processes (12950)
KW - Humans (32796)
KW - Communication (13600)
KW - Neurolinguistics (57250)
KW - Brain (09350)
KW - Social Factors (79910)
KW - article
KW - 4018: psycholinguistics; neurolinguistics
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660012673?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Allba&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Behavioral+and+Brain+Sciences&rft.atitle=Beyond+cry+and+laugh%3A+Toward+a+multilevel+model+of+language+production&rft.au=Bornstein%2C+Marc+H%3BEsposito%2C+Gianluca&rft.aulast=Bornstein&rft.aufirst=Marc&rft.date=2014-12-01&rft.volume=37&rft.issue=6&rft.spage=548&rft.isbn=&rft.btitle=&rft.title=Behavioral+and+Brain+Sciences&rft.issn=0140525X&rft_id=info:doi/
LA - English
DB - Linguistics and Language Behavior Abstracts (LLBA)
N1 - Date revised - 2015-03-01
N1 - Last updated - 2016-09-27
N1 - CODEN - BBSCDH
N1 - SubjectsTermNotLitGenreText - Brain (09350); Cognitive Processes (12950); Neurolinguistics (57250); Social Factors (79910); Communication (13600); Humans (32796)
ER -
TY - JOUR
T1 - Safety and tolerability of chikungunya virus-like particle vaccine in healthy adults: a phase 1 dose-escalation trial
AN - 1654693536; 21143840
AB - Background Chikungunya virus-a mosquito-borne alphavirus-is endemic in Africa and south and southeast Asia and has recently emerged in the Caribbean. No drugs or vaccines are available for treatment or prevention. We aimed to assess the safety, tolerability, and immunogenicity of a new candidate vaccine. Methods VRC 311 was a phase 1, dose-escalation, open-label clinical trial of a virus-like particle (VLP) chikungunya virus vaccine, VRC-CHKVLP059-00-VP, in healthy adults aged 18-50 years who were enrolled at the National Institutes of Health Clinical Center (Bethesda, MD, USA). Participants were assigned to sequential dose level groups to receive vaccinations at 10 mu g, 20 mu g, or 40 mu g on weeks 0, 4, and 20, with follow-up for 44 weeks after enrolment. The primary endpoints were safety and tolerability of the vaccine. Secondary endpoints were chikungunya virus-specific immune responses assessed by ELISA and neutralising antibody assays. This trial is registered with ClinicalTrials.gov, NCT01489358. Findings 25 participants were enrolled from Dec 12, 2011, to March 22, 2012, into the three dosage groups: 10 mu g (n=5), 20 mu g (n=10), and 40 mu g (n=10). The protocol was completed by all five participants at the 10 mu g dose, all ten participants at the 20 mu g dose, and eight of ten participants at the 40 mu g dose; non-completions were for personal circumstances unrelated to adverse events. 73 vaccinations were administered. All injections were well tolerated, with no serious adverse events reported. Neutralising antibodies were detected in all dose groups after the second vaccination (geometric mean titres of the half maximum inhibitory concentration: 2688 in the 10 mu g group, 1775 in the 20 mu g group, and 7246 in the 40 mu g group), and a significant boost occurred after the third vaccination in all dose groups (10 mu g group p=0.0197, 20 mu g group p<0.0001, and 40 mu g group p<0.0001). 4 weeks after the third vaccination, the geometric mean titres of the half maximum inhibitory concentration were 8745 for the 10 mu g group, 4525 for the 20 mu g group, and 5390 for the 40 mu g group. Interpretation The chikungunya VLP vaccine was immunogenic, safe, and well tolerated. This study represents an important step in vaccine development to combat this rapidly emerging pathogen. Further studies should be done in a larger number of participants and in more diverse populations. Funding Intramural Research Program of the Vaccine Research Center, National Institute of Allergy and Infectious Diseases, and National Institutes of Health.
JF - Lancet
AU - Chang, Lee-Jah
AU - Dowd, Kimberly A
AU - Mendoza, Floreliz H
AU - Saunders, Jamie G
AU - Sitar, Sandra
AU - Plummer, Sarah H
AU - Yamshchikov, Galina
AU - Sarwar, Uzma N
AU - Hu, Zonghui
AU - Enama, Mary E
AU - Bailer, Robert T
AU - Koup, Richard A
AU - Schwartz, Richard M
AU - Akahata, Wataru
AU - Nabel, Gary J
AU - Mascola, John R
AU - Pierson, Theodore C
AU - Graham, Barney S
AU - Ledgerwood, Julie E
AD - Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA
Y1 - 2014/12//
PY - 2014
DA - December 2014
SP - 2046
EP - 2052
PB - Elsevier B.V., Radarweg 29 Amsterdam 1043 NX Netherlands
VL - 384
IS - 9959
SN - 0140-6736, 0140-6736
KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Virology & AIDS Abstracts
KW - Virus-like particles
KW - Disease control
KW - Clinical trials
KW - Public health
KW - Hypersensitivity
KW - Endemic species
KW - ASW, Caribbean Sea
KW - Infectious diseases
KW - ELISA
KW - Drugs
KW - Enzyme-linked immunosorbent assay
KW - Chikungunya virus
KW - Pathogens
KW - Vaccination
KW - USA
KW - Antibodies
KW - Immunogenicity
KW - Africa
KW - Immune response
KW - Vaccines
KW - ISEW, Southeast Asia
KW - Research programs
KW - V 22350:Immunology
KW - Q1 08604:Stock assessment and management
KW - Q5 08524:Public health, medicines, dangerous organisms
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1654693536?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Lancet&rft.atitle=Safety+and+tolerability+of+chikungunya+virus-like+particle+vaccine+in+healthy+adults%3A+a+phase+1+dose-escalation+trial&rft.au=Chang%2C+Lee-Jah%3BDowd%2C+Kimberly+A%3BMendoza%2C+Floreliz+H%3BSaunders%2C+Jamie+G%3BSitar%2C+Sandra%3BPlummer%2C+Sarah+H%3BYamshchikov%2C+Galina%3BSarwar%2C+Uzma+N%3BHu%2C+Zonghui%3BEnama%2C+Mary+E%3BBailer%2C+Robert+T%3BKoup%2C+Richard+A%3BSchwartz%2C+Richard+M%3BAkahata%2C+Wataru%3BNabel%2C+Gary+J%3BMascola%2C+John+R%3BPierson%2C+Theodore+C%3BGraham%2C+Barney+S%3BLedgerwood%2C+Julie+E&rft.aulast=Chang&rft.aufirst=Lee-Jah&rft.date=2014-12-01&rft.volume=384&rft.issue=9959&rft.spage=2046&rft.isbn=&rft.btitle=&rft.title=Lancet&rft.issn=01406736&rft_id=info:doi/10.1016%2FS0140-6736%2814%2961185-5
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-02-01
N1 - Last updated - 2016-12-22
N1 - SubjectsTermNotLitGenreText - Endemic species; Antibodies; Infectious diseases; Disease control; ELISA; Pathogens; Vaccines; Vaccination; Public health; Enzyme-linked immunosorbent assay; Virus-like particles; Clinical trials; Hypersensitivity; Immunogenicity; Immune response; Drugs; Research programs; Chikungunya virus; USA; ASW, Caribbean Sea; Africa; ISEW, Southeast Asia
DO - http://dx.doi.org/10.1016/S0140-6736(14)61185-5
ER -
TY - JOUR
T1 - Neural Correlates of Auditory Short-Term Memory in Rostral Superior Temporal Cortex
AN - 1647020733; 21221519
AB - Background: Auditory short-term memory (STM) in the monkey is less robust than visual STM and may depend on a retained sensory trace, which is likely to reside in the higherorder cortical areas of the auditory ventral stream. Results: We recorded from the rostral superior temporal cortex as monkeys performed serial auditory delayed match-tosample (DMS). A subset of neurons exhibited modulations of their firing rate during the delay between sounds, during the sensory response, or during both. This distributed subpopulation carried a predominantly sensory signal modulated by the mnemonic context of the stimulus. Excitatory and suppressive effects on match responses were dissociable in their timing and in their resistance to sounds intervening between the sample and match. Conclusions: Like the monkeys' behavioral performance, these neuronal effects differ from those reported in the same species during visual DMS, suggesting different neural mechanisms for retaining dynamic sounds and static images in STM.
JF - Current Biology
AU - Scott, Brian H
AU - Mortimer, Mishkin
AU - Pingbo, Yin
AD - Laboratory of Neuropsychology, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892, USA, brianscott@mail.nih.gov
Y1 - 2014/12/01/
PY - 2014
DA - 2014 Dec 01
SP - 2767
EP - 2775
PB - Cell Press, 1100 Massachusetts Avenue Cambridge MA 02138 United States
VL - 24
IS - 23
SN - 0960-9822, 0960-9822
KW - CSA Neurosciences Abstracts; Ecology Abstracts
KW - Firing rate
KW - Neuromodulation
KW - Memory
KW - Cortex (visual)
KW - Neurons
KW - Subpopulations
KW - Cortex (temporal)
KW - Cortex (auditory)
KW - Short term memory
KW - Cortex (somatosensory)
KW - N3 11007:Neurobiology
KW - D 04040:Ecosystem and Ecology Studies
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647020733?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aecology&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Current+Biology&rft.atitle=Neural+Correlates+of+Auditory+Short-Term+Memory+in+Rostral+Superior+Temporal+Cortex&rft.au=Scott%2C+Brian+H%3BMortimer%2C+Mishkin%3BPingbo%2C+Yin&rft.aulast=Scott&rft.aufirst=Brian&rft.date=2014-12-01&rft.volume=24&rft.issue=23&rft.spage=2767&rft.isbn=&rft.btitle=&rft.title=Current+Biology&rft.issn=09609822&rft_id=info:doi/10.1016%2Fj.cub.2014.10.004
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-01-01
N1 - Last updated - 2015-11-16
N1 - SubjectsTermNotLitGenreText - Memory; Neuromodulation; Firing rate; Cortex (visual); Subpopulations; Neurons; Cortex (temporal); Cortex (auditory); Short term memory; Cortex (somatosensory)
DO - http://dx.doi.org/10.1016/j.cub.2014.10.004
ER -
TY - JOUR
T1 - Compounds with species and cell type specific toxicity identified in a 2000 compound drug screen of neural stem cells and rat mixed cortical neurons
AN - 1647009959; 21321507
AB - Human primary neural tissue is a vital component for the quick and simple determination of chemical compound neurotoxicity in vitro. In particular, such tissue would be ideal for high-throughput screens that can be used to identify novel neurotoxic or neurotherapeutic compounds. We have previously established a high-throughput screening platform using human induced pluripotent stem cell (iPSC)-derived neural stem cells (NSCs) and neurons. In this study, we conducted a 2000 compound screen with human NSCs and rat cortical cells to identify compounds that are selectively toxic to each group. Approximately 100 of the tested compounds showed specific toxicity to human NSCs. A secondary screen of a small subset of compounds from the primary screen on human iPSCs, NSC-derived neurons, and fetal astrocytes validated the results from >80% of these compounds with some showing cell specific toxicity. Amongst those compounds were several cardiac glycosides, all of which were selectively toxic to the human cells. As the screen was able to reliably identify neurotoxicants, many with species and cell-type specificity, this study demonstrates the feasibility of this NSC-driven platform for higher-throughput neurotoxicity screens.
JF - Neurotoxicology
AU - Malik, Nasir
AU - Efthymiou, Anastasia G
AU - Mather, Karly
AU - Chester, Nathaniel
AU - Wang, Xiantao
AU - Nath, Avindra
AU - Rao, Mahendra S
AU - Steiner, Joseph P
AD - National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, United States
Y1 - 2014/12//
PY - 2014
DA - December 2014
SP - 192
EP - 200
PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands
VL - 45
SN - 0161-813X, 0161-813X
KW - CSA Neurosciences Abstracts; Toxicology Abstracts
KW - Neurotoxicity screening
KW - Neural stem cells
KW - Cardiac glycosides
KW - Cortex
KW - Astrocytes
KW - Neurons
KW - Neurotoxicity
KW - Inhibitory postsynaptic potentials
KW - high-throughput screening
KW - Drugs
KW - Fetuses
KW - N3 11028:Neuropharmacology & toxicology
KW - X 24300:Methods
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647009959?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurotoxicology&rft.atitle=Compounds+with+species+and+cell+type+specific+toxicity+identified+in+a+2000+compound+drug+screen+of+neural+stem+cells+and+rat+mixed+cortical+neurons&rft.au=Malik%2C+Nasir%3BEfthymiou%2C+Anastasia+G%3BMather%2C+Karly%3BChester%2C+Nathaniel%3BWang%2C+Xiantao%3BNath%2C+Avindra%3BRao%2C+Mahendra+S%3BSteiner%2C+Joseph+P&rft.aulast=Malik&rft.aufirst=Nasir&rft.date=2014-12-01&rft.volume=45&rft.issue=&rft.spage=192&rft.isbn=&rft.btitle=&rft.title=Neurotoxicology&rft.issn=0161813X&rft_id=info:doi/10.1016%2Fj.neuro.2014.10.007
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-01-01
N1 - Last updated - 2016-05-13
N1 - SubjectsTermNotLitGenreText - Cortex; Astrocytes; Neurons; Inhibitory postsynaptic potentials; Neurotoxicity; high-throughput screening; Drugs; Neural stem cells; Cardiac glycosides; Fetuses
DO - http://dx.doi.org/10.1016/j.neuro.2014.10.007
ER -
TY - JOUR
T1 - Meeting the healthy people 2020 goals: using the health information national trends survey to monitor progress on health communication objectives
AN - 1646694103; 4635615
AB - The Healthy People initiative outlines a comprehensive set of goals aimed at improving the nation's health and reducing health disparities. Health communication has been included as an explicit goal since the launch of Healthy People 2010. The Health Information National Trends Survey (HINTS) was established as a means of exploring how the changing information environment was affecting the public's health, and is therefore an ideal tool for monitoring key health communication objectives included in the Healthy People agenda. In this article, the authors apply an integrative data analysis strategy to more than 10 years of HINTS data to demonstrate how public health surveillance can be used to evaluate broad national health goals, like those set forth under the Healthy People initiative. The authors analyzed just one item from the HINTS survey regarding Internet access in order to illustrate what public health surveillance tools, like HINTS, can reveal about important indicators that are of interest to all those who work to improve the health of the public. Results show that reported Internet penetration has exceeded the Healthy People 2020 target of 75.4%. HINTS data also allowed modeling of the effects of various sociodemographic factors, which revealed persistent differences on the basis of age and education, with the oldest age groups and those with less than a college education falling short of the Healthy People 2020 target as of 2013. Furthermore, although differences by race/ethnicity were observed, the analyses suggest that race in itself accounts for very little of the variance in Internet access. Reprinted by permission of Taylor & Francis Ltd.
JF - Journal of health communication
AU - Hesse, Bradford W
AU - Gaysynsky, Anna
AU - Ottenbacher, Allison
AU - Moser, Richard P
AU - Blake, Kelly D
AU - Chou, Wen-Ying Sylvia
AU - Vieux, Sana
AU - Beckjord, Ellen
AD - National Cancer Institute ; Patient-Centered Outcomes Research Institute ; University of Pittsburgh
Y1 - 2014/12//
PY - 2014
DA - Dec 2014
SP - 1497
EP - 1509
VL - 19
IS - 12
SN - 1081-0730, 1081-0730
KW - Sociology
KW - Information
KW - Objectivity
KW - Communication
KW - Surveillance
KW - Internet
KW - Public health
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1646694103?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+health+communication&rft.atitle=Meeting+the+healthy+people+2020+goals%3A+using+the+health+information+national+trends+survey+to+monitor+progress+on+health+communication+objectives&rft.au=Hesse%2C+Bradford+W%3BGaysynsky%2C+Anna%3BOttenbacher%2C+Allison%3BMoser%2C+Richard+P%3BBlake%2C+Kelly+D%3BChou%2C+Wen-Ying+Sylvia%3BVieux%2C+Sana%3BBeckjord%2C+Ellen&rft.aulast=Hesse&rft.aufirst=Bradford&rft.date=2014-12-01&rft.volume=19&rft.issue=12&rft.spage=1497&rft.isbn=&rft.btitle=&rft.title=Journal+of+health+communication&rft.issn=10810730&rft_id=info:doi/10.1080%2F10810730.2014.954084
LA - English
DB - International Bibliography of the Social Sciences (IBSS)
N1 - Date revised - 2015-01-20
N1 - Last updated - 2015-01-20
N1 - SubjectsTermNotLitGenreText - 10449 5772; 2572; 6813 6518; 12424 6608 6085; 6515; 8826
DO - http://dx.doi.org/10.1080/10810730.2014.954084
ER -
TY - JOUR
T1 - Immune-based therapies for childhood cancer.
AN - 1645780841; 25348789
AB - After decades of research, immunotherapies for cancer are demonstrating increasing success. These agents can amplify existent antitumour immunity or induce durable antitumour immune responses in a wide array of cancers. The spectrum of immunotherapeutics is broad, spanning monoclonal antibodies and their derivatives, tumour vaccines, and adoptive therapies using T cells and natural killer cells. Only a small number of immunotherapies have been tested in paediatric cancers, but impressive antitumour effects have already been observed. Mononclonal antibodies targeting GD2 that induce antibody-dependent cell-mediated cytotoxicity improve survival in high-risk neuroblastoma. Bi-specific monoclonal antibodies that simultaneously target CD19 and activate T cells can induce remission in acute B-cell lymphoblastic leukaemia (B-ALL) and adoptive immunotherapy using T cells genetically engineered to express chimeric antigen receptors targeting CD19 induce impressive responses in B-ALL. Efforts are underway to generate and test new immunotherapies in a wider array of paediatric cancers. Major challenges include a need to identify immunotherapy targets on the most lethal childhood cancers, to expand availability of technology-intense platforms, such as adoptive cell therapy, to optimize management of novel toxicities associated with this new class of cancer therapies and to determine how best to incorporate these therapies into standard treatment paradigms.
JF - Nature reviews. Clinical oncology
AU - Mackall, Crystal L
AU - Merchant, Melinda S
AU - Fry, Terry J
AD - Paediatric Oncology Branch, Center for Cancer Research, National Cancer Institute, 10 Center Drive, MSC 1104, Bethesda, MD 20892, USA.
Y1 - 2014/12//
PY - 2014
DA - December 2014
SP - 693
EP - 703
VL - 11
IS - 12
KW - Index Medicus
KW - Humans
KW - Immunotherapy, Adoptive
KW - Child
KW - Neoplasms -- drug therapy
KW - Immunotherapy -- methods
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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:
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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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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]
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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:
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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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Canadian+journal+of+statistics&rft.atitle=Stochastic+dynamic+models+and+Chebyshev+splines&rft.au=Fan%2C+Ruzong%3BZhu%2C+Bin%3BWang%2C+Yuedong&rft.aulast=Fan&rft.aufirst=Ruzong&rft.date=2014-12-01&rft.volume=42&rft.issue=3&rft.spage=883&rft.isbn=&rft.btitle=&rft.title=Analytical+and+bioanalytical+chemistry&rft.issn=1618-2650&rft_id=info:doi/10.1007%2Fs00216-014-8118-8
LA - English
DB - International Bibliography of the Social Sciences (IBSS)
N1 - Date revised - 2014-12-16
N1 - Last updated - 2014-12-16
N1 - SubjectsTermNotLitGenreText - 12265 3865 4025 10214 12224 971 12228 10919; 3786 8163; 3555 1073; 5345 971; 12233; 3969 8163; 75 293 14
DO - http://dx.doi.org/10.1002/cjs.11233
ER -
TY - JOUR
T1 - Association of seropositivity to Helicobacter species and biliary tract cancer in the ATBC study
AN - 1635032490; 21045942
AB - Helicobacter have been detected in human bile and hepatobiliary tissue. Despite evidence that Helicobacter species promote gallstone formation and hepatobiliary tumors in laboratory studies, it remains unclear whether Helicobacter species contribute to these cancers in humans. We used a multiplex panel to assess whether seropositivity to 15 Helicobacter pylori proteins was associated with subsequent incidence of hepatobiliary cancers in the Finnish Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study. We included 64 biliary cancers, 122 liver cancers, and 224 age-matched controls which occurred over the course of 22 years. Helicobacter pylori seropositivity was defined as those positive to greater than or equal to 4 antigens. Odds ratios (OR) and 95% confidence intervals were adjusted for major hepatobiliary cancer risk factors. Among the controls, 88% were seropositive to H. pylori at baseline. Among those who subsequently developed hepatobiliary cancer, the prevalence of seropositivity was higher: 100% for gallbladder cancer, 97% of extrahepatic bile duct cancer, 91% of ampula of Vater cancer, 96% of intrahepatic bile duct cancer, and 94% of hepatocellular carcinoma. Although the OR for gallbladder cancer could not be calculated, the OR for the other sites were 7.01 (95% confidence interval [CI]: 0.79-62.33), 2.21 (0.19-25.52), 10.67 (0.76-150.08), and 1.20 (0.42-3.45), respectively, with an OR of 5.47 (95% CI: 1.17-25.65) observed for the biliary tract cancers combined. ORs above 1 were observed for many of the investigated antigens, although most of these associations were not statistically significant. Conclusion: Seropositivity to H. pylori proteins was associated with an increased risk of biliary tract cancers in ATBC. Further studies are needed to confirm our findings and to determine how H. pylori might influence the risk of biliary tract cancer. (Hepatology 2014; 60:1962-1970)
JF - Hepatology
AU - Murphy, Gwen
AU - Michel, Angelika
AU - Taylor, Philip R
AU - Albanes, Demetrius
AU - Weinstein, Stephanie J
AU - Virtamo, Jarmo
AU - Parisi, Dominick
AU - Snyder, Kirk
AU - Butt, Julia
AU - McGlynn, Katherine A
AU - Koshiol, Jill
AU - Pawlita, Michael
AU - Lai, Gabriel Y
AU - Abnet, Christian C
AU - Dawsey, Sanford M
AU - Freedman, Neal D
AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Y1 - 2014/12//
PY - 2014
DA - Dec 2014
SP - 1963
EP - 1971
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 60
IS - 6
SN - 0270-9139, 0270-9139
KW - Microbiology Abstracts B: Bacteriology; Immunology Abstracts
KW - Helicobacter pylori
KW - Gallbladder
KW - Bile duct
KW - Liver cancer
KW - Risk factors
KW - Statistical analysis
KW - Tumors
KW - Biliary tract
KW - Hepatocellular carcinoma
KW - J 02400:Human Diseases
KW - F 06910:Microorganisms & Parasites
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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
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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
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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
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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
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-04-28
N1 - Date created - 2014-11-17
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1002/em.21889
ER -
TY - JOUR
T1 - A DRD1 polymorphism predisposes to lung cancer among those exposed to secondhand smoke during childhood.
AN - 1629965619; 25281486
AB - Lung cancer has a familial component which suggests a genetic contribution to its etiology. Given the strong evidence linking smoking with lung cancer, we studied miRNA-related loci in genes associated with smoking behavior. CHRNA, CHRNB gene families, CYP2A6, and DRD1 (dopamine receptor D1) were mined for SNPs that fell within the seed region of miRNA binding sites and then tested for associations with risk in a three-stage validation approach. A 3'UTR (untranslated region) SNP in DRD1 was associated with a lower risk of lung cancer among individuals exposed to secondhand smoke during childhood [OR, 0.69; 95% confidence interval (CI), 0.60-0.79; P < 0.0001]. This relationship was evident in both ever (OR, 0.74; 95% CI, 0.62-0.88; P = 0.001) and never smokers (OR, 0.61; 95% CI, 0.47-0.79; P < 0.0001), European American (OR, 0.65; 95% CI, 0.53-0.80; P < 0.0001), and African American (OR, 0.73; 95% CI, 0.62-0.88; P = 0.001) populations. Although much remains undefined about the long-term risks associated with exposure to secondhand smoke and heterogeneity between individuals in regard to their susceptibility to the effects of secondhand smoke, our data show an interaction between an SNP in the 3'UTR of DRD1 and exposure to secondhand smoke during childhood. Further work is needed to explore the mechanistic underpinnings of this SNP and the nature of the interaction between DRD1 and exposure to secondhand smoke during childhood.
©2014 American Association for Cancer Research.
JF - Cancer prevention research (Philadelphia, Pa.)
AU - Robles, Ana I
AU - Yang, Ping
AU - Jen, Jin
AU - McClary, Andrew C
AU - Calhoun, Kara
AU - Bowman, Elise D
AU - Vähäkangas, Kirsi
AU - Greathouse, K Leigh
AU - Wang, Yi
AU - Olivo-Marston, Susan
AU - Wenzlaff, Angela S
AU - Deng, Bo
AU - Schwartz, Ann G
AU - Ryan, Bríd M
AD - Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland. ; Mayo Clinic, Department of Health Sciences Research, Rochester, Minnesota. ; Department of Laboratory Medicine and Pathology and Division of Pulmonary and Critical Care Medicine, Mayo Clinic, Rochester, Minnesota. ; Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland. Department of Pathology, Stanford University Hospital and Clinics, Stanford, California. ; School of Pharmacy/Toxicology, Faculty of Health Sciences, University of Eastern Finland, Kuopio, Finland. ; Division of Preventive Medicine, School of Environmental Science and Public Health, Wenzhou Medical University, Wenzhou, Zhejiang, China. Division of Epidemiology, Health Sciences Research, Mayo Clinic, Rochester, Minnesota. ; Division of Epidemiology, College of Public Health, Ohio State University, Columbus, Ohio. ; Karmanos Cancer Institute, Department of Oncology, Wayne State University School of Medicine, Detroit, Michigan. ; Division of Epidemiology, Health Sciences Research, Mayo Clinic, Rochester, Minnesota. Thoracic Surgery Department, Institute of Surgery Research, Daping Hospital, The Third Military Medical University, Chongqing, China. ; Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland. ryanb@mail.nih.gov.
Y1 - 2014/12//
PY - 2014
DA - December 2014
SP - 1210
EP - 1218
VL - 7
IS - 12
KW - 3' Untranslated Regions
KW - 0
KW - CHRNA1 protein, human
KW - CHRNA2 protein, human
KW - DRD1 protein, human
KW - MicroRNAs
KW - Receptors, Dopamine D1
KW - Receptors, Nicotinic
KW - Tobacco Smoke Pollution
KW - CYP2A6 protein, human
KW - EC 1.14.14.1
KW - Cytochrome P-450 CYP2A6
KW - Index Medicus
KW - Neoplasm Staging
KW - MicroRNAs -- genetics
KW - Humans
KW - Prognosis
KW - Aged
KW - Child
KW - Receptors, Nicotinic -- genetics
KW - Cytochrome P-450 CYP2A6 -- genetics
KW - Risk Factors
KW - Case-Control Studies
KW - Follow-Up Studies
KW - Middle Aged
KW - 3' Untranslated Regions -- genetics
KW - Female
KW - Male
KW - Lung Neoplasms -- etiology
KW - Receptors, Dopamine D1 -- genetics
KW - Disease Susceptibility
KW - Polymorphism, Genetic -- genetics
KW - Tobacco Smoke Pollution -- adverse effects
KW - Smoking -- genetics
KW - Lung Neoplasms -- pathology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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:
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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:
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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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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:
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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]
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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:
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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]
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Endocr Relat Cancer. 2001 Mar;8(1):11-31 [11350724]
Biochem J. 2001 Aug 1;357(Pt 3):593-615 [11463332]
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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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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:
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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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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:
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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]
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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:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/carcin/bgu203
ER -
TY - JOUR
T1 - Identification of fragile X syndrome specific molecular markers in human fibroblasts: a useful model to test the efficacy of therapeutic drugs.
AN - 1628238948; 25224527
AB - Fragile X syndrome (FXS) is the most frequent cause of inherited intellectual disability and autism. It is caused by the absence of the fragile X mental retardation 1 (FMR1) gene product, fragile X mental retardation protein (FMRP), an RNA-binding protein involved in the regulation of translation of a subset of brain mRNAs. In Fmr1 knockout mice, the absence of FMRP results in elevated protein synthesis in the brain as well as increased signaling of many translational regulators. Whether protein synthesis is also dysregulated in FXS patients is not firmly established. Here, we demonstrate that fibroblasts from FXS patients have significantly elevated rates of basal protein synthesis along with increased levels of phosphorylated mechanistic target of rapamycin (p-mTOR), phosphorylated extracellular signal regulated kinase 1/2, and phosphorylated p70 ribosomal S6 kinase 1 (p-S6K1). The treatment with small molecules that inhibit S6K1 and a known FMRP target, phosphoinositide 3-kinase (PI3K) catalytic subunit p110β, lowered the rates of protein synthesis in both control and patient fibroblasts. Our data thus demonstrate that fibroblasts from FXS patients may be a useful in vitro model to test the efficacy and toxicity of potential therapeutics prior to clinical trials, as well as for drug screening and designing personalized treatment approaches.
© 2014 WILEY PERIODICALS, INC.
JF - Human mutation
AU - Kumari, Daman
AU - Bhattacharya, Aditi
AU - Nadel, Jeffrey
AU - Moulton, Kristen
AU - Zeak, Nicole M
AU - Glicksman, Anne
AU - Dobkin, Carl
AU - Brick, David J
AU - Schwartz, Philip H
AU - Smith, Carolyn B
AU - Klann, Eric
AU - Usdin, Karen
AD - Laboratory of Cell and Molecular Biology, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland.
Y1 - 2014/12//
PY - 2014
DA - December 2014
SP - 1485
EP - 1494
VL - 35
IS - 12
KW - Biomarkers
KW - 0
KW - FMR1 protein, human
KW - RNA, Messenger
KW - Fragile X Mental Retardation Protein
KW - 139135-51-6
KW - Phosphatidylinositol 3-Kinases
KW - EC 2.7.1.-
KW - Ribosomal Protein S6 Kinases
KW - EC 2.7.11.1
KW - Leucine
KW - GMW67QNF9C
KW - Index Medicus
KW - S6K1
KW - protein synthesis
KW - FMRP
KW - Fragile X syndrome
KW - fibroblasts
KW - FMR1
KW - Protein Biosynthesis
KW - Animals
KW - Phosphatidylinositol 3-Kinases -- metabolism
KW - Humans
KW - Fibroblasts -- cytology
KW - Mice
KW - RNA, Messenger -- genetics
KW - Fibroblasts -- metabolism
KW - Mice, Knockout
KW - Ribosomal Protein S6 Kinases -- metabolism
KW - Cells, Cultured
KW - Leucine -- metabolism
KW - Case-Control Studies
KW - Fragile X Mental Retardation Protein -- genetics
KW - Drug Evaluation, Preclinical
KW - Male
KW - Fragile X Syndrome -- genetics
KW - Biomarkers -- metabolism
KW - Fragile X Syndrome -- drug therapy
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1628238948?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Human+mutation&rft.atitle=Identification+of+fragile+X+syndrome+specific+molecular+markers+in+human+fibroblasts%3A+a+useful+model+to+test+the+efficacy+of+therapeutic+drugs.&rft.au=Kumari%2C+Daman%3BBhattacharya%2C+Aditi%3BNadel%2C+Jeffrey%3BMoulton%2C+Kristen%3BZeak%2C+Nicole+M%3BGlicksman%2C+Anne%3BDobkin%2C+Carl%3BBrick%2C+David+J%3BSchwartz%2C+Philip+H%3BSmith%2C+Carolyn+B%3BKlann%2C+Eric%3BUsdin%2C+Karen&rft.aulast=Kumari&rft.aufirst=Daman&rft.date=2014-12-01&rft.volume=35&rft.issue=12&rft.spage=1485&rft.isbn=&rft.btitle=&rft.title=Human+mutation&rft.issn=1098-1004&rft_id=info:doi/10.1002%2Fhumu.22699
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-07-08
N1 - Date created - 2014-11-25
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Cell. 2011 Jul 22;146(2):247-61 [21784246]
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Genes Brain Behav. 2012 Apr;11(3):332-41 [22268788]
J Neurochem. 2012 May;121(4):672-9 [22393900]
Biochem J. 2010 Oct 15;431(2):245-55 [20704563]
J Neurosci. 2010 Nov 17;30(46):15616-27 [21084617]
Neurobiol Dis. 2011 Feb;41(2):469-80 [21047554]
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Neuron. 2012 Oct 18;76(2):325-37 [23083736]
Hum Mutat. 2013 Jan;34(1):157-66 [22887750]
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Nat Med. 2013 Nov;19(11):1473-7 [24141422]
Biol Psychiatry. 2014 Feb 1;75(3):198-206 [24041505]
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Am J Med Genet A. 2014 Jul;164A(7):1648-58 [24700618]
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Cereb Cortex. 2000 Oct;10(10):1038-44 [11007554]
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Mol Cell Neurosci. 2010 Jan;43(1):43-50 [19837168]
Neurotherapeutics. 2010 Jul;7(3):264-74 [20643379]
J Neurosci. 2010 Aug 11;30(32):10624-38 [20702695]
J Mol Diagn. 2010 Sep;12(5):589-600 [20616364]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1002/humu.22699
ER -
TY - JOUR
T1 - Perceived and objective diet quality in US adults: a cross-sectional analysis of the National Health and Nutrition Examination Survey (NHANES)
AN - 1627977482; 20913351
AB - The Dietary Approaches to Stop Hypertension (DASH) dietary pattern has been shown to reduce cardiometabolic risk. Little is understood about the relationship between objective diet quality and perceived diet quality (PDQ), a potential psychosocial barrier to appropriate dietary intake. We compared PDQ and diet quality measured by a nutrient-based DASH index score in the USA. Cross-sectional study. Participants in the 2005-2006 National Health and Nutrition Examination Survey (NHANES) rated diet quality on a 5-point Likert scale and PDQ scores were generated (low, medium, high). A single 24 h dietary recall was used to estimate DASH index scores (range 0-9 points) by assigning 0, 0.5 or 1 point (optimal) for nine target nutrients: total fat, saturated fat, protein, cholesterol, fibre, Ca, Mg, K and Na. Nationally representative sample of the US population. Adults aged greater than or equal to 19 years in 2005-2006 NHANES (n 4419). Participants with high PDQ (33 %) had higher DASH index scores (mean 3.0 (sd 0.07)) than those with low PDQ (mean 2.5 (sd 0.06), P < 0.001), but average scores did not align with targets for intermediate or optimal DASH accordance. Adults with high PDQ reported higher total fat, saturated fat and Na intakes compared with optimal DASH nutrient goals. Differences between those with high v. low PDQ were similar for Whites and Blacks, but there was no difference between PDQ groups for Mexican Americans. Among Whites and Blacks, but not Mexican Americans, high PDQ may be associated with higher diet quality, but not necessarily a diet meeting DASH nutrient goals. This disconnect between PDQ and actual diet quality may serve as a target in obesity prevention.
JF - Public Health Nutrition
AU - Powell-Wiley, Tiffany M
AU - Miller, Paige E
AU - Agyemang, Priscilla
AU - Agurs-Collins, Tanya
AU - Reedy, Jill
AD - Cardiovascular and Pulmonary Branch, Division of Intramural Research, National Heart, Lung, and Blood Institute, National Institutes of Health, Building 10 - Room 5E3340, Bethesda, MD 20892, USA, tiffany.powell@nih.gov
Y1 - 2014/12//
PY - 2014
DA - Dec 2014
SP - 2641
EP - 2649
PB - Cambridge University Press, The Edinburgh Building, Cambridge CB2 2RU United Kingdom
VL - 17
IS - 12
SN - 1368-9800, 1368-9800
KW - Risk Abstracts
KW - Diets
KW - Obesity
KW - Cholesterol
KW - Ingestion
KW - Nutrition
KW - Health risks
KW - USA
KW - Prevention
KW - Perception
KW - Proteins
KW - Ethnic groups
KW - Hypertension
KW - R2 23110:Psychological aspects
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1627977482?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Public+Health+Nutrition&rft.atitle=Perceived+and+objective+diet+quality+in+US+adults%3A+a+cross-sectional+analysis+of+the+National+Health+and+Nutrition+Examination+Survey+%28NHANES%29&rft.au=Powell-Wiley%2C+Tiffany+M%3BMiller%2C+Paige+E%3BAgyemang%2C+Priscilla%3BAgurs-Collins%2C+Tanya%3BReedy%2C+Jill&rft.aulast=Powell-Wiley&rft.aufirst=Tiffany&rft.date=2014-12-01&rft.volume=17&rft.issue=12&rft.spage=2641&rft.isbn=&rft.btitle=&rft.title=Public+Health+Nutrition&rft.issn=13689800&rft_id=info:doi/10.1017%2FS1368980014000196
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-11-01
N1 - Number of references - 39
N1 - Last updated - 2014-12-24
N1 - SubjectsTermNotLitGenreText - Diets; Health risks; Obesity; Prevention; Perception; Proteins; Cholesterol; Ingestion; Nutrition; Ethnic groups; Hypertension; USA
DO - http://dx.doi.org/10.1017/S1368980014000196
ER -
TY - JOUR
T1 - Peritubular myoid cells participate in male mouse spermatogonial stem cell maintenance.
AN - 1627697485; 25181385
AB - Peritubular myoid (PM) cells surround the seminiferous tubule and together with Sertoli cells form the cellular boundary of the spermatogonial stem cell (SSC) niche. However, it remains unclear what role PM cells have in determining the microenvironment in the niche required for maintenance of the ability of SSCs to undergo self-renewal and differentiation into spermatogonia. Mice with a targeted disruption of the androgen receptor gene (Ar) in PM cells experienced a progressive loss of spermatogonia, suggesting that PM cells require testosterone (T) action to produce factors influencing SSC maintenance in the niche. Other studies showed that glial cell line-derived neurotrophic factor (GDNF) is required for SSC self-renewal and differentiation of SSCs in vitro and in vivo. This led us to hypothesize that T-regulated GDNF expression by PM cells contributes to the maintenance of SSCs. This hypothesis was tested using an adult mouse PM cell primary culture system and germ cell transplantation. We found that T induced GDNF expression at the mRNA and protein levels in PM cells. Furthermore, when thymus cell antigen 1-positive spermatogonia isolated from neonatal mice were cocultured with PM cells with or without T and transplanted to the testes of germ cell-depleted mice, the number and length of transplant-derived colonies was increased considerably by in vitro T treatment. These results support the novel hypothesis that T-dependent regulation of GDNF expression in PM cells has a significant influence on the microenvironment of the niche and SSC maintenance.
JF - Endocrinology
AU - Chen, Liang-Yu
AU - Brown, Paula R
AU - Willis, William B
AU - Eddy, Edward M
AD - Gamete Biology Group (L.-Y.C., W.B.W., E.M.E.) and Reproductive Developmental Biology Group (P.R.B.), Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709.
Y1 - 2014/12//
PY - 2014
DA - December 2014
SP - 4964
EP - 4974
VL - 155
IS - 12
KW - Glial Cell Line-Derived Neurotrophic Factor
KW - 0
KW - Testosterone
KW - 3XMK78S47O
KW - Abridged Index Medicus
KW - Index Medicus
KW - Coculture Techniques
KW - Animals
KW - Mice, Inbred C57BL
KW - Spermatogonia -- physiology
KW - Male
KW - Adult Stem Cells -- transplantation
KW - Testis -- physiology
KW - Glial Cell Line-Derived Neurotrophic Factor -- metabolism
KW - Testosterone -- physiology
KW - Adult Stem Cells -- physiology
KW - Testis -- cytology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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:
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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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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:
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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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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:
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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
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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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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:
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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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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
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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]
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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:
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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
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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
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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
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L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={54C85D94-6D69-4B09-AFAA-502C0E680CA7}
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-12-31
N1 - Last updated - 2015-01-23
ER -
TY - CPAPER
T1 - Fear extinction facilitation by fluoxetine is mediated by basolateral amygdala endocannabinoids
T2 - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014)
AN - 1647639575; 6326372
JF - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014)
AU - Gunduz Cinar, O
AU - Flynn, S
AU - Cinar, R
AU - Ramikie, T
AU - Kunos, G
AU - Patel, S
AU - Holmes, A
Y1 - 2014/11/15/
PY - 2014
DA - 2014 Nov 15
KW - Fluoxetine
KW - Cannabinoids
KW - Extinction
KW - Amygdala
KW - Fear conditioning
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647639575?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.atitle=Fear+extinction+facilitation+by+fluoxetine+is+mediated+by+basolateral+amygdala+endocannabinoids&rft.au=Gunduz+Cinar%2C+O%3BFlynn%2C+S%3BCinar%2C+R%3BRamikie%2C+T%3BKunos%2C+G%3BPatel%2C+S%3BHolmes%2C+A&rft.aulast=Gunduz+Cinar&rft.aufirst=O&rft.date=2014-11-15&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.issn=&rft_id=info:doi/
L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={54C85D94-6D69-4B09-AFAA-502C0E680CA7}
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-12-31
N1 - Last updated - 2015-01-23
ER -
TY - CPAPER
T1 - PET imaging of translocator protein, a neuroinflammatory biomarker, in vivo in patients with temporal lobe epilepsy
T2 - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014)
AN - 1647639556; 6326205
JF - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014)
AU - Dickstein, L
AU - Zanotti-Fregonara, P
AU - Dustin, I
AU - Hong, J
AU - Liow, J
AU - Pike, V
AU - Zoghbi, S
AU - Innis, R
AU - Theodore, W
Y1 - 2014/11/15/
PY - 2014
DA - 2014 Nov 15
KW - Temporal lobe
KW - Bioindicators
KW - Epilepsy
KW - Positron emission tomography
KW - Biomarkers
KW - biomarkers
KW - Imaging techniques
KW - Inflammation
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647639556?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.atitle=PET+imaging+of+translocator+protein%2C+a+neuroinflammatory+biomarker%2C+in+vivo+in+patients+with+temporal+lobe+epilepsy&rft.au=Dickstein%2C+L%3BZanotti-Fregonara%2C+P%3BDustin%2C+I%3BHong%2C+J%3BLiow%2C+J%3BPike%2C+V%3BZoghbi%2C+S%3BInnis%2C+R%3BTheodore%2C+W&rft.aulast=Dickstein&rft.aufirst=L&rft.date=2014-11-15&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.issn=&rft_id=info:doi/
L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={54C85D94-6D69-4B09-AFAA-502C0E680CA7}
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-12-31
N1 - Last updated - 2015-01-23
ER -
TY - CPAPER
T1 - Neuron and astroglia preserve microglial endotoxin tolerance through macrophage colony-stimulating factor
T2 - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014)
AN - 1647639535; 6325946
JF - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014)
AU - Chu, C
AU - Wang, S
AU - Wang, Q
AU - Chen, S
AU - Gao, H
AU - Lu, R.
AU - Hong, J
Y1 - 2014/11/15/
PY - 2014
DA - 2014 Nov 15
KW - Macrophages
KW - Endotoxins
KW - Astrocytes
KW - Neurons
KW - Macrophage colony-stimulating factor
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647639535?accountid=14244
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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:
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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
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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:
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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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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:
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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
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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:
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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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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:
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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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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:
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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
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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
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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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1038/nature13601
ER -
TY - JOUR
T1 - The National Library of Medicine's (NLM) Hazardous Substances Data Bank (HSDB): background, recent enhancements and future plans.
AN - 1612286862; 25223694
AB - The National Library of Medicine's (NLM) Division of Specialized Information Services (SIS) Toxicology and Environmental Health Information Program is responsible for the management of the online Hazardous Substances Data Bank (HSDB). HSDB, a part of NLM's Toxicology Data Network (TOXNET(®)), is a file of chemical/substance information with one record for each specific chemical or substance, or for a category of chemicals or substances. Like the rest of TOXNET's databases and other resources, HSDB is available online at no cost to global users. HSDB has approximately 5600 chemicals and substances, with a focus on toxicology information and also on human exposure, industrial hygiene, emergency handling procedures, environmental fate, regulatory requirements, and related areas of likely interest to HSDB users. All data are from a core set of books, government documents, technical reports, selected primary journal literature, and other online sources of information, with a goal of linking the HSDB content to as much publicly available information as possible. HSDB's content is peer-reviewed by the Scientific Review Panel, a group of experts in the areas covering the scope of HSDB content. Recent enhancements include the addition of chemical structures to HSDB records, the addition of new subfields such as age groups for human data, more occupational exposure standards, and the addition of information on numerous nanomaterials. Examples of future plans include providing more exposure-related information, e.g., uses of a chemical or substance in consumer products; the addition of information summaries aimed towards consumers and other members of the public wanting to learn about a chemical or substance; more visual content such as diagrams (images) of the pathways of metabolism of a substance; and enhanced search features and navigation. Published by Elsevier Ireland Ltd.
JF - Toxicology
AU - Fonger, George Charles
AU - Hakkinen, Pertti
AU - Jordan, Shannon
AU - Publicker, Stephanie
AD - National Library of Medicine, Division of Specialized Information Services, Bethesda, MD 20894, USA. Electronic address: fongerg@mail.nlm.nih.gov. ; National Library of Medicine, Division of Specialized Information Services, Bethesda, MD 20894, USA.
Y1 - 2014/11/05/
PY - 2014
DA - 2014 Nov 05
SP - 209
EP - 216
VL - 325
KW - Hazardous Substances
KW - 0
KW - Index Medicus
KW - Information
KW - Databases
KW - Online
KW - National Library of Medicine
KW - United States
KW - Animals
KW - History, 21st Century
KW - History, 20th Century
KW - Access to Information
KW - Humans
KW - Information Dissemination
KW - Forecasting
KW - Internet
KW - Risk Assessment
KW - Databases, Factual -- trends
KW - Hazardous Substances -- classification
KW - Environmental Health -- trends
KW - National Library of Medicine (U.S.) -- trends
KW - Toxicology -- trends
KW - Toxicology -- history
KW - Environmental Health -- history
KW - Databases, Factual -- history
KW - National Library of Medicine (U.S.) -- history
KW - Hazardous Substances -- toxicity
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1612286862?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology&rft.atitle=The+National+Library+of+Medicine%27s+%28NLM%29+Hazardous+Substances+Data+Bank+%28HSDB%29%3A+background%2C+recent+enhancements+and+future+plans.&rft.au=Fonger%2C+George+Charles%3BHakkinen%2C+Pertti%3BJordan%2C+Shannon%3BPublicker%2C+Stephanie&rft.aulast=Fonger&rft.aufirst=George&rft.date=2014-11-05&rft.volume=325&rft.issue=&rft.spage=209&rft.isbn=&rft.btitle=&rft.title=Toxicology&rft.issn=1879-3185&rft_id=info:doi/10.1016%2Fj.tox.2014.09.003
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-12-18
N1 - Date created - 2014-10-13
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.tox.2014.09.003
ER -
TY - JOUR
T1 - Estimation of the Probability of Exposure to Machining Fluids in a Population-Based Case-Control Study
AN - 1808729120; PQ0003494068
AB - We describe an approach for estimating the probability that study subjects were exposed to metalworking fluids (MWFs) in a population-based case-control study of bladder cancer. Study subject reports on the frequency of machining and use of specific MWFs (straight, soluble, and synthetic/semi-synthetic) were used to estimate exposure probability when available. Those reports also were used to develop estimates for job groups, which were then applied to jobs without MWF reports. Estimates using both cases and controls and controls only were developed. The prevalence of machining varied substantially across job groups (0.1->0.9%), with the greatest percentage of jobs that machined being reported by machinists and tool and die workers. Reports of straight and soluble MWF use were fairly consistent across job groups (generally 50-70%). Synthetic MWF use was lower (13-45%). There was little difference in reports by cases and controls vs. controls only. Approximately, 1% of the entire study population was assessed as definitely exposed to straight or soluble fluids in contrast to 0.2% definitely exposed to synthetic/semi-synthetics. A comparison between the reported use of the MWFs and U.S. production levels found high correlations (r generally >0.7). Overall, the method described here is likely to have provided a systematic and reliable ranking that better reflects the variability of exposure to three types of MWFs than approaches applied in the past. [Supplementary materials are available for this article. Go to the publisher's online edition of Journal of Occupational and Environmental Hygiene for the following free supplemental resources: a list of keywords in the occupational histories that were used to link study subjects to the metalworking fluids (MWFs) modules; recommendations from the literature on selection of MWFs based on type of machining operation, the metal being machined and decade; popular additives to MWFs; the number and proportion of controls who reported various MWF responses by job group; the number and proportion of controls assigned to the MWF types by job group and exposure category; and the distribution of cases and controls assigned various levels of probability by MWF type.]
JF - Journal of Occupational and Environmental Hygiene
AU - Park, Dong-Uk
AU - Colt, Joanne S
AU - Baris, Dalsu
AU - Schwenn, Molly
AU - Karagas, Margaret R
AU - Armenti, Karla R
AU - Johnson, Alison
AU - Silverman, Debra T
AU - Stewart, Patricia A
AD - Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland
Y1 - 2014/11/02/
PY - 2014
DA - 2014 Nov 02
SP - 757
EP - 770
PB - Taylor & Francis Group Ltd., 2 Park Square Oxford OX14 4RN United Kingdom
VL - 11
IS - 11
SN - 1545-9624, 1545-9624
KW - Toxicology Abstracts; Environment Abstracts; Health & Safety Science Abstracts
KW - Historical account
KW - Metals
KW - Urinary bladder
KW - Population studies
KW - Metal-working fluids
KW - Cancer
KW - Workers
KW - Hygiene
KW - Additives
KW - Internet
KW - Occupational exposure
KW - Environmental hygiene
KW - H 1000:Occupational Safety and Health
KW - X 24360:Metals
KW - ENA 02:Toxicology & Environmental Safety
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808729120?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Occupational+and+Environmental+Hygiene&rft.atitle=Estimation+of+the+Probability+of+Exposure+to+Machining+Fluids+in+a+Population-Based+Case-Control+Study&rft.au=Park%2C+Dong-Uk%3BColt%2C+Joanne+S%3BBaris%2C+Dalsu%3BSchwenn%2C+Molly%3BKaragas%2C+Margaret+R%3BArmenti%2C+Karla+R%3BJohnson%2C+Alison%3BSilverman%2C+Debra+T%3BStewart%2C+Patricia+A&rft.aulast=Park&rft.aufirst=Dong-Uk&rft.date=2014-11-02&rft.volume=11&rft.issue=11&rft.spage=757&rft.isbn=&rft.btitle=&rft.title=Journal+of+Occupational+and+Environmental+Hygiene&rft.issn=15459624&rft_id=info:doi/10.1080%2F15459624.2014.918984
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2016-07-01
N1 - Last updated - 2016-09-01
N1 - SubjectsTermNotLitGenreText - Workers; Metals; Urinary bladder; Population studies; Cancer; Occupational exposure; Internet; Environmental hygiene; Historical account; Hygiene; Additives; Metal-working fluids
DO - http://dx.doi.org/10.1080/15459624.2014.918984
ER -
TY - JOUR
T1 - Spoiling and Sustainability: Technology, Water Insecurity, and Visibility in Arctic Alaska
AN - 1622612928; 20825382
AB - One third of households in Alaska Native villages lack running water and sewer services. Historically, this public health need drove policies to improve access to treated water and sanitation. However, despite public health being a stated priority of water infrastructure development, current policies require demonstrated economic sustainability in ways that render suffering from water insecurity invisible. In this article, I situate the introduction of water treatment technologies within the history of domination coproduced with vulnerability. These processes are reflected in local narratives describing the relationships between technology, tradition, and suffering. By drawing attention to the role of the state in creating vulnerability, village leaders are trying to historicize and insert their health concerns into the sustainability conversation using narratives that both fit within and challenge the ideology of sustainability. These narratives are thus central to Inupiat struggles for visibility.
JF - Medical Anthropology
AU - Eichelberger, Laura
AD - Nutritional Epidemiology Branch, Division of Cancer Epidemiology & Genetics, National Cancer Institute, Bethesda, Maryland, USA
Y1 - 2014/11/02/
PY - 2014
DA - 2014 Nov 02
SP - 478
EP - 496
PB - Taylor & Francis Group Ltd., 2 Park Square Oxford OX14 4RN United Kingdom
VL - 33
IS - 6
SN - 0145-9740, 0145-9740
KW - Health & Safety Science Abstracts; Sustainability Science Abstracts
KW - USA, Alaska
KW - Historical account
KW - Anthropology
KW - Polar environments
KW - Traditions
KW - Sustainability
KW - Public health
KW - PN, Arctic
KW - Sanitation
KW - Water treatment
KW - Villages
KW - Households
KW - Economics
KW - Visibility
KW - Vulnerability
KW - Technology
KW - M3 1010:Issues in Sustainable Development
KW - H 12000:Epidemiology and Public Health
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1622612928?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Assamodule&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Medical+Anthropology&rft.atitle=Spoiling+and+Sustainability%3A+Technology%2C+Water+Insecurity%2C+and+Visibility+in+Arctic+Alaska&rft.au=Eichelberger%2C+Laura&rft.aulast=Eichelberger&rft.aufirst=Laura&rft.date=2014-11-02&rft.volume=33&rft.issue=6&rft.spage=478&rft.isbn=&rft.btitle=&rft.title=Medical+Anthropology&rft.issn=01459740&rft_id=info:doi/10.1080%2F01459740.2014.917374
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-11-01
N1 - Last updated - 2014-11-26
N1 - SubjectsTermNotLitGenreText - Historical account; Anthropology; Traditions; Polar environments; Sustainability; Public health; Sanitation; Villages; Water treatment; Households; Economics; Visibility; Vulnerability; Technology; USA, Alaska; PN, Arctic
DO - http://dx.doi.org/10.1080/01459740.2014.917374
ER -
TY - JOUR
T1 - Is CD4 Monitoring Needed Among Ugandan Clients Achieving a Virologic and Immunologic Response to Treatment?
AN - 1827882746; PQ0003681045
AB - It is unclear whether ongoing CD4 monitoring is needed following immunologic and virologic response to antiretroviral therapy (ART). We investigated the proportion of clients who achieved a virologic and immunologic response and then had a subsequent CD4 count <200 cells/ mu L despite continued virologic suppression. Included in this analysis were clients receiving ART through the Rakai Health Sciences Program between June 2004-May 2013 who achieved a CD4 greater than or equal to 200 cells/ mu L and VL less than or equal to 400 copies/mL and who had three sets of CD4 and VL measurements (defined as a sequence) within a 390 day period. A CD4 decline was defined as any drop in CD4 count to <200 cells/ mu L during a period of viral suppression. A total of 1553 clients were included, 68% females, mean age of 35.5 years (SD 8.3), median baseline CD4 count 183 cells/ mu L (IQR 106-224). 43 (2.8%) clients developed CD4 declines, the majority, 32/43 (74%), among individuals whose initial CD4 was <300 cells/ mu L. Of the 43 clients with CD4 declines, 24 had an additional CD4 measurement and 20/24 (83%) achieved a CD4 greater than or equal to 200 cell/ mu L on their next measurement (median 285 cells/ mu L; IQR 220-365). CD4 declines were significantly greater among those with lower CD4 at sequence initiation [adjusted hazard ratio (AHR) 4.3 (95% CI 2.1, 9.0) CD4 200-249 versus greater than or equal to 350 cells/ mu L]. Clients who achieved an immunologic and virologic response to ART were unlikely to experience a subsequent CD4 count decline to <200 cells/ mu L, and among those experiencing a decline, the majority were transient in nature. Thus, ongoing CD4 monitoring could be omitted.
JF - AIDS Patient Care and STDs
AU - Reynolds, Steven J
AU - Sempa, Joseph B
AU - Kiragga, Agnes N
AU - Newell, Kevin
AU - Nakigozi, Gertrude
AU - Galiwango, Ronald
AU - Gray, Ron
AU - Quinn, Thomas C
AU - Serwadda, David
AU - Chang, Larry
AD - Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland.
Y1 - 2014/11//
PY - 2014
DA - November 2014
SP - 575
EP - 578
PB - Mary Ann Liebert, Inc., 2 Madison Ave Larchmont NY 10538 United States
VL - 28
IS - 11
SN - 1087-2914, 1087-2914
KW - Immunology Abstracts; Health & Safety Science Abstracts; Virology & AIDS Abstracts
KW - Acquired immune deficiency syndrome
KW - CD4 antigen
KW - Age
KW - antiretroviral therapy
KW - Antiretroviral agents
KW - Sexually transmitted diseases
KW - V 22360:AIDS and HIV
KW - H 11000:Diseases/Injuries/Trauma
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1827882746?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS+Patient+Care+and+STDs&rft.atitle=Is+CD4+Monitoring+Needed+Among+Ugandan+Clients+Achieving+a+Virologic+and+Immunologic+Response+to+Treatment%3F&rft.au=Reynolds%2C+Steven+J%3BSempa%2C+Joseph+B%3BKiragga%2C+Agnes+N%3BNewell%2C+Kevin%3BNakigozi%2C+Gertrude%3BGaliwango%2C+Ronald%3BGray%2C+Ron%3BQuinn%2C+Thomas+C%3BSerwadda%2C+David%3BChang%2C+Larry&rft.aulast=Reynolds&rft.aufirst=Steven&rft.date=2014-11-01&rft.volume=28&rft.issue=11&rft.spage=575&rft.isbn=&rft.btitle=&rft.title=AIDS+Patient+Care+and+STDs&rft.issn=10872914&rft_id=info:doi/10.1089%2Fapc.2014.0086
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2016-10-01
N1 - Number of references - 17
N1 - Last updated - 2016-10-26
N1 - SubjectsTermNotLitGenreText - Age; CD4 antigen; antiretroviral therapy; Acquired immune deficiency syndrome; Antiretroviral agents; Sexually transmitted diseases
DO - http://dx.doi.org/10.1089/apc.2014.0086
ER -
TY - JOUR
T1 - Predictive prognostic role of miR-181a with discrepancy in the liver and serum of genotype 4 hepatitis C virus patients.
AN - 1826615268; 25279157
AB - microRNA (miRNA) expression in organs does not always represent their quantity in serum. A disparity in the expression of miR-181a has been reported in the tissues and serum of hepatocellular carcinoma (HCC) patients. Since hepatitis C virus (HCV) is a major cause of HCC and miR-181a has never been studied in HCV, the present study aimed to investigate the miR-181a expression profile in genotype 4 (GT4)-HCV patients to evaluate whether this pattern is also apparent in HCV. RNA was extracted from liver tissues, peripheral mononuclear cells (PBMCs) and serum samples from GT4-HCV-infected patients and healthy donors to evaluate the relative miR-181a expression using quantitative reverse transcription-polymerase chain reaction. miR-181a was significantly higher in the serum of naïve patients compared to controls, and an inverse correlation with the viral load and liver enzymes was apparent. By contrast, no difference in miR-181a expression was observed in the liver tissues and PBMCs of patients compared to controls. This expression observed in HCV is conflicting to that previously reported in HCC. The study also demonstrates a significant upregulation of miR-181a post-interferon/ribavirin treatment in the serum of sustained virological responders (SVRs) compared to non-responders and treatment-naïve SVRs. In conclusion, miR-181a may be considered to be a possible prognostic marker in GT4-HCV infection.
JF - Biomedical reports
AU - Elhelw, Dalia Sherif
AU - Mekky, Radwa Yehia
AU - El-Ekiaby, Nada
AU - Ahmed, Rasha
AU - Eldin, Mohammad Ahmed Mohey
AU - El-Sayed, Mohammad
AU - Abouelkhair, Mahmoud Mohammad
AU - Salah, Ayman
AU - Zekri, Abdel Rahman
AU - Esmat, Gamal
AU - Abdelaziz, Ahmed Ihab
AD - The Molecular Pathology Research Group, Department of Pharmacology and Toxicology, German University in Cairo, New Cairo 11835, Egypt. ; Department of Endemic Medicine and Hepatology, Cairo University, Cairo 11562, Egypt. ; Department of Surgery, Cairo University, Cairo 11562, Egypt. ; Virology and Immunology Unit, Cancer Biology Department, National Cancer Institute, Cairo University, Cairo 11976, Egypt.
Y1 - 2014/11//
PY - 2014
DA - November 2014
SP - 843
EP - 848
VL - 2
IS - 6
SN - 2049-9434, 2049-9434
KW - genotype 4
KW - treatment response
KW - microRNA-181a
KW - hepatitis C virus
KW - sustained virological responders
KW - prognosis
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1826615268?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biomedical+reports&rft.atitle=Predictive+prognostic+role+of+miR-181a+with+discrepancy+in+the+liver+and+serum+of+genotype+4+hepatitis+C+virus+patients.&rft.au=Elhelw%2C+Dalia+Sherif%3BMekky%2C+Radwa+Yehia%3BEl-Ekiaby%2C+Nada%3BAhmed%2C+Rasha%3BEldin%2C+Mohammad+Ahmed+Mohey%3BEl-Sayed%2C+Mohammad%3BAbouelkhair%2C+Mahmoud+Mohammad%3BSalah%2C+Ayman%3BZekri%2C+Abdel+Rahman%3BEsmat%2C+Gamal%3BAbdelaziz%2C+Ahmed+Ihab&rft.aulast=Elhelw&rft.aufirst=Dalia&rft.date=2014-11-01&rft.volume=2&rft.issue=6&rft.spage=843&rft.isbn=&rft.btitle=&rft.title=Biomedical+reports&rft.issn=20499434&rft_id=info:doi/
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date created - 2014-10-03
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
ER -
TY - JOUR
T1 - HIV-1 Envelope Glycoprotein Trimer Immunogenicity Elicited in the Presence of Human CD4 Alters the Neutralization Profile
AN - 1768582376; PQ0002687106
AB - The HIV-1 envelope glycoproteins (Env) gp120 and gp41 are the sole virally derived components on the surface of the virus. These glycoproteins mediate receptor binding and entry and are targets for neutralizing antibodies. The most highly validated protein region on Env that is a target for broadly neutralizing antibodies is the conserved CD4 binding site. Mimetics of Env have been used in attempts to elicit antibodies to the CD4 binding site. Some trimers, such as the soluble foldon trimers used here, elicit 5-10% of the Env-directed B cell response to this conserved region. As these trimers, or other Env versions, advance into clinical development, there is both considerable interest and concern as to whether binding to the abundant CD4 present on the surface of T cells and macrophages may blunt potentially protective antibody responses to this site. Here, we utilized rabbits transgenic for human CD4 to evaluate the role of CD4:Env interaction in vivo relative to the elicitation of Env-directed antibodies following immunization. We analyzed responses to trimers both capable and incapable of recognizing human CD4 with high affinity. We demonstrated that the presence of human CD4 in vivo did not significantly affect the overall elicitation of Env binding or CD4bs-directed antibodies. However, the presence of CD4 did reduce the capacity of elicited serum antibodies to neutralize the clade C isolate, MW965. Reduction of HXBc2 neutralization was associated with the CD4 binding-incompetent trimers. These results highlight an important consideration regarding CD4 binding-competent trimeric Env immunogens as they enter the clinic for human vaccine trials.
JF - AIDS Research and Human Retroviruses
AU - Forsell, Mattias NE
AU - McKee, Krisha
AU - Feng, Yu
AU - Mascola, John R
AU - Wyatt, Richard T
AD - Vaccine Research Center, NIAID, National Institutes of Health, Bethesda, Maryland.
Y1 - 2014/11//
PY - 2014
DA - November 2014
SP - 1089
EP - 1098
PB - Mary Ann Liebert, Inc., 140 Huguenot Street New Rochelle NY 10801 United States
VL - 30
IS - 11
SN - 0889-2229, 0889-2229
KW - Immunology Abstracts; Health & Safety Science Abstracts; Virology & AIDS Abstracts
KW - Macrophages
KW - Acquired immune deficiency syndrome
KW - glycoprotein gp41
KW - Lymphocytes B
KW - Clinical trials
KW - Immunization
KW - Glycoprotein gp120
KW - CD4 antigen
KW - Antibodies
KW - Retrovirus
KW - Envelopes
KW - Immunogenicity
KW - Human immunodeficiency virus 1
KW - Lymphocytes T
KW - Proteins
KW - Glycoproteins
KW - Vaccines
KW - Neutralization
KW - H 6000:Natural Disasters/Civil Defense/Emergency Management
KW - V 22360:AIDS and HIV
KW - F 06910:Microorganisms & Parasites
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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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+Journal+of+Health+Psychology&rft.atitle=Concerns+about+unintended+negative+consequences+of+informing+the+public+about+multifactorial+risks+may+be+premature+for+young+adult+smokers&rft.au=Waters%2C+Erika+A%3BKincaid%2C+Caroline%3BKaufman%2C+Annette+R%3BStock%2C+Michelle+L%3BPeterson%2C+Laurel+M%3BMuscanell%2C+Nicole+L%3BGuadagno%2C+Rosanna+E&rft.aulast=Waters&rft.aufirst=Erika&rft.date=2014-11-01&rft.volume=19&rft.issue=4&rft.spage=720&rft.isbn=&rft.btitle=&rft.title=British+Journal+of+Health+Psychology&rft.issn=1359107X&rft_id=info:doi/10.1111%2Fbjhp.12069
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Date revised - 2015-01-09
N1 - Last updated - 2016-05-24
DO - http://dx.doi.org/10.1111/bjhp.12069
ER -
TY - JOUR
T1 - Symptoms of Attention-Deficit/Hyperactivity Disorder and Peer Functioning: a Transactional Model of Development
AN - 1665155814
AB - The goals of this short-term longitudinal study were to investigate differential, independent effects of inattention and hyperactivity/impulsivity on children’s peer relationships and the dynamic, transactional interplay between ADHD symptoms and indices of peer functioning over time. This study used a community sample that included 739 preadolescents (239 fourth graders and 500 fifth graders; 52.23 % boys) from northern Taiwan, who were assessed every six months at three time points. Children’s ADHD symptoms were measured using the parent report on the Swanson, Nolan, and Pelham, version IV scale. Positive and negative facets of peer functioning, including peer rejection, peer acceptance, and the number of friendships, were assessed via peer nomination. Results of cross-lagged models indicated that inattention, but not hyperactivity/impulsivity, predicted subsequent peer impairment (i.e., lower peer acceptance and fewer dyadic friendships). Findings also showed a vicious cycle in which inattentive symptoms predicted later peer impairment, which in turn led to increases in both inattention and hyperactivity/impulsivity. These findings did not differ across gender, and the majority of the findings remained significant even after controlling for age and physical aggression. Taken together, this study demonstrated the detrimental effect of inattention on children’s peer functioning and the transactional and dynamic interplay between inattention and peer impairment in a Chinese culture.
JF - Journal of Abnormal Child Psychology
AU - Tseng, Wan-Ling
AU - Kawabata, Yoshito
AU - Gau, Susan Shur-Fen
AU - Crick, Nicki R
AD - Institute of Child Development, University of Minnesota, Minneapolis, USA wan-ling.tseng@nih.gov wan-ling.tseng@nih.gov wan-ling.tseng@nih.gov; Department of Psychiatry, National Taiwan University Hospital and College of Medicine, 7 Chung-Shan Road, Taipei, 10002, Taiwan gaushufe@ntu.edu.tw; Institute of Child Development, University of Minnesota, Minneapolis, USA
Y1 - 2014/11//
PY - 2014
DA - Nov 2014
SP - 1353
EP - 1365
CY - New York
PB - Springer Science & Business Media
VL - 42
IS - 8
SN - 0091-0627
KW - Medical Sciences--Physical Medicine And Rehabilitation
KW - Acceptance
KW - Aggressive young boys
KW - Aggression
KW - Attention deficit hyperactivity disorder
KW - Attention deficits
KW - Boys
KW - Children
KW - Friendships
KW - Gender
KW - Hyperactivity
KW - Impulsivity
KW - Peer acceptance
KW - Peer rejection
KW - Peer relationships
KW - Rejection
KW - Short term
KW - Taiwan
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665155814?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Abnormal+Child+Psychology&rft.atitle=Symptoms+of+Attention-Deficit%2FHyperactivity+Disorder+and+Peer+Functioning%3A+a+Transactional+Model+of+Development&rft.au=Tseng%2C+Wan-Ling%3BKawabata%2C+Yoshito%3BGau%2C+Susan+Shur-Fen%3BCrick%2C+Nicki+R&rft.aulast=Tseng&rft.aufirst=Wan-Ling&rft.date=2014-11-01&rft.volume=42&rft.issue=8&rft.spage=1353&rft.isbn=&rft.btitle=&rft.title=Journal+of+Abnormal+Child+Psychology&rft.issn=00910627&rft_id=info:doi/10.1007%2Fs10802-014-9883-8
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Date revised - 2015-01-09
N1 - Last updated - 2016-05-12
N1 - SubjectsTermNotLitGenreText - Taiwan
DO - http://dx.doi.org/10.1007/s10802-014-9883-8
ER -
TY - JOUR
T1 - Exploring psychological responses to genetic testing for Lynch Syndrome within the family context
AN - 1665154316
AB - Objective Genetic testing for hereditary cancer susceptibility syndromes is a family-centered process. Nonetheless, little research has explored how the family context affects psychological responses to genetic testing. We examine how personal test results and the test results of immediate and extended family members shape responses to genetic testing. Methods Individuals at risk of carrying a mutation associated with an inherited cancer susceptibility syndrome (Lynch syndrome) received genetic testing. Six months after receiving their results, participants reported on cancer distress, cancer worry, and depressive symptoms. Results Among mutation carriers for Lynch syndrome, the higher the proportion of carriers in their immediate family, the less cancer worry and distress they reported. In contrast, mutation carriers and non-carriers with a high proportion of carriers in their immediate family and mutation carriers with a high proportion of carriers in their extended family were at elevated risk for clinically significant levels of depressive symptoms. Conclusion Personal test results alone are not highly predictive of psychological outcomes. Instead, the interaction between personal and family test results, or in some cases, family test results alone, predict key psychological outcomes. The current research has important implications for genetic counseling and intervention efforts. Published 2014. This article is a U.S. Government work and is in the public domain in the USA.
JF - Psycho-Oncology
AU - Eliezer, Dina
AU - Hadley, Donald W
AU - Koehly, Laura M
AD - National Human Genome Research Institute, Bethesda, MD, USA. ; National Human Genome Research Institute, Bethesda, MD, USA.
Y1 - 2014/11//
PY - 2014
DA - Nov 2014
SP - 1292
EP - 1299
CY - Chichester
PB - Wiley Subscription Services, Inc.
VL - 23
IS - 11
SN - 1057-9249
KW - Medical Sciences--Psychiatry And Neurology
KW - At risk
KW - Cancer
KW - Carriers
KW - Counselling
KW - Depression
KW - Genetic counselling
KW - Genetic screening
KW - Psychological distress
KW - Public domain
KW - Relatives
KW - Susceptibility
KW - Symptoms
KW - United States--US
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665154316?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Psycho-Oncology&rft.atitle=Exploring+psychological+responses+to+genetic+testing+for+Lynch+Syndrome+within+the+family+context&rft.au=Eliezer%2C+Dina%3BHadley%2C+Donald+W%3BKoehly%2C+Laura+M&rft.aulast=Eliezer&rft.aufirst=Dina&rft.date=2014-11-01&rft.volume=23&rft.issue=11&rft.spage=1292&rft.isbn=&rft.btitle=&rft.title=Psycho-Oncology&rft.issn=10579249&rft_id=info:doi/10.1002%2Fpon.3551
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Date revised - 2015-01-09
N1 - Last updated - 2016-05-13
N1 - SubjectsTermNotLitGenreText - United States--US
DO - http://dx.doi.org/10.1002/pon.3551
ER -
TY - JOUR
T1 - Reliability and validity of expert assessment based on airborne and urinary measures of nickel and chromium exposure in the electroplating industry
AN - 1664212763; PQ0001187959
AB - The reliability and validity of six experts' exposure ratings were evaluated for 64 nickel-exposed and 72 chromium-exposed workers from six Shanghai electroplating plants based on airborne and urinary nickel and chromium measurements. Three industrial hygienists and three occupational physicians independently ranked the exposure intensity of each metal on an ordinal scale (1-4) for each worker's job in two rounds: the first round was based on responses to an occupational history questionnaire and the second round also included responses to an electroplating industry-specific questionnaire. The Spearman correlation (r sub(s)) was used to compare each rating's validity to its corresponding subject-specific arithmetic mean of four airborne or four urinary measurements. Reliability was moderately high (weighted kappa range=0.60-0.64). Validity was poor to moderate (r sub(s)=-0.37-0.46) for both airborne and urinary concentrations of both metals. For airborne nickel concentrations, validity differed by plant. For dichotomized metrics, sensitivity and specificity were higher based on urinary measurements (47-78%) than airborne measurements (16-50%). Few patterns were observed by metal, assessment round, or expert type. These results suggest that, for electroplating exposures, experts can achieve moderately high agreement and (reasonably) distinguish between low and high exposures when reviewing responses to in-depth questionnaires used in population-based case-control studies.
JF - Journal of Exposure Science and Environmental Epidemiology
AU - Chen, Yu-Cheng
AU - Coble, Joseph B
AU - Deziel, Nicole C
AU - Ji, Bu-Tian
AU - Xue, Shouzheng
AU - Lu, Wei
AU - Stewart, Patricia A
AU - Friesen, Melissa C
AD - Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland, USA
Y1 - 2014/11//
PY - 2014
DA - November 2014
SP - 622
EP - 628
PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL - 24
IS - 6
SN - 1559-0631, 1559-0631
KW - Toxicology Abstracts; Health & Safety Science Abstracts; Environment Abstracts
KW - Metals
KW - Historical account
KW - Sensitivity
KW - Inventories
KW - Chromium
KW - Heavy metals
KW - Nickel
KW - Mathematics
KW - Urine
KW - Metal finishing industry
KW - China, People's Rep., Shanghai
KW - Occupational exposure
KW - H 1000:Occupational Safety and Health
KW - X 24360:Metals
KW - ENA 02:Toxicology & Environmental Safety
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1664212763?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Exposure+Science+and+Environmental+Epidemiology&rft.atitle=Reliability+and+validity+of+expert+assessment+based+on+airborne+and+urinary+measures+of+nickel+and+chromium+exposure+in+the+electroplating+industry&rft.au=Chen%2C+Yu-Cheng%3BCoble%2C+Joseph+B%3BDeziel%2C+Nicole+C%3BJi%2C+Bu-Tian%3BXue%2C+Shouzheng%3BLu%2C+Wei%3BStewart%2C+Patricia+A%3BFriesen%2C+Melissa+C&rft.aulast=Chen&rft.aufirst=Yu-Cheng&rft.date=2014-11-01&rft.volume=24&rft.issue=6&rft.spage=622&rft.isbn=&rft.btitle=&rft.title=Journal+of+Exposure+Science+and+Environmental+Epidemiology&rft.issn=15590631&rft_id=info:doi/10.1038%2Fjes.2014.22
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-03-01
N1 - Last updated - 2016-03-30
N1 - SubjectsTermNotLitGenreText - Inventories; Chromium; Heavy metals; Nickel; Occupational exposure; Mathematics; Sensitivity; Historical account; Metals; Urine; Metal finishing industry; China, People's Rep., Shanghai
DO - http://dx.doi.org/10.1038/jes.2014.22
ER -
TY - JOUR
T1 - A Research on the Relationship between Exercise Behavior of the Elderly and Medical Frequency as well as Quality of Life
AN - 1660394907; PQ0001022306
AB - Purpose: To understand the impact of exercise frequency (per week of the elderly) on medical inspection frequency and quality of life. Method: Conduct an investigation through questionnaire survey method, aiming at people over 65. Descriptive statistics, t-test, and one-way ANOVA were used to analyze the data including 898 valid questionnaires. Result: 1. Elderly whose exercise more than 5 days a week get higher score in Physical Component Summary (PCS) and Mental Component Summary (MCS), and the inspection frequency was low. 2. The significant differences on medical inspection frequency exist in variables such as exercise frequency, gender, age, hospitalized or not, suffer from chronic diseases or not, and work or not. 3. The medical inspection frequency show sudden deterioration after the age of 75, which means that the age of 75 is a key age point. Conclusion: Elders whose exercise more than 3 days a week only perform better in MCS. However, if the number of days of doing exercise reaches 5 days a week, it will get better scores in not only MCS and PCS, but also reduce the number of medical inspection frequency. We suggest the elderly people should exercise more than five days a week to reduce the medical visits, and enhance the quality of life.
JF - Tiyu Keyan/Sports Science Research
AU - Kao, Hsingkuei
AU - Liu, Zhimin
AD - Taipei Municipal Nei-Hu Junior High School, Taipei, China
Y1 - 2014/11//
PY - 2014
DA - Nov 2014
SP - 17
EP - 22
PB - Shanghai Research Institute of Sports Science, 87 Wu Xing Rd. Shanghai 200030 China, [mailto:shtyky@online.sh.cn], [URL:http://www.shriss.cn]
VL - 35
IS - 6
SN - 1006-1207, 1006-1207
KW - Physical Education Index
KW - Age
KW - Statistics
KW - Research (statistical design)
KW - Gerontology
KW - Surveys
KW - Lifestyle
KW - scoring
KW - Exercise (frequency)
KW - PE 030:Exercise, Health & Physical Fitness
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660394907?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aphysicaleducation&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Tiyu+Keyan%2FSports+Science+Research&rft.atitle=A+Research+on+the+Relationship+between+Exercise+Behavior+of+the+Elderly+and+Medical+Frequency+as+well+as+Quality+of+Life&rft.au=Kao%2C+Hsingkuei%3BLiu%2C+Zhimin&rft.aulast=Kao&rft.aufirst=Hsingkuei&rft.date=2014-11-01&rft.volume=35&rft.issue=6&rft.spage=17&rft.isbn=&rft.btitle=&rft.title=Tiyu+Keyan%2FSports+Science+Research&rft.issn=10061207&rft_id=info:doi/
LA - Chinese
DB - Physical Education Index
N1 - Date revised - 2015-03-01
N1 - Last updated - 2015-11-16
N1 - SubjectsTermNotLitGenreText - Age; Statistics; Research (statistical design); Gerontology; Surveys; Exercise (frequency); scoring; Lifestyle
ER -
TY - JOUR
T1 - A bilingual-monolingual comparison of young children's vocabulary size: Evidence from comprehension and production
AN - 1660012214; 201501679
AB - It is often assumed that young bilinguals are lexically delayed in comparison to monolinguals. A comprehensive comparison of comprehension and production vocabulary in 31 firstborn bilingual and 30 matched monolingual children fails to find empirical foundation for this assumption. Several raters completed Dutch and French adaptations of the MacArthur Communicative Development Inventories for children aged 13 and 20 months. At 13 months, bilinguals understood more words than did monolinguals; at 20 months, monolinguals knew more Dutch words than did bilinguals (combining comprehension and production). There were no group differences for word production or for Dutch word comprehension. Both groups understood and produced the same number of lexicalized meanings; ratios of word comprehension to word production did not differ; interindividual variation was similar. This study underscores the importance of conducting bilingual-monolingual comparisons with matched groups and suggests that if individual bilingual children appear to be slow in early vocabulary development, reasons other than their bilingualism should be investigated. Adapted from the source document
JF - Applied Psycholinguistics
AU - De Houwer, Annick
AU - Bornstein, Marc H
AU - Putnick, Diane L
AD - Erfurt University and Eunice Kennedy Shriver National Institute of Child Health and Human Development annick.dehouwer@uni-erfurt.de
Y1 - 2014/11//
PY - 2014
DA - November 2014
SP - 1189
EP - 1211
VL - 35
IS - 6
SN - 0142-7164, 0142-7164
KW - Vocabulary Size (94862)
KW - Dutch (20100)
KW - Language Acquisition (41600)
KW - Bilingualism (08850)
KW - French (25750)
KW - Comprehension (13950)
KW - Monolingualism (54850)
KW - Children (11850)
KW - article
KW - 4026: psycholinguistics; bilingual language processing
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660012214?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Allba&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Applied+Psycholinguistics&rft.atitle=A+bilingual-monolingual+comparison+of+young+children%27s+vocabulary+size%3A+Evidence+from+comprehension+and+production&rft.au=De+Houwer%2C+Annick%3BBornstein%2C+Marc+H%3BPutnick%2C+Diane+L&rft.aulast=De+Houwer&rft.aufirst=Annick&rft.date=2014-11-01&rft.volume=35&rft.issue=6&rft.spage=1189&rft.isbn=&rft.btitle=&rft.title=Applied+Psycholinguistics&rft.issn=01427164&rft_id=info:doi/
LA - English
DB - Linguistics and Language Behavior Abstracts (LLBA)
N1 - Date revised - 2015-03-01
N1 - Last updated - 2016-09-27
N1 - CODEN - APPSDZ
N1 - SubjectsTermNotLitGenreText - Bilingualism (08850); Comprehension (13950); Children (11850); Dutch (20100); Monolingualism (54850); Vocabulary Size (94862); French (25750); Language Acquisition (41600)
ER -
TY - JOUR
T1 - Improving the specificity and efficacy of CRISPR/CAS9 and gRNA through target specific DNA reporter
AN - 1647013778; 21276148
AB - Genomic engineering by the guide RNA (gRNA)-directed CRISPR/CAS9 is rapidly becoming a method of choice for various biological systems. However, pressing concerns remain regarding its off-target activities and wide variations in efficacies. While next generation sequencing (NGS) has been primarily used to evaluate the efficacies and off-target activities of gRNAs, it only detects the imperfectly repaired double strand DNA breaks (DSB) by the error-prone non-homologous end joining (NHEJ) mechanism and may not faithfully represent the DSB activities because the efficiency of NHEJ-mediated repair varies depending on the local chromatin environment. Here we describe a reporter system for unbiased detection and comparison of DSB activities that promises to improve the chance of success in genomic engineering and to facilitate large-scale screening of CAS9 activities and gRNA libraries. Additionally, we demonstrated that the tolerances to mismatches between a gRNA and the corresponding target DNA can occur at any position of the gRNA, and depend on both specific gRNA sequences and CAS9 constructs used.
JF - Journal of Biotechnology
AU - Zhang, Jian-Hua
AU - Pandey, Mritunjay
AU - Kahler, John F
AU - Loshakov, Anna
AU - Harris, Benjamin
AU - Dagur, Pradeep K
AU - Mo, Yin-Yuan
AU - Simonds, William F
AD - Metabolic Diseases Branch, Bldg. 10, Room 8C-101, National Institute of Diabetes and Digestive and Kidney Diseases, United States
Y1 - 2014/11//
PY - 2014
DA - November 2014
SP - 1
EP - 8
PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands
VL - 189
SN - 0168-1656, 0168-1656
KW - Biochemistry Abstracts 2: Nucleic Acids; Biotechnology and Bioengineering Abstracts
KW - CRISPR
KW - CAS9
KW - gRNA
KW - EGFP reporter
KW - Specificity
KW - CRISPR clustered regularly interspaced short palindromic repeats
KW - CAS9 CRISPR associated protein
KW - gRNA guide RNA
KW - NHEJ none homologous end joining
KW - DSB double strand DNA break
KW - NGS next generation sequencing
KW - DNA damage
KW - Non-homologous end joining
KW - RNA
KW - Chromatin
KW - Nucleotide sequence
KW - genomics
KW - W 30925:Genetic Engineering
KW - N 14820:DNA Metabolism & Structure
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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
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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
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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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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
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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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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]
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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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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:
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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:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/carcin/bgu137
ER -
TY - JOUR
T1 - Definition of smad3 phosphorylation events that affect malignant and metastatic behaviors in breast cancer cells.
AN - 1619317779; 25205100
AB - Smad3, a major intracellular mediator of TGFβ signaling, functions as both a positive and negative regulator in carcinogenesis. In response to TGFβ, the TGFβ receptor phosphorylates serine residues at the Smad3 C-tail. Cancer cells often contain high levels of the MAPK and CDK activities, which can lead to the Smad3 linker region becoming highly phosphorylated. Here, we report, for the first time, that mutation of the Smad3 linker phosphorylation sites markedly inhibited primary tumor growth, but significantly increased lung metastasis of breast cancer cell lines. In contrast, mutation of the Smad3 C-tail phosphorylation sites had the opposite effect. We show that mutation of the Smad3 linker phosphorylation sites greatly intensifies all TGFβ-induced responses, including growth arrest, apoptosis, reduction in the size of putative cancer stem cell population, epithelial-mesenchymal transition, and invasive activity. Moreover, all TGFβ responses were completely lost on mutation of the Smad3 C-tail phosphorylation sites. Our results demonstrate a critical role of the counterbalance between the Smad3 C-tail and linker phosphorylation in tumorigenesis and metastasis. Our findings have important implications for therapeutic intervention of breast cancer.
©2014 American Association for Cancer Research.
JF - Cancer research
AU - Bae, Eunjin
AU - Sato, Misako
AU - Kim, Ran-Ju
AU - Kwak, Mi-Kyung
AU - Naka, Kazuhito
AU - Gim, Jungsoo
AU - Kadota, Mitsutaka
AU - Tang, Binwu
AU - Flanders, Kathleen C
AU - Kim, Tae-Aug
AU - Leem, Sun-Hee
AU - Park, Taesung
AU - Liu, Fang
AU - Wakefield, Lalage M
AU - Kim, Seong-Jin
AU - Ooshima, Akira
AD - CHA Cancer Research Institute, CHA University, Seoul, Korea. ; Laboratory of Cancer Biology and Genetics, National Cancer Institute, Bethesda, Maryland. ; Cancer Research Institute, Kanazawa University, Kanazawa, Ishikawa, Japan. ; Interdisciplinary Program in Bioinformatics, Seoul National University, Seoul, Korea. ; Genome Resource and Analysis Unit, RIKEN Center for Developmental Biology, Kobe, Japan. ; Department of Biology and Biomedical Science, Dong-A University, Busan, Korea. ; Interdisciplinary Program in Bioinformatics, Seoul National University, Seoul, Korea. Department of Statistics, Seoul National University, Seoul, Korea. ; Center for Advanced Biotechnology and Medicine, Susan Lehman Cullman Laboratory for Cancer Research, Department of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers Cancer Institute of New Jersey, Rutgers, The State University of New Jersey, Piscataway, New Jersey. ; CHA Cancer Research Institute, CHA University, Seoul, Korea. aooshima@cha.ac.kr kimsj@cha.ac.kr. ; CHA Cancer Research Institute, CHA University, Seoul, Korea. Laboratory of Cancer Biology and Genetics, National Cancer Institute, Bethesda, Maryland. aooshima@cha.ac.kr kimsj@cha.ac.kr.
Y1 - 2014/11/01/
PY - 2014
DA - 2014 Nov 01
SP - 6139
EP - 6149
VL - 74
IS - 21
KW - Receptors, Transforming Growth Factor beta
KW - 0
KW - SMAD3 protein, human
KW - Smad3 Protein
KW - Transforming Growth Factor beta
KW - Index Medicus
KW - Receptors, Transforming Growth Factor beta -- genetics
KW - Humans
KW - Receptors, Transforming Growth Factor beta -- metabolism
KW - Cell Line, Tumor
KW - Gene Expression Regulation, Neoplastic
KW - Neoplasm Metastasis -- genetics
KW - Phosphorylation -- genetics
KW - Signal Transduction -- genetics
KW - Xenograft Model Antitumor Assays
KW - Neoplasm Metastasis -- pathology
KW - Transforming Growth Factor beta -- genetics
KW - Transforming Growth Factor beta -- metabolism
KW - Mutation
KW - Female
KW - Breast Neoplasms -- genetics
KW - Breast Neoplasms -- pathology
KW - Smad3 Protein -- metabolism
KW - Epithelial-Mesenchymal Transition -- genetics
KW - Cell Transformation, Neoplastic -- genetics
KW - Smad3 Protein -- genetics
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1619317779?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Definition+of+smad3+phosphorylation+events+that+affect+malignant+and+metastatic+behaviors+in+breast+cancer+cells.&rft.au=Bae%2C+Eunjin%3BSato%2C+Misako%3BKim%2C+Ran-Ju%3BKwak%2C+Mi-Kyung%3BNaka%2C+Kazuhito%3BGim%2C+Jungsoo%3BKadota%2C+Mitsutaka%3BTang%2C+Binwu%3BFlanders%2C+Kathleen+C%3BKim%2C+Tae-Aug%3BLeem%2C+Sun-Hee%3BPark%2C+Taesung%3BLiu%2C+Fang%3BWakefield%2C+Lalage+M%3BKim%2C+Seong-Jin%3BOoshima%2C+Akira&rft.aulast=Bae&rft.aufirst=Eunjin&rft.date=2014-11-01&rft.volume=74&rft.issue=21&rft.spage=6139&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=1538-7445&rft_id=info:doi/10.1158%2F0008-5472.CAN-14-0803
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-01-05
N1 - Date created - 2014-11-01
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1158/0008-5472.CAN-14-0803
ER -
TY - JOUR
T1 - Inhibition of NANOG/NANOGP8 downregulates MCL-1 in colorectal cancer cells and enhances the therapeutic efficacy of BH3 mimetics.
AN - 1619317717; 25208882
AB - High levels of BCL-2 family members in colorectal carcinoma cause resistance to treatment. Inhibition of NANOG or its paralog NANOGP8 reduces the proliferation, stemness, and tumorigenicity of colorectal carcinoma cells. Our hypothesis was that inhibition of NANOG/NANOGP8 enhances the cytotoxic effect of BH3 mimetics targeting BCL-2 family members in colorectal carcinoma cells through reducing expression of MCL-1, a prosurvival BCL-2 protein.
Lentiviral vector (LV) shRNA to NANOG (shNG-1) or NANOGP8 (shNp8-1) transduced colorectal carcinoma cells that were also exposed to the BH3 mimetics ABT-737 or ABT-199 in vivo in colorectal carcinoma xenografts and in vitro where proliferation, protein and gene expression, and apoptosis were measured. Clone A and CX-1 were sensitive to ABT-737 and ABT-199 at IC50s of 2 to 9 μmol/L but LS174T was resistant with IC50s of 18 to 30 μmol/L. Resistance was associated with high MCL-1 expression in LS174T. LVshNG-1 or LVshNp8-1 decreased MCL-1 expression, increased apoptosis, and decreased replating efficiency in colorectal carcinoma cells treated with either ABT-737 or ABT-199 compared with the effects of either BH3 mimetic alone. Inhibition or overexpression of MCL-1 alone replicated the effects of LVshNG-1 or LVshNp8-1 in increasing or decreasing the apoptosis caused with the BH3 mimetic. The combination therapy inhibited the growth of LS174T xenografts in vivo compared with untreated controls or treatment with only LV shRNA or ABT-737.
Inhibition of NANOGP8 or NANOG enhances the cytotoxicity of BH3 mimetics that target BCL-2 family members. Gene therapy targeting the NANOGs may increase the efficacy of BH3 mimetics in colorectal carcinoma. ©2014 American Association for Cancer Research.
JF - Clinical cancer research : an official journal of the American Association for Cancer Research
AU - Mattoo, Abid R
AU - Zhang, Jingyu
AU - Espinoza, Luis A
AU - Jessup, J Milburn
AD - Laboratory of Experimental Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland. ; Laboratory of Experimental Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland. Cancer Diagnosis Program, Division of Cancer Treatment and Diagnosis, National Cancer Institute, Bethesda, Maryland. jessupj@mail.nih.gov.
Y1 - 2014/11/01/
PY - 2014
DA - 2014 Nov 01
SP - 5446
EP - 5455
VL - 20
IS - 21
SN - 1078-0432, 1078-0432
KW - ABT-737
KW - 0
KW - BH3 Interacting Domain Death Agonist Protein
KW - Biphenyl Compounds
KW - Bridged Bicyclo Compounds, Heterocyclic
KW - Homeodomain Proteins
KW - MCL1 protein, human
KW - Myeloid Cell Leukemia Sequence 1 Protein
KW - NANOG protein, human
KW - Nanog Homeobox Protein
KW - Nitrophenols
KW - Piperazines
KW - RNA, Small Interfering
KW - Sulfonamides
KW - venetoclax
KW - N54AIC43PW
KW - Index Medicus
KW - Animals
KW - Nitrophenols -- pharmacology
KW - Mice, Inbred NOD
KW - HEK293 Cells
KW - Humans
KW - Biphenyl Compounds -- pharmacology
KW - RNA, Small Interfering -- genetics
KW - Cell Line, Tumor
KW - Mice
KW - Piperazines -- pharmacology
KW - Apoptosis -- genetics
KW - Bridged Bicyclo Compounds, Heterocyclic -- pharmacology
KW - Sulfonamides -- pharmacology
KW - Apoptosis -- drug effects
KW - Xenograft Model Antitumor Assays
KW - HT29 Cells
KW - Mice, SCID
KW - Cell Line
KW - Male
KW - BH3 Interacting Domain Death Agonist Protein -- genetics
KW - Down-Regulation -- genetics
KW - Homeodomain Proteins -- antagonists & inhibitors
KW - Myeloid Cell Leukemia Sequence 1 Protein -- genetics
KW - Colorectal Neoplasms -- genetics
KW - Down-Regulation -- drug effects
KW - Colorectal Neoplasms -- drug therapy
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+cancer+research+%3A+an+official+journal+of+the+American+Association+for+Cancer+Research&rft.atitle=Inhibition+of+NANOG%2FNANOGP8+downregulates+MCL-1+in+colorectal+cancer+cells+and+enhances+the+therapeutic+efficacy+of+BH3+mimetics.&rft.au=Mattoo%2C+Abid+R%3BZhang%2C+Jingyu%3BEspinoza%2C+Luis+A%3BJessup%2C+J+Milburn&rft.aulast=Mattoo&rft.aufirst=Abid&rft.date=2014-11-01&rft.volume=20&rft.issue=21&rft.spage=5446&rft.isbn=&rft.btitle=&rft.title=Clinical+cancer+research+%3A+an+official+journal+of+the+American+Association+for+Cancer+Research&rft.issn=10780432&rft_id=info:doi/10.1158%2F1078-0432.CCR-14-1134
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-07-01
N1 - Date created - 2014-11-01
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1158/1078-0432.CCR-14-1134
ER -
TY - JOUR
T1 - A phase I/II trial of belinostat in combination with cisplatin, doxorubicin, and cyclophosphamide in thymic epithelial tumors: a clinical and translational study.
AN - 1619317602; 25189481
AB - This phase I/II study sought to determine the safety and maximum tolerated dose (MTD) of a novel schedule of belinostat, a histone deacetylase inhibitor (HDAC) administered before and in combination with cisplatin (P), doxorubicin (A), and cyclophosphamide (C) in thymic epithelial tumors (TET). Antitumor activity, pharmacokinetics, and biomarkers of response were also assessed.
Patients with advanced, unresectable TET received increasing doses of belinostat as a continuous intravenous infusion over 48 hours with chemotherapy in 3-week cycles. In phase II, belinostat at the MTD was used. Twenty-six patients were enrolled (thymoma, 12; thymic carcinoma, 14). Dose-limiting toxicities at 2,000 mg/m(2) belinostat were grade 3 nausea and diarrhea and grade 4 neutropenia and thrombocytopenia, respectively, in two patients. Twenty-four patients were treated at the MTD of 1,000 mg/m(2) with chemotherapy (P, 50 mg/m(2) on day 2; A, 25 mg/m(2) on days 2 and 3; C, 500 mg/m(2) on day 3). Objective response rates in thymoma and thymic carcinoma were 64% (95% confidence interval, 30.8%-89.1%) and 21% (4.7%-50.8%), respectively. Modulation of pharmacodynamic markers of HDAC inhibition and declines in regulatory T cell (Treg) and exhausted CD8(+) T-cell populations were observed. Decline in Tregs was associated with response (P = 0.0041) and progression-free survival (P = 0.021). Declines in TIM3(+) CD8(+) T cells were larger in responders than nonresponders (P = 0.049). This study identified the MTD of belinostat in combination with PAC and indicates that the combination is active and feasible in TETs. Immunomodulatory effects on Tregs and TIM3(+) CD8(+) T cells warrant further study.
©2014 American Association for Cancer Research.
JF - Clinical cancer research : an official journal of the American Association for Cancer Research
AU - Thomas, Anish
AU - Rajan, Arun
AU - Szabo, Eva
AU - Tomita, Yusuke
AU - Carter, Corey A
AU - Scepura, Barbara
AU - Lopez-Chavez, Ariel
AU - Lee, Min-Jung
AU - Redon, Christophe E
AU - Frosch, Ari
AU - Peer, Cody J
AU - Chen, Yuanbin
AU - Piekarz, Richard
AU - Steinberg, Seth M
AU - Trepel, Jane B
AU - Figg, William D
AU - Schrump, David S
AU - Giaccone, Giuseppe
AD - Medical Oncology Branch, National Cancer Institute, NIH, Bethesda, Maryland. ; Division of Cancer Prevention, National Cancer Institute, NIH, Bethesda, Maryland. ; Department of Hematology and Oncology, Walter Reed National Military Medical Center, Bethesda, Maryland. ; Laboratory of Molecular Pharmacology, National Cancer Institute, NIH, Bethesda, Maryland. ; Cancer Therapy Evaluation Program, National Cancer Institute, NIH, Bethesda, Maryland. ; Biostatistics and Data Management Section, National Cancer Institute, NIH, Bethesda, Maryland. ; Thoracic Surgery Section, Thoracic and Gastrointestinal Oncology Branch, National Cancer Institute, NIH, Bethesda, Maryland. ; Medical Oncology Branch, National Cancer Institute, NIH, Bethesda, Maryland. gg496@georgetown.edu.
Y1 - 2014/11/01/
PY - 2014
DA - 2014 Nov 01
SP - 5392
EP - 5402
VL - 20
IS - 21
SN - 1078-0432, 1078-0432
KW - Biomarkers, Tumor
KW - 0
KW - Hydroxamic Acids
KW - Sulfonamides
KW - Doxorubicin
KW - 80168379AG
KW - Cyclophosphamide
KW - 8N3DW7272P
KW - belinostat
KW - F4H96P17NZ
KW - Cisplatin
KW - Q20Q21Q62J
KW - Index Medicus
KW - Cyclophosphamide -- administration & dosage
KW - Young Adult
KW - CD8-Positive T-Lymphocytes -- drug effects
KW - Humans
KW - Aged
KW - Translational Medical Research -- methods
KW - Doxorubicin -- administration & dosage
KW - Sulfonamides -- administration & dosage
KW - Cisplatin -- administration & dosage
KW - Biomarkers, Tumor -- metabolism
KW - Hydroxamic Acids -- administration & dosage
KW - Adult
KW - Middle Aged
KW - Maximum Tolerated Dose
KW - Female
KW - Male
KW - Neoplasms, Glandular and Epithelial -- drug therapy
KW - Neoplasms, Glandular and Epithelial -- metabolism
KW - Thymus Neoplasms -- metabolism
KW - Thymus Neoplasms -- drug therapy
KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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:
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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
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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:
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Histol Histopathol. 2014 Mar;29(3):313-21 [24194373]
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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
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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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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]
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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]
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Comment In:
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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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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:
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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:
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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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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
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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
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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:
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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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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
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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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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:
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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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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:
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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]
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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:
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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]
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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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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]
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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
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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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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:
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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
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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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+and+Cellular+Proteomics&rft.atitle=Characterization+of+Functional+Reprogramming+during+Osteoclast+Development+Using+Quantitative+Proteomics+and+mRNA+Profiling&rft.au=An%2C+Eunkyung%3BNarayanan%2C+Manikandan%3BManes%2C+Nathan+P%3BNita-Lazar%2C+Aleksandra&rft.aulast=An&rft.aufirst=Eunkyung&rft.date=2014-10-20&rft.volume=13&rft.issue=10&rft.spage=2687&rft.isbn=&rft.btitle=&rft.title=Molecular+and+Cellular+Proteomics&rft.issn=15359476&rft_id=info:doi/10.1074%2Fmcp.M113.034371
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2016-07-01
N1 - Last updated - 2016-08-17
N1 - SubjectsTermNotLitGenreText - Transformation; Macrophages; Data processing; Immune system; Osteoclasts; Developmental stages; Mitochondria; Peripheral blood; Gene expression; Dendritic cells; Energy flow; Osteoprogenitor cells; Bone resorption; proteomics; Monocytes; Osteoclastogenesis; Metabolism; Signal transduction
DO - http://dx.doi.org/10.1074/mcp.M113.034371
ER -
TY - JOUR
T1 - Formation of epichlorohydrin, a known rodent carcinogen, following oral administration of 1,3-dichloro-2-propanol in rats.
AN - 1614699869; 25254956
AB - The observed toxicity and carcinogenicity of 1,3-dichloro-2-propanol (DCP) in rodents is thought to be due to the formation of reactive metabolites, epichlorohydrin (ECH) and dichloroacetone (DCA). However, there is no direct evidence for the formation of these metabolites from exposure to DCP in rodents due to the challenges of measuring these reactive intermediates directly in vivo. The objective of this work was to investigate the metabolism of DCP to ECH and DCA in vivo by first developing a sensitive analytical method in a suitable biological matrix and analyzing samples from rats administered DCP. DCA reacted rapidly in vitro in rat blood, plasma, and liver homogenate, precluding its detection. Because ECH rapidly disappeared in liver homogenate, but was relatively long-lived in plasma and blood in vitro, blood was selected for analysis of this metabolite. Following a single oral dose of 50 mg/kg DCP in male or female Harlan Sprague-Dawley rats, ECH was detected in blood with a maximum concentration reached at ≤13.7 min. ECH was cleared rapidly with a half-life of ca. 33 and 48 min in males and females, respectively. Following a single oral dose of 25 mg/kg ECH in male and female rats, the elimination half-life of ECH was ca. 34 and 20 min, respectively; the oral bioavailability of ECH was low (males, 5.2%; females, 2.1%), suggesting extensive first pass metabolism of ECH following oral administration. The area under the concentration vs time curve for ECH following oral administration of DCP and intravenous administration of ECH was used to estimate the percent of the DCP dose converted to ECH in rats. On the basis of this analysis, we concluded that in male and female rats following oral administration of 50 mg/kg DCP, ≥1.26% or ≥1.78% of the administered dose was metabolized to ECH, respectively.
JF - Chemical research in toxicology
AU - Waidyanatha, Suramya
AU - Gaudette, Norman F
AU - Hong, Yan
AU - Fennell, Timothy R
AD - Division of National Toxicology Program, National Institute of Environmental Health Sciences , Research Triangle Park, North Carolina 27709, United States.
Y1 - 2014/10/20/
PY - 2014
DA - 2014 Oct 20
SP - 1787
EP - 1795
VL - 27
IS - 10
KW - Epichlorohydrin
KW - 08OOR508C0
KW - 1,3-dichloro-2-propanol
KW - 0F4P2VQC07
KW - alpha-Chlorohydrin
KW - 96-24-2
KW - Index Medicus
KW - Administration, Oral
KW - Animals
KW - Serum -- metabolism
KW - Area Under Curve
KW - ROC Curve
KW - Liver -- metabolism
KW - Mice
KW - Administration, Intravenous
KW - Rats
KW - Rats, Sprague-Dawley
KW - Half-Life
KW - Liver -- drug effects
KW - Gas Chromatography-Mass Spectrometry
KW - Female
KW - Male
KW - alpha-Chlorohydrin -- analogs & derivatives
KW - Epichlorohydrin -- toxicity
KW - Epichlorohydrin -- metabolism
KW - alpha-Chlorohydrin -- metabolism
KW - Epichlorohydrin -- chemistry
KW - alpha-Chlorohydrin -- toxicity
KW - alpha-Chlorohydrin -- chemistry
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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]
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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]
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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:
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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
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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:
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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:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.toxlet.2014.01.038
ER -
TY - JOUR
T1 - Profiling of the Tox21 Chemical Collection for Mitochondrial Function to Identify Compounds that Acutely Decrease Mitochondrial Membrane Potential
AN - 1654685937; PQ0001052561
AB - Background: Mitochondrial dysfunction has been implicated in the pathogenesis of a variety of disorders including cancer, diabetes, and neurodegenerative and cardiovascular diseases. Understanding whether different environmental chemicals and druglike molecules impact mitochondrial function represents an initial step in predicting exposure-related toxicity and defining a possible role for such compounds in the onset of various diseases. Objectives: We sought to identify individual chemicals and general structural features associated with changes in mitochondrial membrane potential (MMP). Methods: We used a multiplexed [two end points in one screen; MMP and adenosine triphosphate (ATP) content] quantitative high throughput screening (qHTS) approach combined with informatics tools to screen the Tox21 library of 10,000 compounds (~ 8,300 unique chemicals) at 15 concentrations each in triplicate to identify chemicals and structural features that are associated with changes in MMP in HepG2 cells. Results: Approximately 11% of the compounds (913 unique compounds) decreased MMP after 1 hr of treatment without affecting cell viability (ATP content). In addition, 309 compounds decreased MMP over a concentration range that also produced measurable cytotoxicity [half maximal inhibitory concentration (IC50) in MMP assay/IC50 in viability assay less than or equal to 3; p < 0.05]. More than 11% of the structural clusters that constitute the Tox21 library (76 of 651 clusters) were significantly enriched for compounds that decreased the MMP. Conclusions: Our multiplexed qHTS approach allowed us to generate a robust and reliable data set to evaluate the ability of thousands of drugs and environmental compounds to decrease MMP. The use of structure-based clustering analysis allowed us to identify molecular features that are likely responsible for the observed activity. Citation: Attene-Ramos MS, Huang R, Michael S, Witt KL, Richard A, Tice RR, Simeonov A, Austin CP, Xia M. 2015. Profiling of the Tox21 chemical collection for mitochondrial function to identify compounds that acutely decrease mitochondrial membrane potential. Environ Health Perspect 123:49-56; http://dx.doi.org/10.1289/ehp.1408642
JF - Environmental Health Perspectives
AU - Attene-Ramos, Matias S
AU - Huang, Ruili
AU - Michael, Sam
AU - Witt, Kristine L
AU - Richard, Ann
AU - Tice, Raymond R
AU - Simeonov, Anton
AU - Austin, Christopher P
AU - Xia, Menghang
AD - National Center for Advancing Translational Sciences, National Institutes of Health (NIH), Department of Health and Human Services (DHHS), Bethesda, Maryland, USA
Y1 - 2014/10/10/
PY - 2014
DA - 2014 Oct 10
SP - 49
EP - 56
PB - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States
VL - 123
IS - 1
SN - 0091-6765, 0091-6765
KW - Environment Abstracts; Health & Safety Science Abstracts
KW - Diabetes mellitus
KW - Cytotoxicity
KW - Membranes
KW - Informatics
KW - Toxicity
KW - Cardiovascular diseases
KW - Drugs
KW - H 4000:Food and Drugs
KW - ENA 07:General
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1654685937?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Health+Perspectives&rft.atitle=Profiling+of+the+Tox21+Chemical+Collection+for+Mitochondrial+Function+to+Identify+Compounds+that+Acutely+Decrease+Mitochondrial+Membrane+Potential&rft.au=Attene-Ramos%2C+Matias+S%3BHuang%2C+Ruili%3BMichael%2C+Sam%3BWitt%2C+Kristine+L%3BRichard%2C+Ann%3BTice%2C+Raymond+R%3BSimeonov%2C+Anton%3BAustin%2C+Christopher+P%3BXia%2C+Menghang&rft.aulast=Attene-Ramos&rft.aufirst=Matias&rft.date=2014-10-10&rft.volume=123&rft.issue=1&rft.spage=49&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1408642
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-02-01
N1 - Last updated - 2015-05-13
N1 - SubjectsTermNotLitGenreText - Diabetes mellitus; Cytotoxicity; Membranes; Informatics; Cardiovascular diseases; Toxicity; Drugs
DO - http://dx.doi.org/10.1289/ehp.1408642
ER -
TY - JOUR
T1 - Milestones in skin carcinogenesis: the biology of multistage carcinogenesis.
AN - 1612289764; 25302469
JF - The Journal of investigative dermatology
AU - Balmain, Allan
AU - Yuspa, Stuart H
AD - Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, San Francisco, California, USA. ; Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, USA.
Y1 - 2014/10/10/
PY - 2014
DA - 2014 Oct 10
SP - E2
EP - E7
VL - 134
KW - DNA
KW - 9007-49-2
KW - Index Medicus
KW - Genes, ras
KW - Animals
KW - Papilloma -- etiology
KW - Humans
KW - DNA -- metabolism
KW - Mutation
KW - Skin Neoplasms -- etiology
KW - Carcinogenesis
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1612289764?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+investigative+dermatology&rft.atitle=Milestones+in+skin+carcinogenesis%3A+the+biology+of+multistage+carcinogenesis.&rft.au=Balmain%2C+Allan%3BYuspa%2C+Stuart+H&rft.aulast=Balmain&rft.aufirst=Allan&rft.date=2014-10-10&rft.volume=134&rft.issue=&rft.spage=E2&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+investigative+dermatology&rft.issn=1523-1747&rft_id=info:doi/10.1038%2Fskinbio.2014.2
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-12-12
N1 - Date created - 2014-10-11
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1038/skinbio.2014.2
ER -
TY - JOUR
T1 - Disordered amyloidogenic peptides may insert into the membrane and assemble into common cyclic structural motifs.
AN - 1561032680; 24566672
AB - Aggregation of disordered amyloidogenic peptides into oligomers is the causative agent of amyloid-related diseases. In solution, disordered protein states are characterized by heterogeneous ensembles. Among these, β-rich conformers self-assemble via a conformational selection mechanism to form energetically-favored cross-β structures, regardless of their precise sequences. These disordered peptides can also penetrate the membrane, and electrophysiological data indicate that they form ion-conducting channels. Based on these and additional data, including imaging and molecular dynamics simulations of a range of amyloid peptides, Alzheimer's amyloid-β (Aβ) peptide, its disease-related variants with point mutations and N-terminal truncated species, other amyloidogenic peptides, as well as a cytolytic peptide and a synthetic gel-forming peptide, we suggest that disordered amyloidogenic peptides can also present a common motif in the membrane. The motif consists of curved, moon-like β-rich oligomers associated into annular organizations. The motif is favored in the lipid bilayer since it permits hydrophobic side chains to face and interact with the membrane and the charged/polar residues to face the solvated channel pores. Such channels are toxic since their pores allow uncontrolled leakage of ions into/out of the cell, destabilizing cellular ionic homeostasis. Here we detail Aβ, whose aggregation is associated with Alzheimer's disease (AD) and for which there are the most abundant data. AD is a protein misfolding disease characterized by a build-up of Aβ peptide as senile plaques, neurodegeneration, and memory loss. Excessively produced Aβ peptides may directly induce cellular toxicity, even without the involvement of membrane receptors through Aβ peptide-plasma membrane interactions.
JF - Chemical Society reviews
AU - Jang, Hyunbum
AU - Arce, Fernando Teran
AU - Ramachandran, Srinivasan
AU - Kagan, Bruce L
AU - Lal, Ratnesh
AU - Nussinov, Ruth
AD - Cancer and Inflammation Program, National Cancer Institute at Frederick, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Frederick, Maryland 21702, USA. jangh2@mail.nih.gov nussinor@helix.nih.gov.
Y1 - 2014/10/07/
PY - 2014
DA - 2014 Oct 07
SP - 6750
EP - 6764
VL - 43
IS - 19
KW - Amyloid beta-Peptides
KW - 0
KW - Lipid Bilayers
KW - Index Medicus
KW - Hydrophobic and Hydrophilic Interactions
KW - Humans
KW - Lipid Bilayers -- chemistry
KW - Molecular Dynamics Simulation
KW - Alzheimer Disease -- metabolism
KW - Protein Structure, Tertiary
KW - Lipid Bilayers -- metabolism
KW - Alzheimer Disease -- pathology
KW - Amyloid beta-Peptides -- metabolism
KW - Amyloid beta-Peptides -- chemistry
KW - Cell Membrane -- chemistry
KW - Cell Membrane -- metabolism
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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:
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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:
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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:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.ejphar.2014.07.025
ER -
TY - JOUR
T1 - Evaluating the NIH Library Editing Service: Pilot Study Used to Analyze Service Impact
AN - 1667947080; 201503151
AB - Evidence-based librarianship drives initiatives and priorities in today's research centers. To evaluate the effectiveness of the National Institutes of Health (NIH) Library's Editing Service, librarians conducted a pilot study comparing edited manuscripts with the published versions. Using a random number generator, five published journal articles were chosen for evaluation from a pool of NIH manuscripts (n = 147) edited between January 2008 and February 2012. A rubric delineating categories of frequently checked writing elements was used to facilitate quantitative analysis. Findings showed that 84 percent of editors' suggestions were accepted for three of the published papers that were submitted to the originally intended journal. Adapted from the source document.
JF - Science & Technology Libraries
AU - Clark, Cindy
AU - Sullivan, Brigit
AD - National Institutes of Health (NIH) Library, Bethesda, Maryland
Y1 - 2014/10/02/
PY - 2014
DA - 2014 Oct 02
SP - 351
EP - 357
PB - Taylor & Francis, Philadelphia PA
VL - 33
IS - 4
SN - 0194-262X, 0194-262X
KW - Evaluation
KW - Scholarly publishing
KW - National libraries
KW - Medicine
KW - Editing
KW - article
KW - 4.15: USER SERVICES
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1667947080?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Alisa&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Science+%26+Technology+Libraries&rft.atitle=Evaluating+the+NIH+Library+Editing+Service%3A+Pilot+Study+Used+to+Analyze+Service+Impact&rft.au=Clark%2C+Cindy%3BSullivan%2C+Brigit&rft.aulast=Clark&rft.aufirst=Cindy&rft.date=2014-10-02&rft.volume=33&rft.issue=4&rft.spage=351&rft.isbn=&rft.btitle=&rft.title=Science+%26+Technology+Libraries&rft.issn=0194262X&rft_id=info:doi/10.1080%2F0194262X.2014.950000
LA - English
DB - Library & Information Science Abstracts (LISA)
N1 - Date revised - 2015-06-01
N1 - Last updated - 2016-09-27
N1 - SubjectsTermNotLitGenreText - Evaluation; National libraries; Medicine; Editing; Scholarly publishing
DO - http://dx.doi.org/10.1080/0194262X.2014.950000
ER -
TY - JOUR
T1 - Ten Years of Change: National Library of Medicine TOXMAP Gets a New Look
AN - 1667945061; 201503265
AB - The United States National Library of Medicine (NLM) TOXNET(TM) databases provide broad coverage of environmental health information covering a wide variety of topics, including access to the U.S. Environment Protection Agency (EPA)'s Toxics Release Inventory (TRI) data. The NLM web-based geographic information system (GIS), TOXMAP(TM) , provides interactive maps which show where TRI chemicals are released into the environment and links to TOXNET for information about these chemicals. TOXMAP also displays locations of Superfund sites on the EPA National Priority List, as well as information about the chemical contaminants at these sites. This column focuses on a new version of TOXMAP which brings it up to date with current web GIS technologies and user expectations. Adapted from the source document.
JF - Medical Reference Services Quarterly
AU - Hochstein, Colette
AU - Gemoets, Darren
AU - Goshorn, Jeanne
AD - Division of Specialized Information Services, National Library of Medicine, Bethesda, Maryland, USA colette@nlm.nih.gov
Y1 - 2014/10/02/
PY - 2014
DA - 2014 Oct 02
SP - 428
EP - 437
PB - Taylor & Francis, Philadelphia PA
VL - 33
IS - 4
SN - 0276-3869, 0276-3869
KW - Product design
KW - Location
KW - Environmental health
KW - Online data bases
KW - Pollution
KW - article
KW - 5.23: SCIENCE, TECHNOLOGY, MEDICINE MATERIALS
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1667945061?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Alisa&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Medical+Reference+Services+Quarterly&rft.atitle=Ten+Years+of+Change%3A+National+Library+of+Medicine+TOXMAP+Gets+a+New+Look&rft.au=Hochstein%2C+Colette%3BGemoets%2C+Darren%3BGoshorn%2C+Jeanne&rft.aulast=Hochstein&rft.aufirst=Colette&rft.date=2014-10-02&rft.volume=33&rft.issue=4&rft.spage=428&rft.isbn=&rft.btitle=&rft.title=Medical+Reference+Services+Quarterly&rft.issn=02763869&rft_id=info:doi/10.1080%2F02763869.2014.957090
LA - English
DB - Library & Information Science Abstracts (LISA)
N1 - Date revised - 2015-06-01
N1 - Last updated - 2016-09-27
N1 - SubjectsTermNotLitGenreText - Online data bases; Environmental health; Pollution; Product design; Location
DO - http://dx.doi.org/10.1080/02763869.2014.957090
ER -
TY - JOUR
T1 - NLM Workshop Marks 20 Years of Community Outreach and Capacity Building in HIV/AIDS
AN - 1667936759; 201503425
AB - The National Library of Medicine's (NLM) AIDS Community Information Outreach Program (ACIOP) was launched in 1994 to provide the HIV/AIDS affected community with access to vital health information resources increasingly becoming available on the Internet. Three hundred awards have been made mostly to community-based organizations. An evaluation in 2012 found that most program objectives are being met; a principal recommendation going forward was that NLM seek to enhance the capacity of community-based awardees to conduct evaluations of their own projects. This article reports on a workshop whose invitees were drawn from AIDS serving organizations, along with scientists, clinicians, and information technologists, to review the evaluation findings and recommendations. They considered alternatives for improving awardees' evaluation capabilities with the help of expert consultation, identified additional steps that could be taken to make individual project results more transparent and sharable, and looked at external influences ranging from mobile health devices to the latest HIV/AIDS scientific research findings that could be used to align future awards with unmet needs in the community. The paper identifies efforts subsequently made by ACIOP managers to prioritize and operationalize guidance from the evaluation and the workshop, and discusses the benefits of community engagement. Adapted from the source document.
JF - Journal of Consumer Health on the Internet
AU - Dancy-Scott, Nicole
AU - Dutcher, Gale A
AU - Keselman, Alla
AU - Siegel, Elliot R
AD - National Library of Medicine, Bethesda, Maryland, USA nicole.scott@nih.gov
Y1 - 2014/10/02/
PY - 2014
DA - 2014 Oct 02
SP - 357
EP - 366
PB - Taylor & Francis, Philadelphia PA
VL - 18
IS - 4
SN - 1539-8285, 1539-8285
KW - Communities
KW - National libraries
KW - Medicine
KW - HIV
KW - Outreach services
KW - article
KW - 10.13: INFORMATION COMMUNICATION - SCIENCE, TECHNOLOGY, MEDICINE
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1667936759?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Alisa&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Consumer+Health+on+the+Internet&rft.atitle=NLM+Workshop+Marks+20+Years+of+Community+Outreach+and+Capacity+Building+in+HIV%2FAIDS&rft.au=Dancy-Scott%2C+Nicole%3BDutcher%2C+Gale+A%3BKeselman%2C+Alla%3BSiegel%2C+Elliot+R&rft.aulast=Dancy-Scott&rft.aufirst=Nicole&rft.date=2014-10-02&rft.volume=18&rft.issue=4&rft.spage=357&rft.isbn=&rft.btitle=&rft.title=Journal+of+Consumer+Health+on+the+Internet&rft.issn=15398285&rft_id=info:doi/10.1080%2F15398285.2014.952999
LA - English
DB - Library & Information Science Abstracts (LISA)
N1 - Date revised - 2015-04-01
N1 - Last updated - 2016-09-27
N1 - SubjectsTermNotLitGenreText - National libraries; Medicine; Outreach services; HIV; Communities
DO - http://dx.doi.org/10.1080/15398285.2014.952999
ER -
TY - JOUR
T1 - Sorafenib and locoregional deep electro-hyperthermia in advanced hepatocellular carcinoma: A phase II study.
AN - 1826611459; 25202410
AB - The standard treatment for advanced hepatocellular carcinoma (HCC) is sorafenib, a multikinase inhibitor of tumor cell proliferation and angiogenesis. Hyperthermia inhibits angiogenesis and promotes apoptosis. Potential synergic antiangiogenic and proapoptotic effects represent the rationale for combining sorafenib with electro-hyperthermia (EHY) in HCC. A total of 21 patients (median age, 64 years; range, 55-73 years) with advanced HCC were enrolled in the current study between February 2009 and September 2010. EHY was achieved by arranging capacitive electrodes with a deep hypothermia radiofrequency field of 13.56 Mhz at 80 W for 60 min, three times per week for six weeks, followed by two weeks without treatment, in combination with sorafenib at a dose of 800 mg every other day. According to the modified Response Evaluation Criteria in Solid Tumors criteria, 50% achieved stable disease, 5% achieved partial response and 45% achieved progressive disease. No complete response was observed. The progression-free survival (PFS) rate at six months was 38%, while the median PFS and overall survival times were 5.2 [95% confidence interval (CI), 4.2-6.2) and 10.4 (95% CI, 10-11) months, respectively. The overall incidence of treatment-related adverse events was 80%, predominantly of grade 1 or 2. Grade 3 toxicity included fatigue, diarrhea, hand-foot skin reaction and hypertension. In the present study, the sorafenib plus EHY combination was feasible and well tolerated, and no major complications were observed. The initial findings indicated that this combination offers a promising option for advanced HCC.
JF - Oncology letters
AU - Gadaleta-Caldarola, Gennaro
AU - Infusino, Stefania
AU - Galise, Ida
AU - Ranieri, Girolamo
AU - Vinciarelli, Gianluca
AU - Fazio, Vito
AU - Divella, Rosa
AU - Daniele, Antonella
AU - Filippelli, Gianfranco
AU - Gadaleta, Cosmo Damiano
AD - Interventional Radiology and Medical Oncology Unit, National Cancer Research Centre, National Cancer Institute 'Giovanni Paolo II', Bari 70124, Italy. ; Medical Oncology Unit, 'S. Francesco di Paola' Hospital, Via Promintesta, Paola 87027, Italy. ; Apulia Cancer Registry, Statistic and Epidemiology Unit, National Cancer Research Centre, National Cancer Institute 'Giovanni Paolo II', Bari 70124, Italy. ; Clinical Pathology Laboratory, National Cancer Research Centre, National Cancer Institute 'Giovanni Paolo II', Bari 70124, Italy.
Y1 - 2014/10//
PY - 2014
DA - October 2014
SP - 1783
EP - 1787
VL - 8
IS - 4
SN - 1792-1074, 1792-1074
KW - electro-hyperthermia
KW - sorafenib
KW - hepatocellular
KW - carcinoma
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1826611459?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncology+letters&rft.atitle=Sorafenib+and+locoregional+deep+electro-hyperthermia+in+advanced+hepatocellular+carcinoma%3A+A+phase+II+study.&rft.au=Gadaleta-Caldarola%2C+Gennaro%3BInfusino%2C+Stefania%3BGalise%2C+Ida%3BRanieri%2C+Girolamo%3BVinciarelli%2C+Gianluca%3BFazio%2C+Vito%3BDivella%2C+Rosa%3BDaniele%2C+Antonella%3BFilippelli%2C+Gianfranco%3BGadaleta%2C+Cosmo+Damiano&rft.aulast=Gadaleta-Caldarola&rft.aufirst=Gennaro&rft.date=2014-10-01&rft.volume=8&rft.issue=4&rft.spage=1783&rft.isbn=&rft.btitle=&rft.title=Oncology+letters&rft.issn=17921074&rft_id=info:doi/
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date created - 2014-09-09
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
ER -
TY - JOUR
T1 - The Yin: An adverse health perspective of nanoceria: uptake, distribution, accumulation, and mechanisms of its toxicity.
AN - 1826601737; 25243070
AB - This critical review evolved from a SNO Special Workshop on Nanoceria panel presentation addressing the toxicological risks of nanoceria: accumulation, target organs, and issues of clearance; how exposure dose/concentration, exposure route, and experimental preparation/model influence the different reported effects of nanoceria; and how can safer by design concepts be applied to nanoceria? It focuses on the most relevant routes of human nanoceria exposure and uptake, disposition, persistence, and resultant adverse effects. The pulmonary, oral, dermal, and topical ocular exposure routes are addressed as well as the intravenous route, as the latter provides a reference for the pharmacokinetic fate of nanoceria once introduced into blood. Nanoceria reaching the blood is primarily distributed to mononuclear phagocytic system organs. Available data suggest nanoceria's distribution is not greatly affected by dose, shape, or dosing schedule. Significant attention has been paid to the inhalation exposure route. Nanoceria distribution from the lung to the rest of the body is less than 1% of the deposited dose, and from the gastrointestinal tract even less. Intracellular nanoceria and organ burdens persist for at least months, suggesting very slow clearance rates. The acute toxicity of nanoceria is very low. However, large/accumulated doses produce granuloma in the lung and liver, and fibrosis in the lung. Toxicity, including genotoxicity, increases with exposure time; the effects disappear slowly, possibly due to nanoceria's biopersistence. Nanoceria may exert toxicity through oxidative stress. Adverse effects seen at sites distal to exposure may be due to nanoceria translocation or released biomolecules. An example is elevated oxidative stress indicators in the brain, in the absence of appreciable brain nanoceria. Nanoceria may change its nature in biological environments and cause changes in biological molecules. Increased toxicity has been related to greater surface Ce3+, which becomes more relevant as particle size decreases and the ratio of surface area to volume increases. Given its biopersistence and resulting increased toxicity with time, there is a risk that long-term exposure to low nanoceria levels may eventually lead to adverse health effects. This critical review provides recommendations for research to resolve some of the many unknowns of nanoceria's fate and adverse effects.
JF - Environmental science. Nano
AU - Yokel, Robert A
AU - Hussain, Salik
AU - Garantziotis, Stavros
AU - Demokritou, Philip
AU - Castranova, Vincent
AU - Cassee, Flemming R
AD - Pharmaceutical Sciences, University of Kentucky, US ; Graduate Center for Toxicology, University of Kentucky, US. ; Clinical Research Unit, National Institute of Environmental Health Sciences, National Institutes of Health, US. ; Environmental Health, Harvard, US. ; National Institute for Occupational Safety and Health, US ; West Virginia University School of Pharmacy, Morgantown, WV, US. ; Centre for Sustainability, Environmental & Health, National Institute for Public Health and the Environment, Bilthoven, the Netherlands ; Institute of Risk Assessment Sciences, Utrecht University, Utrecht, the Netherlands.
Y1 - 2014/10/01/
PY - 2014
DA - 2014 Oct 01
SP - 406
EP - 428
VL - 1
IS - 5
SN - 2051-8153, 2051-8153
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1826601737?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+science.+Nano&rft.atitle=The+Yin%3A+An+adverse+health+perspective+of+nanoceria%3A+uptake%2C+distribution%2C+accumulation%2C+and+mechanisms+of+its+toxicity.&rft.au=Yokel%2C+Robert+A%3BHussain%2C+Salik%3BGarantziotis%2C+Stavros%3BDemokritou%2C+Philip%3BCastranova%2C+Vincent%3BCassee%2C+Flemming+R&rft.aulast=Yokel&rft.aufirst=Robert&rft.date=2014-10-01&rft.volume=1&rft.issue=5&rft.spage=406&rft.isbn=&rft.btitle=&rft.title=Environmental+science.+Nano&rft.issn=20518153&rft_id=info:doi/
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date created - 2014-09-22
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
ER -
TY - JOUR
T1 - THE FAMILY HOUSEHOLD AND INFORMAL OLD AGE CARE IN MEXICO: A RESEARCH NOTE
AN - 1728661355; 201535886
AB - Mexican society has traditionally expected the family to care for of its older people but the current situation is being strained by demographic, social and economic changes. This research note outlines the situation and provides some basic information on current caretakers using data from the Mexican National Time Use Survey of 2009. The survey identifies six different caretaking tasks, three of which are performed predominantly by women. Since most health and personal care occurs within the household, the physical and psychological burdens, as well as opportunity costs involved, are seldom recognised by health and social development ministries. This remains a main challenge to be addressed in order to develop optimal targeted support for older adults and their caregivers. Adapted from the source document.
JF - International Journal of Sociology of the Family
AU - Lopez-Ortega, Mariana
AD - National Institute of Geriatrics, National Institutes of Health, Mexico
Y1 - 2014/10//
PY - 2014
DA - October 2014
SP - 235
EP - 246
PB - Serials Publications, Delhi, India
VL - 40
IS - 2
SN - 0973-2039, 0973-2039
KW - Caregivers
KW - Time
KW - Mexico
KW - Elderly
KW - Social Development
KW - Females
KW - Health Care Costs
KW - article
KW - 1941: the family and socialization; sociology of the family, marriage, & divorce
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1728661355?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Asocabs&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Sociology+of+the+Family&rft.atitle=THE+FAMILY+HOUSEHOLD+AND+INFORMAL+OLD+AGE+CARE+IN+MEXICO%3A+A+RESEARCH+NOTE&rft.au=Lopez-Ortega%2C+Mariana&rft.aulast=Lopez-Ortega&rft.aufirst=Mariana&rft.date=2014-10-01&rft.volume=40&rft.issue=2&rft.spage=235&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Sociology+of+the+Family&rft.issn=09732039&rft_id=info:doi/
LA - English
DB - Sociological Abstracts
N1 - Date revised - 2015-11-01
N1 - Number of references - 24
N1 - Last updated - 2016-09-28
N1 - CODEN - IJSFAK
N1 - SubjectsTermNotLitGenreText - Elderly; Mexico; Health Care Costs; Caregivers; Time; Females; Social Development
ER -
TY - JOUR
T1 - US state variation in Autism insurance mandates: Balancing access and fairness
AN - 1698882292
AB - This article examines how nations split decision-making about health services between federal and sub-federal levels, creating variation between states or provinces. When is this variation ethically acceptable? We identify three sources of ethical acceptability—procedural fairness, value pluralism, and substantive fairness—and examine these sources with respect to a case study: the fact that only 30 out of 51 US states or territories passed mandates requiring private insurers to offer extensive coverage of Autism behavioral therapies, creating variation for privately insured children living in different US states. Is this variation ethically acceptable? To address this question, we need to analyze whether mandates go to more or less needy states and whether the mandates reflect value pluralism between states regarding government’s role in health care. Using time-series logistic regressions and data from National Survey of Children with Special Health Care Needs, Individual with Disabilities Education Act, legislature political composition, and American Board of Pediatrics workforce data, we find that the states in which mandates are passed are less needy than states in which mandates have not been passed, what we call a cumulative advantage outcome that increases between-state disparities rather than a compensatory outcome that decreases between-state disparities. Concluding, we discuss the implications of our analysis for broader discussions of variation in health services provision.
JF - Autism
AU - Johnson, Rebecca A
AU - Danis, Marion
AU - Hafner-Eaton, Chris
AD - Department of Bioethics, National Institutes of Health, USA ; Division of Science Policy and Science Liaison, National Institutes of Health, USA ; Department of Bioethics, National Institutes of Health, USA
Y1 - 2014/10//
PY - 2014
DA - Oct 2014
SP - 803
EP - 814
CY - London
PB - SAGE PUBLICATIONS, INC.
VL - 18
IS - 7
SN - 1362-3613
KW - Psychology
KW - Autism
KW - distributive justice
KW - ethics
KW - health policy
KW - private insurance mandates
KW - Autistic children
KW - Health inequalities
KW - Health insurance
KW - Health services
KW - Insurance
KW - Labour force
KW - Paediatrics
KW - Pluralism
KW - Procedural justice
KW - Provinces
KW - Service delivery
KW - Service provision
KW - Special needs children
KW - Territories
KW - Behaviour
KW - Children
KW - Composition
KW - Coverage
KW - Decision making
KW - Distributive justice
KW - Ethics
KW - Fairness
KW - Health care
KW - United States--US
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1698882292?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Autism&rft.atitle=US+state+variation+in+Autism+insurance+mandates%3A+Balancing+access+and+fairness&rft.au=Johnson%2C+Rebecca+A%3BDanis%2C+Marion%3BHafner-Eaton%2C+Chris&rft.aulast=Johnson&rft.aufirst=Rebecca&rft.date=2014-10-01&rft.volume=18&rft.issue=7&rft.spage=803&rft.isbn=&rft.btitle=&rft.title=Autism&rft.issn=13623613&rft_id=info:doi/10.1177%2F1362361314529191
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Name - American Board of Pediatrics
N1 - Date revised - 2015-07-07
N1 - Last updated - 2016-05-13
N1 - SubjectsTermNotLitGenreText - United States--US
DO - http://dx.doi.org/10.1177/1362361314529191
ER -
TY - JOUR
T1 - Maternal hormonal contraceptive use and offspring overweight or obesity
AN - 1680439030; 20867364
AB - Background/ objectives: Experiments in animal models have shown a positive association between in utero exposure to pharmacologic sex hormones and offspring obesity. The developmental effects of such hormones on human obesity are unknown.Subjects/ methods: Using data from a large, prospective pregnancy cohort study (n=19 652), with linkage to a national prescription registry, we evaluated the association between use of hormonal contraceptives before and after conception (defined from dispensed prescription data and characterized by last date of use relative to conception, 12 to >4 months before (n=3392), 4 to >1 months before (n=2541), 1 to >0 months before (n=2997) and 0-12 weeks after (n=567)) in relation to offspring overweight or obesity at age 3 years. Results: We observed a weak, inverse association between early pregnancy use of a combination oral contraceptive and offspring overweight or obesity at age 3 (adjusted odds ratio (OR): 0.75, 95% confidence interval (CI): 0.53, 1.08) and a positive, but imprecise, association with use of a progestin-only oral contraceptive in early pregnancy (adjusted OR: 1.26, 95% CI: 0.79, 2.02). In general, no association was observed between the use of a hormonal contraceptive before conception and offspring overweight or obesity. A sensitivity analysis comparing combination oral contraceptive users in early pregnancy to other unplanned pregnancies without hormonal contraceptive use further strengthened the inverse association (adjusted OR: 0.70, 95% CI: 0.48, 1.02). Other sensitivity analyses were conducted to evaluate the robustness of the associations observed given varying assumptions. Conclusions: Pharmacologic sex hormones in early pregnancy may be inversely or positively associated with offspring overweight or obesity at age 3, depending on the specific formulation used. The present study provides support for the potential for environmental sources of hormonally active agents to exert developmental effects.
JF - International Journal of Obesity
AU - Jensen, E T
AU - Daniels, J L
AU - Stuermer, T
AU - Robinson, W R
AU - Williams, C J
AU - Moster, D
AU - Juliusson, P B
AU - Vejrup, K
AU - Magnus, P
AU - Longnecker, M P
AD - 1] Department of Epidemiology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, USA [2] Department of Epidemiology, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC, USA
Y1 - 2014/10//
PY - 2014
DA - Oct 2014
SP - 1275
EP - 1281
PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL - 38
IS - 10
SN - 0307-0565, 0307-0565
KW - Physical Education Index
KW - Human relations
KW - Obesity
KW - Analysis
KW - Recruiting
KW - Hormones
KW - Pregnancy
KW - Sex
KW - PE 030:Exercise, Health & Physical Fitness
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1680439030?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aphysicaleducation&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Obesity&rft.atitle=Maternal+hormonal+contraceptive+use+and+offspring+overweight+or+obesity&rft.au=Jensen%2C+E+T%3BDaniels%2C+J+L%3BStuermer%2C+T%3BRobinson%2C+W+R%3BWilliams%2C+C+J%3BMoster%2C+D%3BJuliusson%2C+P+B%3BVejrup%2C+K%3BMagnus%2C+P%3BLongnecker%2C+M+P&rft.aulast=Jensen&rft.aufirst=E&rft.date=2014-10-01&rft.volume=38&rft.issue=10&rft.spage=1275&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Obesity&rft.issn=03070565&rft_id=info:doi/10.1038%2Fijo.2014.114
LA - English
DB - Physical Education Index
N1 - Date revised - 2015-05-01
N1 - Last updated - 2015-06-12
N1 - SubjectsTermNotLitGenreText - Human relations; Obesity; Analysis; Recruiting; Hormones; Sex; Pregnancy
DO - http://dx.doi.org/10.1038/ijo.2014.114
ER -
TY - JOUR
T1 - Liminality as a Conceptual Frame for Understanding the Family Caregiving Rite of Passage: An Integrative Review
AN - 1665167736
AB - Family caregiving is a significant rite of passage experienced by family caregivers of individuals with protracted illness or injury. In an integrative review of 26 studies, we characterized family caregiving from the sociocultural perspective of liminality and explored associated psychosocial implications. Analysis of published evidence on this dynamic and formative transition produced a range of themes. While role ambiguity resolved for most, for others, uncertainty and suffering continued. The process of becoming a caregiver was transformative and can be viewed as a rebirth that is largely socially and culturally driven. The transition to family caregiving model produced by this review provides a holistic perspective on this phenomenon and draws attention to aspects of the experience previously underappreciated. Published 2014. This article is a U.S. Government work and is in the public domain in the USA.
JF - Research in Nursing & Health
AU - Gibbons, Susanne W
AU - Ross, Alyson
AU - Bevans, Margaret
AD - Assistant Professor, Daniel K. Inouye Graduate School of Nursing, Uniformed Services University of the Health Sciences, Bethesda, MD. ; IRTA Postdoctoral Research Fellow, National Institutes of Health Clinical Center, Bethesda, MD. ; Clinical Nurse Scientist, National Institutes of Health Clinical Center, 10 Center Drive MSC 1151, Bethesda, MD, 20892. ; Assistant Professor, Daniel K. Inouye Graduate School of Nursing, Uniformed Services University of the Health Sciences, Bethesda, MD.
Y1 - 2014/10//
PY - 2014
DA - Oct 2014
SP - 423
EP - 436
CY - New York
PB - Wiley Subscription Services, Inc.
VL - 37
IS - 5
SN - 0160-6891
KW - Medical Sciences--Nurses And Nursing
KW - Ambiguity
KW - Carers
KW - Injuries
KW - Psychosocial factors
KW - Public domain
KW - Role ambiguity
KW - Sociocultural factors
KW - Suffering
KW - Uncertainty
KW - United States--US
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665167736?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Research+in+Nursing+%26+Health&rft.atitle=Liminality+as+a+Conceptual+Frame+for+Understanding+the+Family+Caregiving+Rite+of+Passage%3A+An+Integrative+Review&rft.au=Gibbons%2C+Susanne+W%3BRoss%2C+Alyson%3BBevans%2C+Margaret&rft.aulast=Gibbons&rft.aufirst=Susanne&rft.date=2014-10-01&rft.volume=37&rft.issue=5&rft.spage=423&rft.isbn=&rft.btitle=&rft.title=Research+in+Nursing+%26+Health&rft.issn=01606891&rft_id=info:doi/10.1002%2Fnur.21622
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Copyright - Copyright Wiley Subscription Services, Inc. Oct 2014
N1 - Date revised - 2015-01-09
N1 - Last updated - 2016-10-06
N1 - SubjectsTermNotLitGenreText - United States--US
DO - http://dx.doi.org/10.1002/nur.21622
ER -
TY - JOUR
T1 - NETWORK STRUCTURE MODERATES INTERGROUP DIFFERENTIATION OF STEREOTYPED RUMORS
AN - 1665157664
AB - The role of network structure in intergroup differentiation—the bipolarization of stereotypes that are defensive (ingroup-positive/outgroup-negative) and non-defensive (outgroup-positive/ingroup-negative)—was investigated using a Dynamic Social Impact Theory (DSIT) framework. Three computer-mediated laboratory social network experiments were pooled to test the interaction of network clustering (cliquish structure) and segregation (personal network homogeneity) on intergroup differentiation. Democrats and Republicans during the five months preceding the 2008 U.S. Presidential election, deaf and hearing persons, and women and men participated. Twenty-six 16-person groups (e.g., 8 Democrats, 8 Republicans) serially discussed nine controversial stereotyped rumors in lattice (unclustered) or "family" (clustered) network structures. Support was found on an Ingroup Echo Chamber Effect: segregation led to intergroup differentiation (stronger defensive belief, weaker non-defensive belief) in clustered, but not un-clustered, structures. At the individual level, network clustering amplified ingroup neighbor social ifluence, leading participants to think more positively of their ingroup and more negatively of their outgroup.
JF - Social Cognition
AU - DiFonzo, Nicholas
AU - Suls, Jerry
AU - Beckstead, Jason W
AU - Bourgeois, Martin J
AU - Homan, Christopher M
AU - Brougher, Samuel
AU - Younge, Andrew J
AU - Terpstra-Schwab, Nicholas
AD - Department of Psychology, Rochester Institute of Technology, 18 Lomb Memorial Drive, Rochester, NY 14623 ; National Cancer Institute ; University of South Florida ; Florida Gulf Coast University ; Rochester Institute of Technology ; University of Wyoming ; Department of Psychology, Rochester Institute of Technology, 18 Lomb Memorial Drive, Rochester, NY 14623
Y1 - 2014/10//
PY - 2014
DA - Oct 2014
SP - 409
EP - 448
CY - New York
PB - Guilford Publications, Inc.
VL - 32
IS - 5
SN - 0278-016X
KW - Psychology
KW - Intergroup differentiation
KW - Hearing
KW - Segregation
KW - Deaf
KW - Social networks
KW - Clustering
KW - Differentiation
KW - Stereotypes
KW - Social impact
KW - United States--US
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665157664?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Social+Cognition&rft.atitle=NETWORK+STRUCTURE+MODERATES+INTERGROUP+DIFFERENTIATION+OF+STEREOTYPED+RUMORS&rft.au=DiFonzo%2C+Nicholas%3BSuls%2C+Jerry%3BBeckstead%2C+Jason+W%3BBourgeois%2C+Martin+J%3BHoman%2C+Christopher+M%3BBrougher%2C+Samuel%3BYounge%2C+Andrew+J%3BTerpstra-Schwab%2C+Nicholas&rft.aulast=DiFonzo&rft.aufirst=Nicholas&rft.date=2014-10-01&rft.volume=32&rft.issue=5&rft.spage=409&rft.isbn=&rft.btitle=&rft.title=Social+Cognition&rft.issn=0278016X&rft_id=info:doi/
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Date revised - 2015-01-09
N1 - Last updated - 2016-05-13
N1 - SubjectsTermNotLitGenreText - United States--US
ER -
TY - JOUR
T1 - Innate immunity is sufficient for the clearance of Chlamydia trachomatis from the female mouse genital tract
AN - 1660408991; PQ0001030385
AB - Chlamydia muridarum and Chlamydia trachomatis, mouse and human strains, respectively, have been used to study immunity in a murine model of female genital tract infection. Despite evidence that unique genes of these otherwise genomically similar strains could play a role in innate immune evasion in their respective mouse and human hosts, there have been no animal model findings to directly support this conclusion. Here, we infected C57BL/6 and adaptive immune-deficient Rag1 super(-/-) female mice with these strains and evaluated their ability to spontaneously resolve genital infection. Predictably, C57BL/6 mice spontaneously cleared infection caused by both chlamydial strains. In contrast, Rag1 super(-/-) mice which lack mature T and B cell immunity but maintain functional innate immune effectors were incapable of resolving C. muridarum infection but spontaneously cleared C. trachomatis infection. This distinct dichotomy in adaptive and innate immune-mediated clearance between mouse and human strains has important cautionary implications for the study of natural immunity and vaccine development in the mouse model. We show using Rag1-deficient mice that genital tract infections caused by human and murine chlamydial strains are differentially resolved by innate and adaptive immune mechanisms.
JF - Pathogens and Disease
AU - Sturdevant, Gail L
AU - Caldwell, Harlan D
AD - Laboratory of Intracellular Parasites, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT, USA.
Y1 - 2014/10//
PY - 2014
DA - Oct 2014
SP - 70
EP - 73
PB - Wiley Subscription Services, Inc., 1105 N Market St Wilmington DE 19801 England
VL - 72
IS - 1
SN - 2049-632X, 2049-632X
KW - Microbiology Abstracts B: Bacteriology
KW - Lymphocytes B
KW - Animal models
KW - Chlamydia trachomatis
KW - Genital tract
KW - Immunity
KW - Vaccines
KW - Pathogens
KW - Infection
KW - J 02350:Immunology
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660408991?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pathogens+and+Disease&rft.atitle=Innate+immunity+is+sufficient+for+the+clearance+of+Chlamydia+trachomatis+from+the+female+mouse+genital+tract&rft.au=Sturdevant%2C+Gail+L%3BCaldwell%2C+Harlan+D&rft.aulast=Sturdevant&rft.aufirst=Gail&rft.date=2014-10-01&rft.volume=72&rft.issue=1&rft.spage=70&rft.isbn=&rft.btitle=&rft.title=Pathogens+and+Disease&rft.issn=2049632X&rft_id=info:doi/10.1111%2F2049-632X.12164
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-03-01
N1 - Last updated - 2015-11-16
N1 - SubjectsTermNotLitGenreText - Lymphocytes B; Animal models; Genital tract; Pathogens; Vaccines; Immunity; Infection; Chlamydia trachomatis
DO - http://dx.doi.org/10.1111/2049-632X.12164
ER -
TY - JOUR
T1 - A combined prognostic serum interleukin-8 and interleukin-6 classifier for stage 1 lung cancer in the prostate, lung, colorectal, and ovarian cancer screening trial.
AN - 1639978378; 25170636
AB - The advent of low-dose helical computed tomography for lung cancer screening will likely lead to an increase in the detection of stage I lung cancer. Presently, these patients are primarily treated with surgery alone and approximately 30% will develop recurrence and die. Biomarkers that can identify patients for whom adjuvant chemotherapy would be a benefit could significantly reduce both patient morbidity and mortality. Herein, we sought to build a prognostic inflammatory-based classifier for stage I lung cancer.
We performed a retrospective analysis of 548 European American lung cancer cases prospectively enrolled in the Prostate, Lung, Colorectal and Ovarian study. C-reactive protein, interleukin (IL)-6, IL-8, tumor necrosis factor-α, and IL-1β were measured using an ultrasensitive electrochemiluminescence immunoassay in serum samples collected at the time of study entry. IL-6 and IL-8 were each associated with significantly shorter survival (hazard ratio [HR], 1.33; 95% confidence interval [CI], 1.08-1.64; p = 0.007; and HR, 1.3; 95% CI, 1.09-1.67; p = 0.005, respectively). Moreover, a combined classifier of IL-6 and IL-8 were significantly associated with poor outcome in stage I lung cancer patients (HR, 3.39; 95% CI, 1.54-7.48, p = 0.002) and in stage 1 patients with more than or equal to 30 pack-years of smoking (HR, 3.15; 95% CI, 1.54-6.46, p = 0.002). These results further support the association between inflammatory markers and lung cancer outcome and suggest that a combined serum IL-6/IL-8 classifier could be a useful tool for guiding therapeutic decisions in patients with stage I lung cancer.
JF - Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
AU - Ryan, Bríd M
AU - Pine, Sharon R
AU - Chaturvedi, Anil K
AU - Caporaso, Neil
AU - Harris, Curtis C
AD - *Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, MD; †Department of Medicine, Rutgers Cancer Institute of New Jersey, Rutgers, The State University of New Jersey, New Brunswick, NJ; ‡Infections and Immunoepidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD; and §Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD.
Y1 - 2014/10//
PY - 2014
DA - October 2014
SP - 1494
EP - 1503
VL - 9
IS - 10
KW - Biomarkers, Tumor
KW - 0
KW - Interleukin-6
KW - Interleukin-8
KW - Index Medicus
KW - Neoplasm Staging
KW - Risk Factors
KW - Humans
KW - Retrospective Studies
KW - Prognosis
KW - Aged
KW - Middle Aged
KW - Neoplasm Recurrence, Local
KW - Early Detection of Cancer -- methods
KW - Male
KW - Female
KW - Interleukin-6 -- blood
KW - Lung Neoplasms -- blood
KW - Biomarkers, Tumor -- blood
KW - Interleukin-8 -- blood
KW - Lung Neoplasms -- pathology
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1639978378?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+thoracic+oncology+%3A+official+publication+of+the+International+Association+for+the+Study+of+Lung+Cancer&rft.atitle=A+combined+prognostic+serum+interleukin-8+and+interleukin-6+classifier+for+stage+1+lung+cancer+in+the+prostate%2C+lung%2C+colorectal%2C+and+ovarian+cancer+screening+trial.&rft.au=Ryan%2C+Br%C3%ADd+M%3BPine%2C+Sharon+R%3BChaturvedi%2C+Anil+K%3BCaporaso%2C+Neil%3BHarris%2C+Curtis+C&rft.aulast=Ryan&rft.aufirst=Br%C3%ADd&rft.date=2014-10-01&rft.volume=9&rft.issue=10&rft.spage=1494&rft.isbn=&rft.btitle=&rft.title=Journal+of+thoracic+oncology+%3A+official+publication+of+the+International+Association+for+the+Study+of+Lung+Cancer&rft.issn=1556-1380&rft_id=info:doi/10.1097%2FJTO.0000000000000278
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-09-03
N1 - Date created - 2014-12-20
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1097/JTO.0000000000000278
ER -
TY - JOUR
T1 - Association of cancer worry and perceived risk with doctor avoidance: an analysis of information avoidance in a nationally representative US sample
AN - 1627734018
AB - Fear of receiving bad news about one’s health can lead people to avoid seeking out health information that, ironically, may be crucial for health maintenance. Using a nationally representative US sample, the present study examined whether perceived likelihood of developing cancer and worry about cancer were associated with reports of avoiding visits to one’s doctor, in respondents under and over age 50. Cancer worry, but not perceived risk of cancer, predicted doctor avoidance in respondents aged 50 and older, whereas the opposite pattern held for respondents under age 50. Moreover, in respondents aged 50 and older, cancer worry and perceived cancer risk interacted such that cancer worry was linked to doctor avoidance only when respondents also perceived a high likelihood of cancer. The latter result is consistent with the notion that worry may motivate information seeking when people expect information to dispel worry and information avoidance when the information is seen as highly likely to confirm one’s fears. Findings suggest a need for communication strategies that can influence worry and perceived risk differentially. Research should also assess the effectiveness of other behavioral strategies (e.g., automatic scheduling of appointments) as a means for reducing doctor avoidance.
JF - Journal of Behavioral Medicine
AU - Persoskie, Alexander
AU - Ferrer, Rebecca A
AU - Klein, William M P
AD - Behavioral Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, 9609 Medical Center Drive, Floor 3 East Tower, Bethesda, MD, 20892–9761, USA persoskieai@mail.nih.gov persoskieai@mail.nih.gov persoskieai@mail.nih.gov; Behavioral Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, 9609 Medical Center Drive, Floor 3 East Tower, Bethesda, MD, 20892–9761, USA
Y1 - 2014/10//
PY - 2014
DA - Oct 2014
SP - 977
EP - 987
CY - New York
PB - Springer Science & Business Media
VL - 37
IS - 5
SN - 0160-7715
KW - Psychology
KW - Appointments
KW - Avoidance
KW - Bad news
KW - Cancer
KW - Communication strategies
KW - Fear
KW - Health
KW - Health information
KW - News
KW - Risk perception
KW - Worry
KW - United States--US
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1627734018?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Behavioral+Medicine&rft.atitle=Association+of+cancer+worry+and+perceived+risk+with+doctor+avoidance%3A+an+analysis+of+information+avoidance+in+a+nationally+representative+US+sample&rft.au=Persoskie%2C+Alexander%3BFerrer%2C+Rebecca+A%3BKlein%2C+William+M+P&rft.aulast=Persoskie&rft.aufirst=Alexander&rft.date=2014-10-01&rft.volume=37&rft.issue=5&rft.spage=977&rft.isbn=&rft.btitle=&rft.title=Journal+of+Behavioral+Medicine&rft.issn=01607715&rft_id=info:doi/10.1007%2Fs10865-013-9537-2
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Date revised - 2014-11-10
N1 - Last updated - 2016-05-13
N1 - SubjectsTermNotLitGenreText - United States--US
DO - http://dx.doi.org/10.1007/s10865-013-9537-2
ER -
TY - JOUR
T1 - Attitudes About Internet Support Groups Among Adolescents and Young Adults with Neurofibromatosis Type 1 and their Parents
AN - 1627732009
AB - Youth with neurofibromatosis type 1 (NF1) have multiple, complex symptoms associated with physical, social-emotional, and cognitive difficulties. In addition, caring for a child with NF1 can be extremely challenging for parents. Since research with other chronic illness populations suggests that social support, including internet support groups (ISGs), can be beneficial, this survey study aimed to determine the attitudes and preferences of adolescents and young adults with NF1 and parents of a child with NF1 regarding ISGs. Thirty patients and 30 caregivers completed a 24-item survey about ISGs. Many patients and parents are not aware of any ISGs for NF1, but are interested in using one in the future for a variety of reasons, including to get answers to their questions about NF1, to find out about research studies, and to discuss problems and concerns about NF1. Specific concerns of interest include physical, social-emotional, and cognitive aspects of NF1. ISGs have potential as a social support intervention within the NF1 community. ISGs for the NF1 population should include patients with NF1 (or parents of children with NF1) as well as a health professional, and both chat rooms and discussion boards likely would be well-received.
JF - Journal of Genetic Counseling
AU - Martin, Staci
AU - Wolters, Pamela L
AU - Baldwin, Andrea
AU - Roderick, Marie Claire
AU - Toledo-Tamula, Mary Anne
AU - Gillespie, Andrea
AU - Widemann, Brigitte
AD - Pediatric Oncology Branch, National Cancer Institute, Building 82, Room 107 9030 Old Georgetown Road, Bethesda, MD, 20892-8200, USA martins@mail.nih.gov martins@mail.nih.gov martins@mail.nih.gov martins@mail.nih.gov martins@mail.nih.gov; Pediatric Oncology Branch, National Cancer Institute, Building 82, Room 107 9030 Old Georgetown Road, Bethesda, MD, 20892-8200, USA, Institute for Psychological Sciences, Arlington, VA, USA ; Clinical Research Directorate/CMRP, SAIC-Frederick, Inc., Frederick National Laboratory for Cancer Research, Frederick, MD, USA ; Pediatric Oncology Branch, National Cancer Institute, Building 82, Room 107 9030 Old Georgetown Road, Bethesda, MD, 20892-8200, USA
Y1 - 2014/10//
PY - 2014
DA - Oct 2014
SP - 796
EP - 804
CY - New York
PB - Springer Science & Business Media
VL - 23
IS - 5
SN - 1059-7700
KW - Psychology
KW - Adolescents
KW - Social support
KW - Support groups
KW - Young adults
KW - Attitudes
KW - Carers
KW - Caring
KW - Chat rooms
KW - Children
KW - Chronic sickness
KW - Cognitive aspects
KW - Health
KW - Internet
KW - Multiple symptoms
KW - Neurofibromatosis
KW - Parents
KW - Physical symptoms
KW - Preferences
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1627732009?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Genetic+Counseling&rft.atitle=Attitudes+About+Internet+Support+Groups+Among+Adolescents+and+Young+Adults+with+Neurofibromatosis+Type+1+and+their+Parents&rft.au=Martin%2C+Staci%3BWolters%2C+Pamela+L%3BBaldwin%2C+Andrea%3BRoderick%2C+Marie+Claire%3BToledo-Tamula%2C+Mary+Anne%3BGillespie%2C+Andrea%3BWidemann%2C+Brigitte&rft.aulast=Martin&rft.aufirst=Staci&rft.date=2014-10-01&rft.volume=23&rft.issue=5&rft.spage=796&rft.isbn=&rft.btitle=&rft.title=Journal+of+Genetic+Counseling&rft.issn=10597700&rft_id=info:doi/10.1007%2Fs10897-014-9688-5
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Date revised - 2014-11-10
N1 - Last updated - 2016-05-13
DO - http://dx.doi.org/10.1007/s10897-014-9688-5
ER -
TY - JOUR
T1 - HIV Testing Histories and Risk Factors Among Migrants and Recent Immigrants Who Received Rapid HIV Testing from Three Community-Based Organizations
AN - 1627731003
AB - Migrants and recent immigrants in the US constitute a large population that is vulnerable to HIV. From March 2005 to February 2007, three community-based organizations conducted rapid HIV testing among migrants in five states. Participants were asked to complete a survey on sociodemographics, HIV-risk behaviors, and HIV-testing histories with the aim of understanding factors associated with HIV testing. Among 5,247 persons tested, 6 (0.1 %) were HIV-positive. Among 3,135 persons who completed surveys, more than half had never been tested for HIV previously (59 %). Participants reported high levels of HIV-risk behaviors in the past year, including 2 or more sex partners (45 %), sex while high/drunk (30 %), and transactional sex (29 %). Multivariate analysis identified several factors independently associated with decreased likelihood of prior HIV testing, including poor spoken English. Continued efforts are needed to ensure that migrant populations have improved access to HIV testing and prevention services. Understanding factors associated with migrants’ lack of previous HIV testing may help focus these efforts.
JF - Journal of Immigrant and Minority Health
AU - Schulden, Jeffrey D
AU - Painter, Thomas M
AU - Song, Binwei
AU - Valverde, Eduardo
AU - Borman, Mary Ann
AU - Monroe-Spencer, Kyle
AU - Bautista, Greg
AU - Saleheen, Hassan
AU - Voetsch, Andrew C
AU - Heffelfinger, James D
AD - National Institute on Drug Abuse (NIDA), National Institutes of Health (NIH), 6001 Executive Blvd, MSC 9589, Bethesda, MD, 20892, USA schuldenj@nida.nih.gov; National Center for HIV/AIDS, Viral Hepatitis, STD, and TB Prevention, Centers for Disease Control and Prevention (CDC), Atlanta, GA, USA ; United Migrant Opportunity Services, Milwaukee, WI, USA ; AIDGwinnett, Lawrenceville, GA, USA ; Connecticut Children’s Medical Center, Hartford, CT, USA ; National Institute on Drug Abuse (NIDA), National Institutes of Health (NIH), 6001 Executive Blvd, MSC 9589, Bethesda, MD, 20892, USA
Y1 - 2014/10//
PY - 2014
DA - Oct 2014
SP - 798
EP - 810
CY - New York
PB - Springer Science & Business Media
VL - 16
IS - 5
SN - 1557-1912
KW - Medical Sciences
KW - Community based
KW - Risk behaviour
KW - HIV
KW - Immigrants
KW - Migrants
KW - Multivariate analysis
KW - Preventive health care
KW - Preventive programmes
KW - Risk factors
KW - Safe sexual practices
KW - Sex education
KW - Testing
KW - United States--US
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1627731003?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Immigrant+and+Minority+Health&rft.atitle=HIV+Testing+Histories+and+Risk+Factors+Among+Migrants+and+Recent+Immigrants+Who+Received+Rapid+HIV+Testing+from+Three+Community-Based+Organizations&rft.au=Schulden%2C+Jeffrey+D%3BPainter%2C+Thomas+M%3BSong%2C+Binwei%3BValverde%2C+Eduardo%3BBorman%2C+Mary+Ann%3BMonroe-Spencer%2C+Kyle%3BBautista%2C+Greg%3BSaleheen%2C+Hassan%3BVoetsch%2C+Andrew+C%3BHeffelfinger%2C+James+D&rft.aulast=Schulden&rft.aufirst=Jeffrey&rft.date=2014-10-01&rft.volume=16&rft.issue=5&rft.spage=798&rft.isbn=&rft.btitle=&rft.title=Journal+of+Immigrant+and+Minority+Health&rft.issn=15571912&rft_id=info:doi/10.1007%2Fs10903-013-9811-y
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Date revised - 2014-11-10
N1 - Last updated - 2016-05-13
N1 - SubjectsTermNotLitGenreText - United States--US
DO - http://dx.doi.org/10.1007/s10903-013-9811-y
ER -
TY - JOUR
T1 - Do Childhood Externalizing Disorders Predict Adult Depression? A Meta-Analysis
AN - 1627730686
AB - Childhood externalizing disorders have been linked to adult affective disorders, although some studies fail to substantiate this finding. Multiple longitudinal cohort studies identifying childhood psychopathology and their association with adult psychiatric illness have been published. To examine the association between childhood externalizing symptoms or disorders and the development of adult depression across cohorts, a meta-analysis was performed. Potential studies were identified using a PubMed search through November 2013. All published, prospective, longitudinal, community-sampled cohort studies of children (≤ 13 years) with externalizing symptoms or disorders (aggression, conduct problems, oppositional defiant disorder, conduct disorder), reassessed in adulthood (≥ 18 years) for depressive disorders (major depressive disorder, depressive disorder NOS, or dysthymic disorder) were included. A random effects model was used to summarize the pooled effect sizes. Ancillary analyses considered covariates that could account for variance among studies. Ten studies representing eight cohorts of children initially assessed at age 13 or younger (N=17,712) were included in the meta-analysis. Childhood externalizing behavior was associated with adult depressive disorders (OR=1.52, 95 % confidence interval=1.27–1.80, p<0.0001). Utilizing Orwin’s Fail-safe N approach, 263 studies with a mean odds ratio of 1.0 would have to be added to the analysis before the cumulative effect would become trivial. Externalizing psychopathology in childhood is associated with the development of unipolar depressive disorders in adulthood.
JF - Journal of Abnormal Child Psychology
AU - Loth, Annemarie K
AU - Drabick, Deborah A G
AU - Leibenluft, Ellen
AU - Hulvershorn, Leslie A
AD - Department of Psychiatry, Indiana University School of Medicine, Riley Hospital for Children, 705 Riley Hospital Drive, Room 4300, Indianapolis, IN, 46202, USA lhulvers@iupui.edu lhulvers@iupui.edu; Department of Psychology, Temple University, Philadelphia, PA, USA ; Section on Bipolar Spectrum Disorders, Emotion and Development Branch, National Institute of Mental Health, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, USA ; Department of Psychiatry, Indiana University School of Medicine, Riley Hospital for Children, 705 Riley Hospital Drive, Room 4300, Indianapolis, IN, 46202, USA
Y1 - 2014/10//
PY - 2014
DA - Oct 2014
SP - 1103
EP - 1113
CY - New York
PB - Springer Science & Business Media
VL - 42
IS - 7
SN - 0091-0627
KW - Medical Sciences--Physical Medicine And Rehabilitation
KW - Predictors
KW - Adults
KW - Analysis
KW - Adulthood
KW - Affective disorders
KW - Aggression
KW - Childhood
KW - Children
KW - Cohort analysis
KW - Conduct disorders
KW - Depression
KW - Depressive personality disorders
KW - Externalizing behaviour
KW - Externalizing problems
KW - Oppositional defiant disorder
KW - Psychopathology
KW - Random effects
KW - Symptoms
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1627730686?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Abnormal+Child+Psychology&rft.atitle=Do+Childhood+Externalizing+Disorders+Predict+Adult+Depression%3F+A+Meta-Analysis&rft.au=Loth%2C+Annemarie+K%3BDrabick%2C+Deborah+A+G%3BLeibenluft%2C+Ellen%3BHulvershorn%2C+Leslie+A&rft.aulast=Loth&rft.aufirst=Annemarie&rft.date=2014-10-01&rft.volume=42&rft.issue=7&rft.spage=1103&rft.isbn=&rft.btitle=&rft.title=Journal+of+Abnormal+Child+Psychology&rft.issn=00910627&rft_id=info:doi/10.1007%2Fs10802-014-9867-8
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Date revised - 2014-11-10
N1 - Last updated - 2016-05-13
DO - http://dx.doi.org/10.1007/s10802-014-9867-8
ER -
TY - JOUR
T1 - Approaches to integrating germline and tumor genomic data in cancer research.
AN - 1623291726; 25115441
AB - Cancer is characterized by a diversity of genetic and epigenetic alterations occurring in both the germline and somatic (tumor) genomes. Hundreds of germline variants associated with cancer risk have been identified, and large amounts of data identifying mutations in the tumor genome that participate in tumorigenesis have been generated. Increasingly, these two genomes are being explored jointly to better understand how cancer risk alleles contribute to carcinogenesis and whether they influence development of specific tumor types or mutation profiles. To understand how data from germline risk studies and tumor genome profiling is being integrated, we reviewed 160 articles describing research that incorporated data from both genomes, published between January 2009 and December 2012, and summarized the current state of the field. We identified three principle types of research questions being addressed using these data: (i) use of tumor data to determine the putative function of germline risk variants; (ii) identification and analysis of relationships between host genetic background and particular tumor mutations or types; and (iii) use of tumor molecular profiling data to reduce genetic heterogeneity or refine phenotypes for germline association studies. We also found descriptive studies that compared germline and tumor genomic variation in a gene or gene family, and papers describing research methods, data sources, or analytical tools. We identified a large set of tools and data resources that can be used to analyze and integrate data from both genomes. Finally, we discuss opportunities and challenges for cancer research that integrates germline and tumor genomics data.
Published by Oxford University Press 2014.
JF - Carcinogenesis
AU - Feigelson, Heather Spencer
AU - Goddard, Katrina A B
AU - Hollombe, Celine
AU - Tingle, Sharna R
AU - Gillanders, Elizabeth M
AU - Mechanic, Leah E
AU - Nelson, Stefanie A
AD - Institute for Health Research, Kaiser Permanente Colorado, Denver, CO, USA, Center for Health Research, Kaiser Permanente Northwest, Portland, OR, USA and Epidemiology and Genomics Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, Rockville, MD, USA. ; Center for Health Research, Kaiser Permanente Northwest, Portland, OR, USA and. ; Epidemiology and Genomics Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, Rockville, MD, USA.
Y1 - 2014/10//
PY - 2014
DA - October 2014
SP - 2157
EP - 2163
VL - 35
IS - 10
KW - Index Medicus
KW - Gene Expression Regulation, Neoplastic
KW - Humans
KW - Genetic Predisposition to Disease
KW - Databases, Genetic
KW - Genomics -- methods
KW - Germ-Line Mutation
KW - Neoplasms -- genetics
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1623291726?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Approaches+to+integrating+germline+and+tumor+genomic+data+in+cancer+research.&rft.au=Feigelson%2C+Heather+Spencer%3BGoddard%2C+Katrina+A+B%3BHollombe%2C+Celine%3BTingle%2C+Sharna+R%3BGillanders%2C+Elizabeth+M%3BMechanic%2C+Leah+E%3BNelson%2C+Stefanie+A&rft.aulast=Feigelson&rft.aufirst=Heather&rft.date=2014-10-01&rft.volume=35&rft.issue=10&rft.spage=2157&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgu165
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-05-11
N1 - Date created - 2014-09-30
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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Methods Mol Biol. 2010;576:61-87 [19882258]
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Breast Cancer Res. 2010;12(6):R93 [21062454]
Genes Dev. 2011 Mar 15;25(6):534-55 [21406553]
Cancer Res. 2011 Apr 1;71(7):2423-7 [21292812]
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Nature. 2011 Jun 30;474(7353):609-15 [21720365]
Cancer Sci. 2011 Oct;102(10):1874-81 [21740479]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/carcin/bgu165
ER -
TY - JOUR
T1 - An analysis of genetic factors related to risk of inflammatory bowel disease and colon cancer
AN - 1622607920; 20875936
AB - Background and aims Patients with inflammatory bowel disease (IBD) have a higher risk of developing colorectal cancer than the general population. Genome-wide association studies have identified and replicated several loci associated with risk of IBD; however, it is currently unknown whether these loci are also associated with colon cancer risk. Methods We selected 15 validated SNPs associated with risk of either Crohn's disease, ulcerative colitis, or both in previous GWAS and tested whether these loci were also associated with colon cancer risk in a two-stage study design. Results We found that rs744166 in STAT3 was associated with colon cancer risk in two studies; however, the direction of the observation was reversed in TP53 mutant tumors possibly due to a nullification of the effect by mutant p53. The SNP, which lies within intron 1 of the STAT3 gene, was associated with lower expression of STAT3 mRNA in TP53 wild-type, but not mutant, tumors. Conclusions These data suggest that the STAT3 locus is associated with both IBD and cancer. Further understanding the function of this variant in relation to TP53 could possibly explain the role of this gene in autoimmunity and cancer. Furthermore, an analysis of this locus, specifically in a population with IBD, could help to resolve the relationship between this SNP and cancer.
JF - Cancer Epidemiology
AU - Ryan, Brid M
AU - Wolff, Roger K
AU - Valeri, Nicola
AU - Khan, Mohammed
AU - Robinson, Dillon
AU - Paone, Alessio
AU - Bowman, Elise D
AU - Lundgreen, Abbie
AU - Caan, Bette
AU - Potter, John
AU - Brown, Derek
AU - Croce, Carlo
AU - Slattery, Martha L
AU - Harris, Curtis C
AD - Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA
Y1 - 2014/10//
PY - 2014
DA - Oct 2014
SP - 583
EP - 590
PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom
VL - 38
IS - 5
SN - 1877-7821, 1877-7821
KW - Genetics Abstracts; Risk Abstracts
KW - Inflammatory bowel disease
KW - Colon cancer
KW - STAT3
KW - Genetic factors
KW - Ulcerative colitis
KW - Colorectal cancer
KW - Autoimmunity
KW - Mutants
KW - Gene expression
KW - Risk factors
KW - Crohn's disease
KW - Data processing
KW - Stat3 protein
KW - Tumors
KW - Cancer
KW - mRNA
KW - p53 protein
KW - Health risks
KW - Inflammatory bowel diseases
KW - Single-nucleotide polymorphism
KW - Introns
KW - Colorectal carcinoma
KW - G 07880:Human Genetics
KW - R2 23060:Medical and environmental health
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Epidemiology&rft.atitle=An+analysis+of+genetic+factors+related+to+risk+of+inflammatory+bowel+disease+and+colon+cancer&rft.au=Ryan%2C+Brid+M%3BWolff%2C+Roger+K%3BValeri%2C+Nicola%3BKhan%2C+Mohammed%3BRobinson%2C+Dillon%3BPaone%2C+Alessio%3BBowman%2C+Elise+D%3BLundgreen%2C+Abbie%3BCaan%2C+Bette%3BPotter%2C+John%3BBrown%2C+Derek%3BCroce%2C+Carlo%3BSlattery%2C+Martha+L%3BHarris%2C+Curtis+C&rft.aulast=Ryan&rft.aufirst=Brid&rft.date=2014-10-01&rft.volume=38&rft.issue=5&rft.spage=583&rft.isbn=&rft.btitle=&rft.title=Cancer+Epidemiology&rft.issn=18777821&rft_id=info:doi/10.1016%2Fj.canep.2014.07.003
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-11-01
N1 - Last updated - 2015-01-07
N1 - SubjectsTermNotLitGenreText - Crohn's disease; Genetic factors; Data processing; Stat3 protein; Ulcerative colitis; Colorectal cancer; Autoimmunity; Colon cancer; Tumors; p53 protein; mRNA; Gene expression; Inflammatory bowel diseases; Single-nucleotide polymorphism; Risk factors; Introns; Health risks; Colorectal carcinoma; Cancer; Mutants
DO - http://dx.doi.org/10.1016/j.canep.2014.07.003
ER -
TY - JOUR
T1 - NUCLEAR MEDICINE PRACTICES IN THE 1950s THROUGH THE MID-1970S AND OCCUPATIONAL RADIATION DOSES TO TECHNOLOGISTS FROM DIAGNOSTIC RADIOISOTOPE PROCEDURES
AN - 1622607874; 20802508
AB - Data on occupational radiation exposure from nuclear medicine procedures for the time period of the 1950s through the 1970s is important for retrospective health risk studies of medical personnel who conducted those activities. To better understand and characterize historical radiation exposures to technologists, the authors collected information on nuclear medicine practices in the 1950s, 1960s, and 1970s. To collect historical data needed to reconstruct doses to technologists, a focus group interview was held with experts who began using radioisotopes in medicine in the 1950s and the 1960s. The doses estimated in this study show that the introduction of [sup 99m]Tc resulted in an increase in occupational doses per procedure.
JF - Health Physics
AU - Drozdovitch, Vladimir
AU - Brill, Aaron B
AU - Mettler, Fred A, Jr
AU - Beckner, William M
AU - Goldsmith, Stanley J
AU - Gross, Milton D
AU - Hays, Marguerite T
AU - Kirchner, Peter T
AU - Langan, James K
AU - Reba, Richard C
AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, 9609 Medical Center Drive, Room 7E548, MSC 9778, Bethesda, MD 20892-9778, drozdovv@mail.nih.gov
Y1 - 2014/10//
PY - 2014
DA - Oct 2014
SP - 300
EP - 310
PB - Williams & Wilkins, 351 W. Camden St. Baltimore MD 21201 United States
VL - 107
IS - 4
SN - 0017-9078, 0017-9078
KW - Risk Abstracts; Health & Safety Science Abstracts
KW - dose assessment
KW - historical profiles
KW - nuclear medicine
KW - radiation, medical
KW - Historical account
KW - Health risks
KW - Radiation
KW - Radioisotopes
KW - Occupational exposure
KW - Medical personnel
KW - R2 23060:Medical and environmental health
KW - H 1000:Occupational Safety and Health
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Health+Physics&rft.atitle=NUCLEAR+MEDICINE+PRACTICES+IN+THE+1950s+THROUGH+THE+MID-1970S+AND+OCCUPATIONAL+RADIATION+DOSES+TO+TECHNOLOGISTS+FROM+DIAGNOSTIC+RADIOISOTOPE+PROCEDURES&rft.au=Drozdovitch%2C+Vladimir%3BBrill%2C+Aaron+B%3BMettler%2C+Fred+A%2C+Jr%3BBeckner%2C+William+M%3BGoldsmith%2C+Stanley+J%3BGross%2C+Milton+D%3BHays%2C+Marguerite+T%3BKirchner%2C+Peter+T%3BLangan%2C+James+K%3BReba%2C+Richard+C&rft.aulast=Drozdovitch&rft.aufirst=Vladimir&rft.date=2014-10-01&rft.volume=107&rft.issue=4&rft.spage=300&rft.isbn=&rft.btitle=&rft.title=Health+Physics&rft.issn=00179078&rft_id=info:doi/10.1097%2FHP.0000000000000107
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-11-01
N1 - Last updated - 2015-05-27
N1 - SubjectsTermNotLitGenreText - Health risks; Historical account; Radiation; Radioisotopes; Medical personnel; Occupational exposure
DO - http://dx.doi.org/10.1097/HP.0000000000000107
ER -
TY - JOUR
T1 - Alterations in leukocyte telomere length in workers occupationally exposed to benzene
AN - 1622606180; 20840744
AB - Exposure to benzene, a known leukemogen and probable lymphomagen, has been demonstrated to result in oxidative stress, which has previously been associated with altered telomere length (TL). TL specifically has been associated with several health outcomes in epidemiologic studies, including cancer risk, and has been demonstrated to be altered following exposure to a variety of chemical agents. To evaluate the association between benzene exposure and TL, we measured TL by monochrome multiplex quantitative PCR in 43 workers exposed to high levels of benzene and 43 age and sex-matched unexposed workers in Shanghai, China. Benzene exposure levels were monitored using organic vapor passive dosimetry badges before phlebotomy. The median benzene exposure level in exposed workers was 31 ppm. The mean TL in controls, workers exposed to levels of benzene below the median ( less than or equal to 31 ppm), and above the median (>31 ppm) was 1.26 plus or minus 0.17, 1.25 plus or minus 0.16, and 1.37 plus or minus 0.23, respectively. Mean TL was significantly elevated in workers exposed to >31 ppm of benzene compared with controls (P=0.03). Our findings provide evidence that high levels of occupational benzene exposure are associated with TL. Environ. Mol. Mutagen. 55:673-678, 2014. Published [2014]. This article is a U.S. Government work and is in the public domain in the USA.
JF - Environmental and Molecular Mutagenesis
AU - Bassig, Bryan A
AU - Zhang, Luoping
AU - Cawthon, Richard M
AU - Smith, Martyn T
AU - Yin, Songnian
AU - Li, Guilan
AU - Hu, Wei
AU - Shen, Min
AU - Rappaport, Stephen
AU - Barone-Adesi, Francesco
AU - Rothman, Nathaniel
AU - Vermeulen, Roel
AU - Lan, Qing
AD - Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Bethesda, Maryland.
Y1 - 2014/10//
PY - 2014
DA - Oct 2014
SP - 673
EP - 678
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 55
IS - 8
SN - 0893-6692, 0893-6692
KW - Health & Safety Science Abstracts; Risk Abstracts; Toxicology Abstracts; Genetics Abstracts
KW - Mutagens
KW - Age
KW - Dosimetry
KW - Leukocytes
KW - Benzene
KW - Cancer
KW - Mutagenesis
KW - Health risks
KW - Telomeres
KW - USA
KW - Vapors
KW - Oxidative stress
KW - Polymerase chain reaction
KW - China, People's Rep.
KW - China, People's Rep., Shanghai
KW - Occupational exposure
KW - H 1000:Occupational Safety and Health
KW - R2 23060:Medical and environmental health
KW - G 07730:Development & Cell Cycle
KW - X 24350:Industrial Chemicals
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1622606180?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+and+Molecular+Mutagenesis&rft.atitle=Alterations+in+leukocyte+telomere+length+in+workers+occupationally+exposed+to+benzene&rft.au=Bassig%2C+Bryan+A%3BZhang%2C+Luoping%3BCawthon%2C+Richard+M%3BSmith%2C+Martyn+T%3BYin%2C+Songnian%3BLi%2C+Guilan%3BHu%2C+Wei%3BShen%2C+Min%3BRappaport%2C+Stephen%3BBarone-Adesi%2C+Francesco%3BRothman%2C+Nathaniel%3BVermeulen%2C+Roel%3BLan%2C+Qing&rft.aulast=Bassig&rft.aufirst=Bryan&rft.date=2014-10-01&rft.volume=55&rft.issue=8&rft.spage=673&rft.isbn=&rft.btitle=&rft.title=Environmental+and+Molecular+Mutagenesis&rft.issn=08936692&rft_id=info:doi/10.1002%2Fem.21880
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-11-01
N1 - Last updated - 2015-10-28
N1 - SubjectsTermNotLitGenreText - Mutagens; Telomeres; Age; Vapors; Oxidative stress; Leukocytes; Dosimetry; Polymerase chain reaction; Cancer; Occupational exposure; Benzene; Mutagenesis; Health risks; USA; China, People's Rep., Shanghai; China, People's Rep.
DO - http://dx.doi.org/10.1002/em.21880
ER -
TY - JOUR
T1 - Statin use and risk of hepatocellular carcinoma in a U.S. population
AN - 1622603586; 20875946
AB - Purpose Statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) are medications widely prescribed to reduce cholesterol levels. Observational studies in high-risk populations, mostly in Asia, have suggested that statins are associated with a reduced risk of hepatocellular carcinoma (HCC). The current study sought to evaluate the association of statin use and HCC in a U.S.-based, low-risk, general population. Methods A nested case-control study was conducted among members of the Health Alliance Plan HMO of the Henry Ford Health System enrolled between 1999 and 2010. Electronic pharmacy records of statin use were compared among tumor registry-confirmed cases of HCC (n=94) and controls (n=468) matched on age, sex, diagnosis date, and length of HMO enrolment. Results In multivariate analyses, ever-use of statins was significantly inversely associated with development of HCC (Odds ratio (OR): 0.32, 95%CI: 0.15-0.67). No clear dose-response relationship was evident as statin use for 2 years (OR=0.31, 95CI%=0.12-9.81) resulted in very similar ORs. Conclusions The use of statins among populations in low-risk HCC areas may be associated with decreased risk of HCC.
JF - Cancer Epidemiology
AU - McGlynn, Katherine A
AU - Divine, George W
AU - Sahasrabuddhe, Vikrant V
AU - Engel, Lawrence S
AU - VanSlooten, Ashley
AU - Wells, Karen
AU - Yood, Marianne Ulcickas
AU - Alford, Sharon Hensley
AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, United States
Y1 - 2014/10//
PY - 2014
DA - Oct 2014
SP - 523
EP - 527
PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom
VL - 38
IS - 5
SN - 1877-7821, 1877-7821
KW - Risk Abstracts
KW - Statins
KW - Liver cancer
KW - Epidemiology
KW - Health risks
KW - Age
KW - Dose-response effects
KW - Risk reduction
KW - Tumors
KW - Cholesterol
KW - Asia
KW - Drugs
KW - Cancer
KW - R2 23060:Medical and environmental health
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Epidemiology&rft.atitle=Statin+use+and+risk+of+hepatocellular+carcinoma+in+a+U.S.+population&rft.au=McGlynn%2C+Katherine+A%3BDivine%2C+George+W%3BSahasrabuddhe%2C+Vikrant+V%3BEngel%2C+Lawrence+S%3BVanSlooten%2C+Ashley%3BWells%2C+Karen%3BYood%2C+Marianne+Ulcickas%3BAlford%2C+Sharon+Hensley&rft.aulast=McGlynn&rft.aufirst=Katherine&rft.date=2014-10-01&rft.volume=38&rft.issue=5&rft.spage=523&rft.isbn=&rft.btitle=&rft.title=Cancer+Epidemiology&rft.issn=18777821&rft_id=info:doi/10.1016%2Fj.canep.2014.06.009
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-11-01
N1 - Last updated - 2014-11-26
N1 - SubjectsTermNotLitGenreText - Health risks; Age; Statins; Dose-response effects; Cholesterol; Tumors; Risk reduction; Drugs; Cancer; Asia
DO - http://dx.doi.org/10.1016/j.canep.2014.06.009
ER -
TY - JOUR
T1 - Chloroquine Remains Effective for Treating Plasmodium vivax Malaria in Pursat Province, Western Cambodia
AN - 1622601429; 20856093
AB - Chloroquine (CQ) is used to treat Plasmodium vivax malaria in areas where CQ resistance has not been reported. The use of artemisinin (ART)-based combination therapies (ACTs) to treat CQ-sensitive P. vivax infections is effective and convenient but may promote the emergence and worsening of ART resistance in sympatric Plasmodium falciparum populations. Here, we show that CQ effectively treats P. vivax malaria in Pursat Province, western Cambodia, where ART-resistant P. falciparum is highly prevalent and spreading. (This study has been registered at ClinicalTrials.gov under registration no. NCT00663546.)
JF - Antimicrobial Agents & Chemotherapy
AU - Amaratunga, Chanaki
AU - Sreng, Sokunthea
AU - Mao, Sivanna
AU - Tullo, Gregory S
AU - Anderson, Jennifer M
AU - Chuor, Char Meng
AU - Suon, Seila
AU - Fairhurst, Rick M
AD - Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA, rfairhurst@niaid.nih.gov.
Y1 - 2014/10//
PY - 2014
DA - October 2014
SP - 6270
EP - 6272
PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL - 58
IS - 10
SN - 0066-4804, 0066-4804
KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts A: Industrial & Applied Microbiology
KW - Parasites
KW - Human diseases
KW - Spreading
KW - Sympatric populations
KW - Therapy
KW - Chloroquine
KW - Plasmodium vivax
KW - Malaria
KW - Plasmodium falciparum
KW - Infection
KW - Public health
KW - Cambodia
KW - artemisinin
KW - K 03340:Effects of Physical & Chemical Factors
KW - A 01340:Antibiotics & Antimicrobials
KW - Q1 08485:Species interactions: pests and control
KW - Q5 08524:Public health, medicines, dangerous organisms
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Antimicrobial+Agents+%26+Chemotherapy&rft.atitle=Chloroquine+Remains+Effective+for+Treating+Plasmodium+vivax+Malaria+in+Pursat+Province%2C+Western+Cambodia&rft.au=Amaratunga%2C+Chanaki%3BSreng%2C+Sokunthea%3BMao%2C+Sivanna%3BTullo%2C+Gregory+S%3BAnderson%2C+Jennifer+M%3BChuor%2C+Char+Meng%3BSuon%2C+Seila%3BFairhurst%2C+Rick+M&rft.aulast=Amaratunga&rft.aufirst=Chanaki&rft.date=2014-10-01&rft.volume=58&rft.issue=10&rft.spage=6270&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+Agents+%26+Chemotherapy&rft.issn=00664804&rft_id=info:doi/10.1128%2FAAC.03026-14
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-11-01
N1 - Number of references - 17
N1 - Last updated - 2016-02-04
N1 - SubjectsTermNotLitGenreText - Parasites; Human diseases; Therapy; Malaria; Public health; Spreading; Sympatric populations; Chloroquine; artemisinin; Infection; Plasmodium vivax; Plasmodium falciparum; Cambodia
DO - http://dx.doi.org/10.1128/AAC.03026-14
ER -
TY - JOUR
T1 - Combined Effects of the Structural Heterogeneity and Dynamics of Flaviviruses on Antibody Recognition
AN - 1622598932; 20856421
AB - Flaviviruses are thought to sample an ensemble of structures at equilibrium. One consequence of a structurally dynamic virion is the observed time-dependent increases in neutralization sensitivity that can occur after prolonged incubation with antibody. Differences in how virus strains "breathe" may affect epitope exposure and contribute to the underlying mechanisms of strain-dependent neutralization sensitivity. Beyond the contribution of structural dynamics, flaviviruses exist as a structurally heterogeneous population due to an inefficient virion maturation process. Here, we investigate the interplay between virion maturation and structural dynamics that contributes to antibody-mediated neutralization. Using West Nile (WNV) and dengue (DENV) viruses produced under conditions that modify the extent of virion maturation, we investigated time-dependent changes in neutralization sensitivity associated with structural dynamics. Our results identify distinct patterns of neutralization against viruses that vary markedly with respect to the extent of virion maturation. Reducing the efficiency of virion maturation resulted in greater time-dependent changes in neutralization potency and a marked reduction in the stability of the particle at 37 degree C compared to more mature virus. The fact that the neutralization sensitivity of WNV and DENV did not increase after prolonged incubation in the absence of antibody, regardless of virion maturation, suggests that the dynamic processes that govern epitope accessibility on infectious viruses are reversible. Against the backdrop of heterogeneous flavivirus structures, differences in the pathways by which viruses "breathe" represent an additional layer of complexity in understanding maturation state-dependent patterns of antibody recognition. IMPORTANCE Flaviviruses exist as a group of related structures at equilibrium that arise from the dynamic motion of E proteins that comprise the antigenic surface of the mature virion. This process has been characterized for numerous viruses and is referred to as viral "breathing." Additionally, flaviviruses are structurally heterogeneous due to an inefficient maturation process responsible for cleaving prM on the virion surface. Both of these mechanisms vary the exposure of antigenic sites available for antibody binding and impact the ability of antibodies to neutralize infection. We demonstrate that virions with inefficient prM cleavage "breathe" differently than their more mature counterparts, resulting in distinct patterns of neutralization sensitivity. Additionally, the maturation state was found to impact virus stability in solution. Our findings provide insight into the complex flavivirus structures that contribute to infection with the potential to impact antibody recognition.
JF - Journal of Virology
AU - Dowd, Kimberly A
AU - Mukherjee, Swati
AU - Kuhn, Richard J
AU - Pierson, Theodore C
AD - Viral Pathogenesis Section, Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA, piersontc@mail.nih.gov.
Y1 - 2014/10//
PY - 2014
DA - October 2014
SP - 11726
EP - 11737
PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL - 88
IS - 20
SN - 0022-538X, 0022-538X
KW - ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Virology & AIDS Abstracts
KW - Virions
KW - Virology
KW - Respiration
KW - Viruses
KW - Environmental impact
KW - Infection
KW - E protein
KW - Flavivirus
KW - Antibodies
KW - Viral diseases
KW - Dengue
KW - Sexual maturity
KW - Structural dynamics
KW - Epitopes
KW - Q1 08442:Population dynamics
KW - V 22320:Replication
KW - Q5 08524:Public health, medicines, dangerous organisms
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Virology&rft.atitle=Combined+Effects+of+the+Structural+Heterogeneity+and+Dynamics+of+Flaviviruses+on+Antibody+Recognition&rft.au=Dowd%2C+Kimberly+A%3BMukherjee%2C+Swati%3BKuhn%2C+Richard+J%3BPierson%2C+Theodore+C&rft.aulast=Dowd&rft.aufirst=Kimberly&rft.date=2014-10-01&rft.volume=88&rft.issue=20&rft.spage=11726&rft.isbn=&rft.btitle=&rft.title=Journal+of+Virology&rft.issn=0022538X&rft_id=info:doi/10.1128%2FJVI.01140-14
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-11-01
N1 - Number of references - 56
N1 - Last updated - 2016-12-22
N1 - SubjectsTermNotLitGenreText - Virology; Antibodies; Viral diseases; Structural dynamics; Sexual maturity; Viruses; Environmental impact; Virions; Dengue; Respiration; Infection; E protein; Epitopes; Flavivirus
DO - http://dx.doi.org/10.1128/JVI.01140-14
ER -
TY - JOUR
T1 - The role of acculturation and collectivism in cancer screening for Vietnamese American women
AN - 1622301416; 4614933
AB - The aim of this study was to examine the influence of demographic variables and the interplay between collectivism and acculturation on breast and cervical cancer screening outcomes among Vietnamese American women. Convenience sampling was used to recruit 111 Vietnamese women from the Richmond, VA, metropolitan area, who participated in a larger cancer screening intervention. All participants completed measures on demographic variables, collectivism, acculturation, and cancer-screening- related variables (i.e., attitudes, self-efficacy, and screening behavior). Findings indicated that collectivism predicted both positive attitudes and higher levels of self-efficacy with regard to breast and cervical cancer screening. Collectivism also moderated the relationship between acculturation and attitudes toward breast cancer screening such that for women with low levels of collectivistic orientation, increasing acculturation predicted less positive attitudes towards breast cancer screening. This relationship was not found for women with high levels of collectivistic orientation. The current findings highlight the important roles that sociodemographic and cultural variables play in affecting health attitudes, self- efficacy, and behavior among Vietnamese women. The findings potentially inform screening programs that rely on culturally relevant values in helping increase Vietnamese women's motivation to screen. Reprinted by permission of Taylor & Francis Ltd.
JF - Health care for women international
AU - Nguyen, Anh B
AU - Clark, Trenette T
AD - US National Cancer Institute ; University of North Carolina, Chapel Hill
Y1 - 2014/10//
PY - 2014
DA - Oct 2014
SP - 1162
EP - 1180
VL - 35
IS - 10
SN - 0739-9332, 0739-9332
KW - Sociology
KW - Acculturation
KW - Health care
KW - Motivation
KW - Collectivism
KW - Women
KW - U.S.A.
KW - Cancer
KW - Vietnam
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1622301416?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Health+care+for+women+international&rft.atitle=The+role+of+acculturation+and+collectivism+in+cancer+screening+for+Vietnamese+American+women&rft.au=Nguyen%2C+Anh+B%3BClark%2C+Trenette+T&rft.aulast=Nguyen&rft.aufirst=Anh&rft.date=2014-10-01&rft.volume=35&rft.issue=10&rft.spage=1162&rft.isbn=&rft.btitle=&rft.title=Health+care+for+women+international&rft.issn=07399332&rft_id=info:doi/10.1080%2F07399332.2013.863317
LA - English
DB - International Bibliography of the Social Sciences (IBSS)
N1 - Date revised - 2014-11-10
N1 - Last updated - 2014-11-11
N1 - SubjectsTermNotLitGenreText - 1939 3617 6220; 2491 5676; 8322; 13598 5421 6091; 5775 13521; 539 3105 3198; 449 393 30; 433 293 14
DO - http://dx.doi.org/10.1080/07399332.2013.863317
ER -
TY - JOUR
T1 - MMS exposure promotes increased MtDNA mutagenesis in the presence of replication-defective disease-associated DNA polymerase γ variants.
AN - 1618161204; 25340760
AB - Mitochondrial DNA (mtDNA) encodes proteins essential for ATP production. Mutant variants of the mtDNA polymerase cause mutagenesis that contributes to aging, genetic diseases, and sensitivity to environmental agents. We interrogated mtDNA replication in Saccharomyces cerevisiae strains with disease-associated mutations affecting conserved regions of the mtDNA polymerase, Mip1, in the presence of the wild type Mip1. Mutant frequency arising from mtDNA base substitutions that confer erythromycin resistance and deletions between 21-nucleotide direct repeats was determined. Previously, increased mutagenesis was observed in strains encoding mutant variants that were insufficient to maintain mtDNA and that were not expected to reduce polymerase fidelity or exonuclease proofreading. Increased mutagenesis could be explained by mutant variants stalling the replication fork, thereby predisposing the template DNA to irreparable damage that is bypassed with poor fidelity. This hypothesis suggests that the exogenous base-alkylating agent, methyl methanesulfonate (MMS), would further increase mtDNA mutagenesis. Mitochondrial mutagenesis associated with MMS exposure was increased up to 30-fold in mip1 mutants containing disease-associated alterations that affect polymerase activity. Disrupting exonuclease activity of mutant variants was not associated with increased spontaneous mutagenesis compared with exonuclease-proficient alleles, suggesting that most or all of the mtDNA was replicated by wild type Mip1. A novel subset of C to G transversions was responsible for about half of the mutants arising after MMS exposure implicating error-prone bypass of methylated cytosines as the predominant mutational mechanism. Exposure to MMS does not disrupt exonuclease activity that suppresses deletions between 21-nucleotide direct repeats, suggesting the MMS-induce mutagenesis is not explained by inactivated exonuclease activity. Further, trace amounts of CdCl2 inhibit mtDNA replication but suppresses MMS-induced mutagenesis. These results suggest a novel mechanism wherein mutations that lead to hypermutation by DNA base-damaging agents and associate with mitochondrial disease may contribute to previously unexplained phenomena, such as the wide variation of age of disease onset and acquired mitochondrial toxicities.
JF - PLoS genetics
AU - Stumpf, Jeffrey D
AU - Copeland, William C
AD - Mitochondrial DNA Replication Group, Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, NIH, DHHS, Research Triangle Park, North Carolina, United States of America.
Y1 - 2014/10//
PY - 2014
DA - October 2014
SP - 1
VL - 10
IS - 10
KW - DNA, Mitochondrial
KW - 0
KW - Saccharomyces cerevisiae Proteins
KW - Adenosine Triphosphate
KW - 8L70Q75FXE
KW - Methyl Methanesulfonate
KW - AT5C31J09G
KW - DNA Polymerase I
KW - EC 2.7.7.-
KW - DNA polymerase gamma
KW - DNA-Directed DNA Polymerase
KW - EC 2.7.7.7
KW - MIP1 protein, S cerevisiae
KW - Index Medicus
KW - DNA Repair -- genetics
KW - DNA Replication -- genetics
KW - Humans
KW - Point Mutation
KW - Mutagenesis -- genetics
KW - DNA Replication -- drug effects
KW - DNA Repair -- drug effects
KW - Adenosine Triphosphate -- biosynthesis
KW - Sequence Deletion
KW - Saccharomyces cerevisiae
KW - Methyl Methanesulfonate -- pharmacology
KW - Mitochondrial Diseases -- genetics
KW - Mitochondrial Diseases -- metabolism
KW - Saccharomyces cerevisiae Proteins -- genetics
KW - Mitochondrial Diseases -- etiology
KW - DNA Polymerase I -- genetics
KW - DNA-Directed DNA Polymerase -- genetics
KW - DNA, Mitochondrial -- genetics
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1618161204?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PLoS+genetics&rft.atitle=MMS+exposure+promotes+increased+MtDNA+mutagenesis+in+the+presence+of+replication-defective+disease-associated+DNA+polymerase+%CE%B3+variants.&rft.au=Stumpf%2C+Jeffrey+D%3BCopeland%2C+William+C&rft.aulast=Stumpf&rft.aufirst=Jeffrey&rft.date=2014-10-01&rft.volume=10&rft.issue=10&rft.spage=e1004748&rft.isbn=&rft.btitle=&rft.title=PLoS+genetics&rft.issn=1553-7404&rft_id=info:doi/10.1371%2Fjournal.pgen.1004748
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-06-30
N1 - Date created - 2014-10-24
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1371/journal.pgen.1004748
ER -
TY - JOUR
T1 - Lessons from a BACE1 inhibitor trial: off-site but not off base.
AN - 1618140880; 24530026
AB - Alzheimer's disease (AD) is characterized by formation of neuritic plaque primarily composed of a small filamentous protein called amyloid-β peptide (Aβ). The rate-limiting step in the production of Aβ is the processing of Aβ precursor protein (APP) by β-site APP-cleaving enzyme (BACE1). Hence, BACE1 activity plausibly plays a rate-limiting role in the generation of potentially toxic Aβ within brain and the development of AD, thereby making it an interesting drug target. A phase II trial of the promising LY2886721 inhibitor of BACE1 was suspended in June 2013 by Eli Lilly and Co., due to possible liver toxicity. This outcome was apparently a surprise to the study's team, particularly since BACE1 knockout mice and mice treated with the drug did not show such liver toxicity. Lilly proposed that the problem was not due to LY2886721 anti-BACE1 activity. We offer an alternative hypothesis, whereby anti-BACE1 activity may induce apparent hepatotoxicity through inhibiting BACE1's processing of β-galactoside α-2,6-sialyltransferase I (STGal6 I). In knockout mice, paralogues, such as BACE2 or cathepsin D, could partially compensate. Furthermore, the short duration of animal studies and short lifespan of study animals could mask effects that would require several decades to accumulate in humans. Inhibition of hepatic BACE1 activity in middle-aged humans would produce effects not detectable in mice. We present a testable model to explain the off-target effects of LY2886721 and highlight more broadly that so-called off-target drug effects might actually represent off-site effects that are not necessarily off-target. Consideration of this concept in forthcoming drug design, screening, and testing programs may prevent such failures in the future. Copyright © 2014 The Alzheimer's Association. All rights reserved.
JF - Alzheimer's & dementia : the journal of the Alzheimer's Association
AU - Lahiri, Debomoy K
AU - Maloney, Bryan
AU - Long, Justin M
AU - Greig, Nigel H
AD - Laboratory of Molecular Neurogenetics, Department of Psychiatry, Institute of Psychiatric Research, Indiana University School of Medicine, Indianapolis, IN, USA; Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN, USA. Electronic address: dlahiri@iupui.edu. ; Laboratory of Molecular Neurogenetics, Department of Psychiatry, Institute of Psychiatric Research, Indiana University School of Medicine, Indianapolis, IN, USA. ; Laboratory of Translational Gerontology, Intramural Research Program, National Institute of Aging, National Institutes of Health, Baltimore, MD, USA.
Y1 - 2014/10//
PY - 2014
DA - October 2014
SP - S411
EP - S419
VL - 10
IS - 5 Suppl
KW - Heterocyclic Compounds, 2-Ring
KW - 0
KW - N-(3-(2-amino-4a,5,7,7a-tetrahydro-4H-furo(3,4-d)(1,3)thiazin-7a-yl)-4-fluorophenyl)-5-fluoropicolinamide
KW - Nootropic Agents
KW - Picolinic Acids
KW - Protease Inhibitors
KW - Amyloid Precursor Protein Secretases
KW - EC 3.4.-
KW - Aspartic Acid Endopeptidases
KW - EC 3.4.23.-
KW - BACE1 protein, human
KW - EC 3.4.23.46
KW - Bace1 protein, mouse
KW - Index Medicus
KW - Liver damage
KW - ROS
KW - Neuronal death
KW - CNS
KW - Aging
KW - Human studies
KW - Demyelination
KW - Drug trial
KW - Brain disorder
KW - Animal model
KW - Sialylation
KW - Melatonin
KW - Secretase
KW - Dementia
KW - Side effects
KW - Heterocyclic Compounds, 2-Ring -- therapeutic use
KW - Animals
KW - Picolinic Acids -- therapeutic use
KW - Picolinic Acids -- adverse effects
KW - Alzheimer Disease -- drug therapy
KW - Alzheimer Disease -- physiopathology
KW - Brain -- drug effects
KW - Humans
KW - Clinical Trials as Topic
KW - Disease Models, Animal
KW - Heterocyclic Compounds, 2-Ring -- adverse effects
KW - Nootropic Agents -- pharmacology
KW - Nootropic Agents -- adverse effects
KW - Models, Biological
KW - Heterocyclic Compounds, 2-Ring -- pharmacology
KW - Mice, Knockout
KW - Brain -- physiopathology
KW - Liver -- physiopathology
KW - Liver -- drug effects
KW - Nootropic Agents -- therapeutic use
KW - Picolinic Acids -- pharmacology
KW - Protease Inhibitors -- therapeutic use
KW - Protease Inhibitors -- pharmacology
KW - Protease Inhibitors -- adverse effects
KW - Aspartic Acid Endopeptidases -- genetics
KW - Amyloid Precursor Protein Secretases -- antagonists & inhibitors
KW - Aspartic Acid Endopeptidases -- metabolism
KW - Aspartic Acid Endopeptidases -- antagonists & inhibitors
KW - Amyloid Precursor Protein Secretases -- metabolism
KW - Amyloid Precursor Protein Secretases -- genetics
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-07-13
N1 - Date created - 2014-10-24
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
J Neurosci. 2013 May 1;33(18):7856-69 [23637177]
Alzheimers Dement. 2013 Mar;9(2):208-45 [23507120]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.jalz.2013.11.004
ER -
TY - JOUR
T1 - Cross-national comparison of prenatal methamphetamine exposure on infant and early child physical growth: a natural experiment
AN - 1610988995; 4605836
AB - The current study seeks to compare the effects of prenatal methamphetamine exposure (PME) on infant and child physical growth between the USA and New Zealand (NZ). This cross-national comparison provides a unique opportunity to examine the potential impact of services provided to drug using mothers on child health. The longitudinal Infant Development, Environment and Lifestyle study of PME from birth to 36_months was conducted in the USA and NZ. The US cohort included 204 children with PME and 212 non-PME matched comparisons (NPME); the NZ cohort included 108 children with PME and 115 NPME matched comparisons. Latent growth curve models were used to examine effects of PME, country of origin, and the country × PME interaction on growth in length/height and weight. In regard to length/height, PME and country of origin were associated with initial length and growth over time. There was also a significant interaction effect, such that children with PME in the USA were shorter at birth than children with PME in NZ after controlling for other prenatal exposures, infant set, socioeconomic status, and maternal height. In regard to weight, there was only an effect of country of origin. Effects of PME on infant and child growth were shown to differ across countries, with exposed children in NZ faring better than exposed children in the USA. Implications for prevention programs and public policy are discussed. Reprinted by permission of Springer
JF - Prevention science
AU - Abar, Beau
AU - LaGasse, Linda L
AU - Wouldes, Trecia
AU - Derauf, Chris
AU - Newman, Elana
AU - Shah, Rizwan
AU - Smith, Lynne M
AU - Arria, Amelia M
AU - Huestis, Marilyn A
AU - DellaGrotta, Sheri
AU - Dansereau, Lynne M
AU - Wilcox, Tara
AU - Neal, Charles R
AU - Lester, Barry M
AD - Brown University ; University of Auckland ; University of Hawaii ; University of Tulsa ; Harbor-UCLA Medical Center ; University of Maryland School of Public Health ; National Institute on Drug Abuse
Y1 - 2014/10//
PY - 2014
DA - Oct 2014
SP - 767
EP - 776
VL - 15
IS - 5
SN - 1389-4986, 1389-4986
KW - Sociology
KW - Prevention
KW - Socioeconomic status
KW - U.S.A.
KW - Drugs
KW - New Zealand
KW - Child health
KW - Infants
KW - Cross-national analysis
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Prevention+science&rft.atitle=Cross-national+comparison+of+prenatal+methamphetamine+exposure+on+infant+and+early+child+physical+growth%3A+a+natural+experiment&rft.au=Abar%2C+Beau%3BLaGasse%2C+Linda+L%3BWouldes%2C+Trecia%3BDerauf%2C+Chris%3BNewman%2C+Elana%3BShah%2C+Rizwan%3BSmith%2C+Lynne+M%3BArria%2C+Amelia+M%3BHuestis%2C+Marilyn+A%3BDellaGrotta%2C+Sheri%3BDansereau%2C+Lynne+M%3BWilcox%2C+Tara%3BNeal%2C+Charles+R%3BLester%2C+Barry+M&rft.aulast=Abar&rft.aufirst=Beau&rft.date=2014-10-01&rft.volume=15&rft.issue=5&rft.spage=767&rft.isbn=&rft.btitle=&rft.title=Prevention+science&rft.issn=13894986&rft_id=info:doi/10.1007%2Fs11121-013-0431-5
LA - English
DB - International Bibliography of the Social Sciences (IBSS)
N1 - Date revised - 2014-10-14
N1 - Last updated - 2014-10-14
N1 - SubjectsTermNotLitGenreText - 3060 971; 6495 2212; 10072; 2199 5772; 3755; 11988 4011 3974 9390 11932 2328 11935 5837 2360 2688 2449 10404 11936; 286 309; 433 293 14
DO - http://dx.doi.org/10.1007/s11121-013-0431-5
ER -
TY - JOUR
T1 - TRIM28 regulates RNA polymerase II promoter-proximal pausing and pause release.
AN - 1609505644; 25173174
AB - Promoter-proximal pausing of RNA polymerase II (Pol II) is a major checkpoint in transcription. An unbiased search for new human proteins that could regulate paused Pol II at the HSPA1B gene identified TRIM28. In vitro analyses indicated HSF1-dependent attenuation of Pol II pausing upon TRIM28 depletion, whereas in vivo data revealed de novo expression of HSPA1B and other known genes regulated by paused Pol II upon TRIM28 knockdown. These results were supported by genome-wide ChIP-sequencing analyses of Pol II occupancy that revealed a global role for TRIM28 in regulating Pol II pausing and pause release. Furthermore, in vivo and in vitro mechanistic studies suggest that transcription-coupled phosphorylation regulates Pol II pause release by TRIM28. Collectively, our findings identify TRIM28 as a new factor that modulates Pol II pausing and transcriptional elongation at a large number of mammalian genes.
JF - Nature structural & molecular biology
AU - Bunch, Heeyoun
AU - Zheng, Xiaofeng
AU - Burkholder, Adam
AU - Dillon, Simon T
AU - Motola, Shmulik
AU - Birrane, Gabriel
AU - Ebmeier, Christopher C
AU - Levine, Stuart
AU - Fargo, David
AU - Hu, Guang
AU - Taatjes, Dylan J
AU - Calderwood, Stuart K
AD - Department of Radiation Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA. ; 1] Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA. [2]. ; 1] Integrative Bioinformatics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA. [2]. ; 1] Department of Radiation Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA. [2] Genomics and Proteomics Center, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA. ; BioMicro Center, Massachusetts Institute of Technology, Cambridge, Massachusetts, USA. ; 1] Department of Radiation Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA. [2] Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA. ; Department of Chemistry and Biochemistry, University of Colorado, Boulder, Boulder, Colorado, USA. ; Integrative Bioinformatics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA. ; Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA.
Y1 - 2014/10//
PY - 2014
DA - October 2014
SP - 876
EP - 883
VL - 21
IS - 10
KW - DNA-Binding Proteins
KW - 0
KW - HSP70 Heat-Shock Proteins
KW - HSPA1B protein, human
KW - Repressor Proteins
KW - TRIM28 protein, human
KW - Transcription Factors
KW - heat shock transcription factor
KW - ATM protein, human
KW - EC 2.7.11.1
KW - Ataxia Telangiectasia Mutated Proteins
KW - DNA-Activated Protein Kinase
KW - RNA Polymerase II
KW - EC 2.7.7.-
KW - Index Medicus
KW - DNA-Activated Protein Kinase -- antagonists & inhibitors
KW - Transcription Factors -- antagonists & inhibitors
KW - Phosphorylation
KW - HeLa Cells
KW - Humans
KW - HEK293 Cells
KW - DNA-Binding Proteins -- genetics
KW - Transcription, Genetic -- genetics
KW - DNA-Binding Proteins -- antagonists & inhibitors
KW - Cell Line, Tumor
KW - Transcription Factors -- genetics
KW - Ataxia Telangiectasia Mutated Proteins -- antagonists & inhibitors
KW - HSP70 Heat-Shock Proteins -- genetics
KW - HSP70 Heat-Shock Proteins -- biosynthesis
KW - RNA Polymerase II -- genetics
KW - Repressor Proteins -- metabolism
KW - Promoter Regions, Genetic -- genetics
KW - Repressor Proteins -- genetics
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+structural+%26+molecular+biology&rft.atitle=TRIM28+regulates+RNA+polymerase+II+promoter-proximal+pausing+and+pause+release.&rft.au=Bunch%2C+Heeyoun%3BZheng%2C+Xiaofeng%3BBurkholder%2C+Adam%3BDillon%2C+Simon+T%3BMotola%2C+Shmulik%3BBirrane%2C+Gabriel%3BEbmeier%2C+Christopher+C%3BLevine%2C+Stuart%3BFargo%2C+David%3BHu%2C+Guang%3BTaatjes%2C+Dylan+J%3BCalderwood%2C+Stuart+K&rft.aulast=Bunch&rft.aufirst=Heeyoun&rft.date=2014-10-01&rft.volume=21&rft.issue=10&rft.spage=876&rft.isbn=&rft.btitle=&rft.title=Nature+structural+%26+molecular+biology&rft.issn=1545-9985&rft_id=info:doi/10.1038%2Fnsmb.2878
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-01-07
N1 - Date created - 2014-10-08
N1 - Date revised - 2017-01-14
N1 - Genetic sequence - GSE48253; GEO
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1038/nsmb.2878
ER -
TY - JOUR
T1 - The crystal structure of the phosphatidylinositol 4-kinase IIα.
AN - 1586095389; 25168678
AB - Phosphoinositides are a class of phospholipids generated by the action of phosphoinositide kinases with key regulatory functions in eukaryotic cells. Here, we present the atomic structure of phosphatidylinositol 4-kinase type IIα (PI4K IIα), in complex with ATP solved by X-ray crystallography at 2.8 Å resolution. The structure revealed a non-typical kinase fold that could be divided into N- and C-lobes with the ATP binding groove located in between. Surprisingly, a second ATP was found in a lateral hydrophobic pocket of the C-lobe. Molecular simulations and mutagenesis analysis revealed the membrane binding mode and the putative function of the hydrophobic pocket. Taken together, our results suggest a mechanism of PI4K IIα recruitment, regulation, and function at the membrane.
© 2014 The Authors.
JF - EMBO reports
AU - Baumlova, Adriana
AU - Chalupska, Dominika
AU - Róźycki, Bartosz
AU - Jovic, Marko
AU - Wisniewski, Eva
AU - Klima, Martin
AU - Dubankova, Anna
AU - Kloer, Daniel P
AU - Nencka, Radim
AU - Balla, Tamas
AU - Boura, Evzen
AD - Institute of Organic Chemistry and Biochemistry AS CR, Prague, Czech Republic. ; Institute of Physics Polish Academy of Sciences, Warsaw, Poland. ; Section on Molecular Signal Transduction, Program for Developmental Neuroscience, NICHD NIH, Bethesda, MD, USA. ; Syngenta Jealott's Hill Internation Research Centre, Bracknell, UK. ; Institute of Organic Chemistry and Biochemistry AS CR, Prague, Czech Republic boura@uochb.cas.cz.
Y1 - 2014/10//
PY - 2014
DA - October 2014
SP - 1085
EP - 1092
VL - 15
IS - 10
KW - Minor Histocompatibility Antigens
KW - 0
KW - Phosphatidylinositols
KW - Inositol
KW - 4L6452S749
KW - Phosphotransferases (Alcohol Group Acceptor)
KW - EC 2.7.1.-
KW - phosphatidylinositol phosphate 4-kinase
KW - EC 2.7.1.67
KW - Index Medicus
KW - kinase
KW - Monte Carlo simulations
KW - membrane
KW - crystal structure
KW - phosphatidyl inositol
KW - Membranes -- chemistry
KW - Humans
KW - Monte Carlo Method
KW - Inositol -- chemistry
KW - Protein Binding
KW - Signal Transduction
KW - Binding Sites
KW - Phosphotransferases (Alcohol Group Acceptor) -- chemistry
KW - Phosphatidylinositols -- chemistry
KW - Phosphatidylinositols -- metabolism
KW - Crystallography, X-Ray
KW - Phosphotransferases (Alcohol Group Acceptor) -- ultrastructure
KW - Phosphotransferases (Alcohol Group Acceptor) -- metabolism
KW - Protein Conformation
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=EMBO+reports&rft.atitle=The+crystal+structure+of+the+phosphatidylinositol+4-kinase+II%CE%B1.&rft.au=Baumlova%2C+Adriana%3BChalupska%2C+Dominika%3BR%C3%B3%C5%BAycki%2C+Bartosz%3BJovic%2C+Marko%3BWisniewski%2C+Eva%3BKlima%2C+Martin%3BDubankova%2C+Anna%3BKloer%2C+Daniel+P%3BNencka%2C+Radim%3BBalla%2C+Tamas%3BBoura%2C+Evzen&rft.aulast=Baumlova&rft.aufirst=Adriana&rft.date=2014-10-01&rft.volume=15&rft.issue=10&rft.spage=1085&rft.isbn=&rft.btitle=&rft.title=EMBO+reports&rft.issn=1469-3178&rft_id=info:doi/10.15252%2Fembr.201438841
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-06-11
N1 - Date created - 2014-10-02
N1 - Date revised - 2017-01-14
N1 - Genetic sequence - 4PLA; PDB
N1 - SuppNotes - Cited By:
J Biol Chem. 2001 May 18;276(20):16635-40 [11279162]
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Mol Biol Cell. 2007 Jul;18(7):2646-55 [17494868]
Biochem J. 2008 Jan 15;409(2):501-9 [17927563]
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Mol Biol Cell. 2008 Apr;19(4):1415-26 [18256276]
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Subcell Biochem. 2012;59:255-70 [22374093]
Subcell Biochem. 2012;58:1-24 [22403072]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.15252/embr.201438841
ER -
TY - JOUR
T1 - Smoothness of in vivo spectral baseline determined by mean-square error
AN - 1566849715; 20749130
AB - Purpose A nonparametric smooth line is usually added to the spectral model to account for background signals in vivo magnetic resonance spectroscopy (MRS). The assumed smoothness of the baseline significantly influences quantitative spectral fitting. In this paper, a method is proposed to minimize baseline influences on the estimated spectral parameters. Methods The nonparametric baseline function with a given smoothness was treated as a function of spectral parameters. Its uncertainty was measured by root-mean-square error (RMSE). The proposed method was demonstrated with a simulated spectrum and in vivo spectra of both short echo time and averaged echo times. The estimated in vivo baselines were compared with the metabolite-nulled spectra and the LCModel-estimated baselines. The accuracies of estimated baseline and metabolite concentrations were further verified via cross-validation. Results An optimal smoothness condition was found that led to the minimal baseline RMSE. In this condition, the best fit was balanced against minimal baseline influences on metabolite concentration estimates. Conclusion Baseline RMSE can be used to indicate estimated baseline uncertainties and serve as the criterion for determining the baseline smoothness of in vivo MRS. Magn Reson Med 72:913-922, 2014. copyright 2013 Wiley Periodicals, Inc.
JF - Magnetic Resonance in Medicine
AU - Zhang, Yan
AU - Shen, Jun
AD - MR Spectroscopy Core Facility, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland, USA.
Y1 - 2014/10//
PY - 2014
DA - Oct 2014
SP - 913
EP - 922
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 72
IS - 4
SN - 0740-3194, 0740-3194
KW - Biotechnology and Bioengineering Abstracts
KW - Magnetic resonance spectroscopy
KW - Metabolites
KW - N.M.R.
KW - Models
KW - W 30910:Imaging
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Magnetic+Resonance+in+Medicine&rft.atitle=Smoothness+of+in+vivo+spectral+baseline+determined+by+mean-square+error&rft.au=Zhang%2C+Yan%3BShen%2C+Jun&rft.aulast=Zhang&rft.aufirst=Yan&rft.date=2014-10-01&rft.volume=72&rft.issue=4&rft.spage=913&rft.isbn=&rft.btitle=&rft.title=Magnetic+Resonance+in+Medicine&rft.issn=07403194&rft_id=info:doi/10.1002%2Fmrm.25013
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-09-01
N1 - Last updated - 2014-10-15
N1 - SubjectsTermNotLitGenreText - Magnetic resonance spectroscopy; N.M.R.; Metabolites; Models
DO - http://dx.doi.org/10.1002/mrm.25013
ER -
TY - JOUR
T1 - N-acetyl-aspartyl-glutamate detection in the human brain at 7 Tesla by echo time optimization and improved Wiener filtering
AN - 1566845802; 20749125
AB - Purpose To report enhanced signal detection for measuring N-acetyl-aspartyl-glutamate (NAAG) in the human brain at 7 Tesla by echo time (TE) -optimized point-resolved spectroscopy (PRESS) and improved Wiener filtering. Methods Using a highly efficient in-house developed numerical simulation program, a PRESS sequence with (TE sub(1), TE sub(2))=(26, 72) ms was found to maximize the NAAG signals relative to the overlapping Glu signals. A new Wiener filtering water reference deconvolution method was developed to reduce broadening and distortions of metabolite peaks caused by B sub(0) inhomogeneity and eddy currents. Results Monte Carlo simulation results demonstrated that the new Wiener filtering method offered higher spectral resolution, reduced spectral artifacts, and higher accuracy in NAAG quantification compared with the original Wiener filtering method. In vivo spectra and point spread functions of signal distortion confirmed that the new Wiener filtering method lead to improved spectral resolution and reduced spectral artifacts. Conclusion TE-optimized PRESS in combination with a new Wiener filtering method made it possible to fully use both the NAAG singlet signal at 2.05 ppm and the NAAG multiplet signal at 2.18 ppm in the quantification of NAAG. A more accurate characterization of lineshape distortion for Wiener filtering needs B sub(0) field maps and segmented anatomical images to exclude contribution from cerebral spinal fluid. Magn Reson Med 72:903-912, 2014. copyright 2013 Wiley Periodicals, Inc.
JF - Magnetic Resonance in Medicine
AU - An, Li
AU - Li, Shizhe
AU - Wood, Emily T
AU - Reich, Daniel S
AU - Shen, Jun
AD - National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland, USA.
Y1 - 2014/10//
PY - 2014
DA - Oct 2014
SP - 903
EP - 912
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 72
IS - 4
SN - 0740-3194, 0740-3194
KW - Biotechnology and Bioengineering Abstracts
KW - Monte Carlo simulation
KW - N-Acetylaspartylglutamic acid
KW - Cerebrospinal fluid
KW - Mathematical models
KW - Brain
KW - N.M.R.
KW - Metabolites
KW - Maps
KW - Spectroscopy
KW - W 30910:Imaging
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Magnetic+Resonance+in+Medicine&rft.atitle=N-acetyl-aspartyl-glutamate+detection+in+the+human+brain+at+7+Tesla+by+echo+time+optimization+and+improved+Wiener+filtering&rft.au=An%2C+Li%3BLi%2C+Shizhe%3BWood%2C+Emily+T%3BReich%2C+Daniel+S%3BShen%2C+Jun&rft.aulast=An&rft.aufirst=Li&rft.date=2014-10-01&rft.volume=72&rft.issue=4&rft.spage=903&rft.isbn=&rft.btitle=&rft.title=Magnetic+Resonance+in+Medicine&rft.issn=07403194&rft_id=info:doi/10.1002%2Fmrm.25007
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-09-01
N1 - Last updated - 2014-10-15
N1 - SubjectsTermNotLitGenreText - Monte Carlo simulation; Cerebrospinal fluid; N-Acetylaspartylglutamic acid; Mathematical models; Brain; Metabolites; N.M.R.; Spectroscopy; Maps
DO - http://dx.doi.org/10.1002/mrm.25007
ER -
TY - JOUR
T1 - NIH Workshop on Clinical Translation of Molecular Imaging Probes and Technology-Meeting Report
AN - 1566844270; 20740778
AB - A workshop on "Clinical Translation of Molecular Imaging Probes and Technology" was held August 2, 2013 in Bethesda, Maryland, organized and supported by the National Institute of Biomedical Imaging and Bioengineering (NIBIB). This workshop brought together researchers, clinicians, representatives from pharmaceutical companies, molecular probe developers, and regulatory science experts. Attendees met to talk over current challenges in the discovery, validation, and translation of molecular imaging (MI) probes for key clinical applications. Participants also discussed potential strategies to address these challenges. The workshop consisted of 4 sessions, with 14 presentations and 2 panel discussions. Topics of discussion included (1) challenges and opportunities for clinical research and patient care, (2) advances in molecular probe design, (3) current approaches used by industry and pharmaceutical companies, and (4) clinical translation of MI probes. In the presentations and discussions, there were general agreement that while the barriers for validation and translation of MI probes remain high, there are pressing clinical needs and development opportunities for targets in cardiovascular, cancer, endocrine, neurological, and inflammatory diseases. The strengths of different imaging modalities, and the synergy of multimodality imaging, were highlighted. Participants also underscored the continuing need for close interactions and collaborations between academic and industrial partners, and federal agencies in the imaging probe development process.
JF - Molecular Imaging and Biology
AU - Liu, Christina H
AU - Sastre, Antonio
AU - Conroy, Richard
AU - Seto, Belinda
AU - Pettigrew, Roderic I
AD - National Institute of Biomedical Imaging and Bioengineering, 6707 Democracy Blvd., Suite 200, Bethesda, MD, 20892, USA, Christina.liu@nih.gov
Y1 - 2014/10//
PY - 2014
DA - Oct 2014
SP - 595
EP - 604
PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL - 16
IS - 5
SN - 1536-1632, 1536-1632
KW - Biotechnology and Bioengineering Abstracts
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-09-01
N1 - Number of references - 95
N1 - Last updated - 2014-10-02
DO - http://dx.doi.org/10.1007/s11307-014-0746-z
ER -
TY - JOUR
T1 - The evidence base for the use of internal dosimetry in the clinical practice of molecular radiotherapy
AN - 1566838182; 20719981
AB - Molecular radiotherapy (MRT) has demonstrated unique therapeutic advantages in the treatment of an increasing number of cancers. As with other treatment modalities, there is related toxicity to a number of organs at risk. Despite the large number of clinical trials over the past several decades, considerable uncertainties still remain regarding the optimization of this therapeutic approach and one of the vital issues to be answered is whether an absorbed radiation dose-response exists that could be used to guide personalized treatment. There are only limited and sporadic data investigating MRT dosimetry. The determination of dose-effect relationships for MRT has yet to be the explicit aim of a clinical trial. The aim of this article was to collate and discuss the available evidence for an absorbed radiation dose-effect relationships in MRT through a review of published data. Based on a PubMed search, 92 papers were found. Out of 79 studies investigating dosimetry, an absorbed dose-effect correlation was found in 48. The application of radiobiological modelling to clinical data is of increasing importance and the limited published data on absorbed dose-effect relationships based on these models are also reviewed. Based on National Cancer Institute guideline definition, the studies had a moderate or low rate of clinical relevance due to the limited number of studies investigating overall survival and absorbed dose. Nevertheless, the evidence strongly implies a correlation between the absorbed doses delivered and the response and toxicity, indicating that dosimetry-based personalized treatments would improve outcome and increase survival.
JF - European Journal of Nuclear Medicine and Molecular Imaging
AU - Strigari, Lidia
AU - Konijnenberg, Mark
AU - Chiesa, Carlo
AU - Bardies, Manuel
AU - Du, Yong
AU - Gleisner, Katarina Sjogreen
AU - Lassmann, Michael
AU - Flux, Glenn
AD - Laboratory of Medical Physics and Expert Systems, Regina Elena National Cancer Institute, via E. Chianesi 53, 00144, Rome, Italy, strigari@ifo.it
Y1 - 2014/10//
PY - 2014
DA - Oct 2014
SP - 1976
EP - 1988
PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL - 41
IS - 10
SN - 1619-7070, 1619-7070
KW - Biotechnology and Bioengineering Abstracts
KW - Data processing
KW - Radiation
KW - Reviews
KW - Dosimetry
KW - Survival
KW - Radiotherapy
KW - Nuclear medicine
KW - Toxicity
KW - Clinical trials
KW - Cancer
KW - Models
KW - W 30910:Imaging
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-09-01
N1 - Number of references - 75
N1 - Last updated - 2014-10-02
N1 - SubjectsTermNotLitGenreText - Data processing; Radiation; Reviews; Dosimetry; Nuclear medicine; Radiotherapy; Survival; Toxicity; Clinical trials; Cancer; Models
DO - http://dx.doi.org/10.1007/s00259-014-2824-5
ER -
TY - JOUR
T1 - [ super(18)F]Fluciclatide in the in vivo evaluation of human melanoma and renal tumors expressing alpha sub(v) beta sub(3) and alpha sub(v) beta sub(5) integrins
AN - 1566837864; 20719972
AB - Purpose: [ super(18)F]Fluciclatide is an integrin-targeted PET radiopharmaceutical. alpha sub(v) beta sub(3) and alpha sub(v) beta sub(5) are upregulated in tumor angiogenesis as well as on some tumor cell surfaces. Our aim was to use [ super(18)F]fluciclatide (formerly known as [ super(18)F]AH111585) for PET imaging of angiogenesis in melanoma and renal tumors and compare with tumor integrin expression. Methods: Eighteen evaluable patients with solid tumors greater than or equal to 2.0 cm underwent [ super(18)F]fluciclatide PET/CT. All patients underwent surgery and tumor tissue samples were obtained. Immunohistochemical (IHC) staining with mouse monoclonal antibodies and diaminobenzidine (DAB) was applied to snap-frozen tumor specimens, and additional IHC was done on formalin-fixed paraffin-embedded samples. DAB optical density (OD) data from digitized whole-tissue sections were compared with PET SUV sub(80% max), and Patlak influx rate constant (K sub(i)) data, tumor by tumor. Results: Tumors from all 18 patients demonstrated measurable [ super(18)F]fluciclatide uptake. At the final dynamic time-point (55 min after injection), renal malignancies (in 11 patients) demonstrated an average SUV sub(80% max) of 6.4 plus or minus 2.0 (range 3.8 - 10.0), while the average SUV sub(80% max) for metastatic melanoma lesions (in 6 patients) was 3.0 plus or minus 2.0 (range 0.7 - 6.5). There was a statistically significant difference in [ super(18)F]fluciclatide uptake between chromophobe and nonchromophobe renal cell carcinoma (RCCs, with SUV sub(80% max) of 8.2 plus or minus 1.8 and 5.4 plus or minus 1.4 (P=0.020) and tumor-to-normal kidney (T/N) ratios of 1.5 plus or minus 0.4 and 0.9 plus or minus 0.2, respectively (P=0.029). The highest Pearson's correlation coefficients were obtained when comparing Patlak K sub(i) and alpha sub(v) beta sub(5) OD when segregating the patient population between melanoma and RCC (r=0.83 for K sub(i) vs. melanoma and r=0.91 for K sub(i) vs. RCC). SUV sub(80% max) showed a moderate correlation with alpha sub(v) beta sub(5) and alpha sub(v) beta sub(3) OD. Conclusion: [ super(18)F]Fluciclatide PET imaging was well tolerated and demonstrated favorable characteristics for imaging alpha sub(v) beta sub(3) and alpha sub(v) beta sub(5) expression in melanoma and RCC. Higher uptake was observed in chromophobe than in nonchromophobe RCC. [ super(18)F]Fluciclatide may be a useful radiotracer to improve knowledge of integrin expression.
JF - European Journal of Nuclear Medicine and Molecular Imaging
AU - Mena, Esther
AU - Owenius, Rikard
AU - Turkbey, Baris
AU - Sherry, Richard
AU - Bratslavsky, Gennady
AU - Macholl, Sven
AU - Miller, Matthew P
AU - Somer, Ed J
AU - Lindenberg, Liza
AU - Adler, Stephen
AU - Shih, Joanna
AU - Choyke, Peter
AU - Kurdziel, Karen
AD - Molecular Imaging Program, NCI, NIH, Bethesda, MD, USA, liza.lindenberg@nih.gov
Y1 - 2014/10//
PY - 2014
DA - Oct 2014
SP - 1879
EP - 1888
PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL - 41
IS - 10
SN - 1619-7070, 1619-7070
KW - Biotechnology and Bioengineering Abstracts
KW - Data processing
KW - Monoclonal antibodies
KW - Solid tumors
KW - Statistical analysis
KW - Angiogenesis
KW - Tumors
KW - Tumor cells
KW - Melanoma
KW - Metastases
KW - Malignancy
KW - renal cell carcinoma
KW - Integrins
KW - Surgery
KW - Optical density
KW - Computed tomography
KW - Radioisotopes
KW - Kidney
KW - Pharmaceuticals
KW - Nuclear medicine
KW - W 30910:Imaging
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+Journal+of+Nuclear+Medicine+and+Molecular+Imaging&rft.atitle=%5B+super%2818%29F%5DFluciclatide+in+the+in+vivo+evaluation+of+human+melanoma+and+renal+tumors+expressing+alpha+sub%28v%29+beta+sub%283%29+and+alpha+sub%28v%29+beta+sub%285%29+integrins&rft.au=Mena%2C+Esther%3BOwenius%2C+Rikard%3BTurkbey%2C+Baris%3BSherry%2C+Richard%3BBratslavsky%2C+Gennady%3BMacholl%2C+Sven%3BMiller%2C+Matthew+P%3BSomer%2C+Ed+J%3BLindenberg%2C+Liza%3BAdler%2C+Stephen%3BShih%2C+Joanna%3BChoyke%2C+Peter%3BKurdziel%2C+Karen&rft.aulast=Mena&rft.aufirst=Esther&rft.date=2014-10-01&rft.volume=41&rft.issue=10&rft.spage=1879&rft.isbn=&rft.btitle=&rft.title=European+Journal+of+Nuclear+Medicine+and+Molecular+Imaging&rft.issn=16197070&rft_id=info:doi/10.1007%2Fs00259-014-2791-x
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-09-01
N1 - Number of references - 36
N1 - Last updated - 2014-10-02
N1 - SubjectsTermNotLitGenreText - Data processing; Solid tumors; Monoclonal antibodies; Angiogenesis; Statistical analysis; Tumors; Tumor cells; Melanoma; Metastases; Malignancy; renal cell carcinoma; Integrins; Surgery; Computed tomography; Optical density; Kidney; Radioisotopes; Nuclear medicine; Pharmaceuticals
DO - http://dx.doi.org/10.1007/s00259-014-2791-x
ER -
TY - JOUR
T1 - Value of super(18)F-FDG uptake on PET/CT and CEA level to predict epidermal growth factor receptor mutations in pulmonary adenocarcinoma
AN - 1566828838; 20719976
AB - Purpose: The identification of the mutation status of the epidermal growth factor receptor (EGFR) is important for the optimization of treatment in patients with pulmonary adenocarcinoma. The acquisition of adequate tissues for EGFR mutational analysis is sometimes not feasible, especially in advanced-stage patients. The aim of this study was to predict EGFR mutation status in patients with pulmonary adenocarcinoma based on super(18)F-fluorodeoxyglucose (FDG) uptake and imaging features in positron emission tomography/computed tomography (PET/CT), as well as on the serum carcinoembryonic antigen (CEA) level. Methods: We retrospectively reviewed 132 pulmonary adenocarcinoma patients who underwent EGFR mutation testing, pretreatment FDG PET/CT and serum CEA analysis. The associations between EGFR mutations and patient characteristics, maximal standard uptake value (SUVmax) of primary tumors, serum CEA level and CT imaging features were analyzed. Receiver-operating characteristic (ROC) curve analysis was performed to quantify the predictive value of these factors. Results: EGFR mutations were identified in 69 patients (52.2 %). Patients with SUVmax greater than or equal to 6 (p=0.002) and CEA level greater than or equal to 5 (p=0.013) were more likely to have EGFR mutations. The CT characteristics of larger tumors ( greater than or equal to 3 cm) (p=0.023) and tumors with a nonspiculated margin (p=0.026) were also associated with EGFR mutations. Multivariate analysis showed that higher SUVmax and CEA level, never smoking and a nonspiculated tumor margin were the most significant predictors of EGFR mutation. The combined use of these four criteria yielded a higher area under the ROC curve (0.82), suggesting a good discrimination. Conclusion: The combined evaluation of FDG uptake, CEA level, smoking status and tumor margins may be helpful in predicting EGFR mutation status in patients with pulmonary adenocarcinoma, especially when the tumor sample is inadequate for genetic analysis or genetic testing is not available. Further large-scale prospective studies are needed to validate these results.
JF - European Journal of Nuclear Medicine and Molecular Imaging
AU - Ko, Kai-Hsiung
AU - Hsu, Hsian-He
AU - Huang, Tsai-Wang
AU - Gao, Hong-Wei
AU - Shen, Daniel HY
AU - Chang, Wei-Chou
AU - Hsu, Yi-Chih
AU - Chang, Tsun-Hou
AU - Chu, Chi-Ming
AU - Ho, Ching-Liang
AU - Chang, Hung
AD - Department of Radiology, Tri-Service General Hospital and National Defense Medical Center, 325, Section 2, Cheng-Gong Road, Nei-Hu, Taipei 114, Taiwan, Republic of China, hsianhe@yahoo.com.tw
Y1 - 2014/10//
PY - 2014
DA - Oct 2014
SP - 1889
EP - 1897
PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL - 41
IS - 10
SN - 1619-7070, 1619-7070
KW - Biotechnology and Bioengineering Abstracts
KW - Genetic analysis
KW - Carcinoembryonic antigen
KW - Epidermal growth factor receptors
KW - Tumors
KW - Smoking
KW - Multivariate analysis
KW - Lung
KW - Computed tomography
KW - Positron emission tomography
KW - Genetic screening
KW - Nuclear medicine
KW - Adenocarcinoma
KW - Mutation
KW - W 30910:Imaging
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+Journal+of+Nuclear+Medicine+and+Molecular+Imaging&rft.atitle=Value+of+super%2818%29F-FDG+uptake+on+PET%2FCT+and+CEA+level+to+predict+epidermal+growth+factor+receptor+mutations+in+pulmonary+adenocarcinoma&rft.au=Ko%2C+Kai-Hsiung%3BHsu%2C+Hsian-He%3BHuang%2C+Tsai-Wang%3BGao%2C+Hong-Wei%3BShen%2C+Daniel+HY%3BChang%2C+Wei-Chou%3BHsu%2C+Yi-Chih%3BChang%2C+Tsun-Hou%3BChu%2C+Chi-Ming%3BHo%2C+Ching-Liang%3BChang%2C+Hung&rft.aulast=Ko&rft.aufirst=Kai-Hsiung&rft.date=2014-10-01&rft.volume=41&rft.issue=10&rft.spage=1889&rft.isbn=&rft.btitle=&rft.title=European+Journal+of+Nuclear+Medicine+and+Molecular+Imaging&rft.issn=16197070&rft_id=info:doi/10.1007%2Fs00259-014-2802-y
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-09-01
N1 - Number of references - 30
N1 - Last updated - 2014-10-02
N1 - SubjectsTermNotLitGenreText - Carcinoembryonic antigen; Genetic analysis; Epidermal growth factor receptors; Tumors; Smoking; Lung; Multivariate analysis; Computed tomography; Positron emission tomography; Nuclear medicine; Genetic screening; Adenocarcinoma; Mutation
DO - http://dx.doi.org/10.1007/s00259-014-2802-y
ER -
TY - JOUR
T1 - N-methylnicotinamide and nicotinamide N-methyltransferase are associated with microRNA-1291-altered pancreatic carcinoma cell metabolome and suppressed tumorigenesis.
AN - 1566824134; 25115443
AB - The cell metabolome comprises abundant information that may be predictive of cell functions in response to epigenetic or genetic changes at different stages of cell proliferation and metastasis. An unbiased ultra-performance liquid chromatography-mass spectrometry-based metabolomics study revealed a significantly altered metabolome for human pancreatic carcinoma PANC-1 cells with gain-of-function non-coding microRNA-1291 (miR-1291), which led to a lower migration and invasion capacity as well as suppressed tumorigenesis in a xenograft tumor mouse model. A number of metabolites, including N-methylnicotinamide, involved in nicotinamide metabolism, and l-carnitine, isobutyryl-carnitine and isovaleryl-carnitine, involved in fatty acid metabolism, were elevated in miR-1291-expressing PANC-1. Notably, N-methylnicotinamide was elevated to the greatest extent, and this was associated with a sharp increase in nicotinamide N-methyltransferase (NNMT) mRNA level in miR-1291-expressing PANC-1 cells. In addition, expression of NNMT mRNA was inversely correlated with pancreatic tumor size in the xenograft mouse model. These results indicate that miR-1291-altered PANC-1 cell function is associated with the increase in N-methylnicotinamide level and NNMT expression, and in turn NNMT may be indicative of the extent of pancreatic carcinogenesis.
Published by Oxford University Press 2014.
JF - Carcinogenesis
AU - Bi, Hui-Chang
AU - Pan, Yu-Zhuo
AU - Qiu, Jing-Xin
AU - Krausz, Kristopher W
AU - Li, Fei
AU - Johnson, Caroline H
AU - Jiang, Chang-Tao
AU - Gonzalez, Frank J
AU - Yu, Ai-Ming
AD - School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China, Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. ; Department of Pharmaceutical Sciences, SUNY-Buffalo, Buffalo, NY 14214, USA, Department of Biochemistry & Molecular Medicine, UC Davis Medical Center, Sacramento, CA 95817, USA and. ; Department of Pathology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA. ; Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. ; School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China. ; Department of Pharmaceutical Sciences, SUNY-Buffalo, Buffalo, NY 14214, USA, Department of Biochemistry & Molecular Medicine, UC Davis Medical Center, Sacramento, CA 95817, USA and aimyu@ucdavis.edu.
Y1 - 2014/10//
PY - 2014
DA - October 2014
SP - 2264
EP - 2272
VL - 35
IS - 10
KW - Biomarkers, Tumor
KW - 0
KW - MIRN1291 microRNA, human
KW - MicroRNAs
KW - Niacinamide
KW - 25X51I8RD4
KW - NNMT protein, human
KW - EC 2.1.1.1
KW - Nicotinamide N-Methyltransferase
KW - N-methylnicotinamide
KW - X3I82S5L8I
KW - Index Medicus
KW - Cell Movement
KW - Animals
KW - Humans
KW - Aged
KW - Mice, Nude
KW - Mice
KW - Cell Line, Tumor
KW - Biomarkers, Tumor -- metabolism
KW - Gene Expression Regulation, Neoplastic
KW - Metabolome
KW - Aged, 80 and over
KW - Adult
KW - Xenograft Model Antitumor Assays
KW - Middle Aged
KW - Female
KW - Male
KW - Nicotinamide N-Methyltransferase -- genetics
KW - Pancreatic Neoplasms -- pathology
KW - Pancreatic Neoplasms -- mortality
KW - Pancreatic Neoplasms -- metabolism
KW - MicroRNAs -- genetics
KW - Nicotinamide N-Methyltransferase -- metabolism
KW - Niacinamide -- analogs & derivatives
KW - Pancreatic Neoplasms -- genetics
KW - Niacinamide -- metabolism
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=N-methylnicotinamide+and+nicotinamide+N-methyltransferase+are+associated+with+microRNA-1291-altered+pancreatic+carcinoma+cell+metabolome+and+suppressed+tumorigenesis.&rft.au=Bi%2C+Hui-Chang%3BPan%2C+Yu-Zhuo%3BQiu%2C+Jing-Xin%3BKrausz%2C+Kristopher+W%3BLi%2C+Fei%3BJohnson%2C+Caroline+H%3BJiang%2C+Chang-Tao%3BGonzalez%2C+Frank+J%3BYu%2C+Ai-Ming&rft.aulast=Bi&rft.aufirst=Hui-Chang&rft.date=2014-10-01&rft.volume=35&rft.issue=10&rft.spage=2264&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgu174
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-05-11
N1 - Date created - 2014-09-30
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/carcin/bgu174
ER -
TY - JOUR
T1 - Household air pollution and lung cancer in China: a review of studies in Xuanwei.
AN - 1566822185; 25223911
AB - Over half of the world's population is exposed to household air pollution from the burning of solid fuels at home. Household air pollution from solid fuel use is a leading risk factor for global disease and remains a major public health problem, especially in low- and mid-income countries. This is a particularly serious problem in China, where many people in rural areas still use coal for household heating and cooking. This review focuses on several decades of research carried out in Xuanwei County, Yunnan Province, where household coal use is a major source of household air pollution and where studies have linked household air pollution exposure to high rates of lung cancer. We conducted a series of case-control and cohort studies in Xuanwei to characterize the lung cancer risk in this population and the factors associated with it. We found lung cancer risk to vary substantially between different coal types, with a higher risk associated with smoky (i.e., bituminous) coal use compared to smokeless (i.e., anthracite) coal use. The installation of a chimney in homes resulted in a substantial reduction in lung cancer incidence and mortality. Overall, our research underscores the need among existing coal users to improve ventilation, use the least toxic fuel, and eventually move toward the use of cleaner fuels, such as gas and electricity.
JF - Chinese journal of cancer
AU - Seow, Wei Jie
AU - Hu, Wei
AU - Vermeulen, Roel
AU - Hosgood Iii, H Dean
AU - Downward, George S
AU - Chapman, Robert S
AU - He, Xingzhou
AU - Bassig, Bryan A
AU - Kim, Christopher
AU - Wen, Cuiju
AU - Rothman, Nathaniel
AU - Lan, Qing
AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD 20850, USA. weijie.seow2@nih.gov.
Y1 - 2014/10//
PY - 2014
DA - October 2014
SP - 471
EP - 475
VL - 33
IS - 10
SN - 1000-467X, 1000-467X
KW - Coal
KW - 0
KW - Fossil Fuels
KW - Smoke
KW - Index Medicus
KW - Smoking
KW - Heating
KW - Risk Factors
KW - Humans
KW - Cooking
KW - Cohort Studies
KW - Incidence
KW - China
KW - Smoke -- adverse effects
KW - Air Pollution, Indoor -- adverse effects
KW - Lung Neoplasms -- etiology
KW - Coal -- adverse effects
KW - Coal -- classification
KW - Lung Neoplasms -- mortality
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chinese+journal+of+cancer&rft.atitle=Household+air+pollution+and+lung+cancer+in+China%3A+a+review+of+studies+in+Xuanwei.&rft.au=Seow%2C+Wei+Jie%3BHu%2C+Wei%3BVermeulen%2C+Roel%3BHosgood+Iii%2C+H+Dean%3BDownward%2C+George+S%3BChapman%2C+Robert+S%3BHe%2C+Xingzhou%3BBassig%2C+Bryan+A%3BKim%2C+Christopher%3BWen%2C+Cuiju%3BRothman%2C+Nathaniel%3BLan%2C+Qing&rft.aulast=Seow&rft.aufirst=Wei&rft.date=2014-10-01&rft.volume=33&rft.issue=10&rft.spage=471&rft.isbn=&rft.btitle=&rft.title=Chinese+journal+of+cancer&rft.issn=1000467X&rft_id=info:doi/10.5732%2Fcjc.014.10132
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-09-01
N1 - Date created - 2014-09-30
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Cancer Epidemiol Biomarkers Prev. 2000 Jun;9(6):605-8 [10868696]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.5732/cjc.014.10132
ER -
TY - JOUR
T1 - Assay of lapatinib in murine models of cigarette smoke carcinogenesis.
AN - 1566821174; 25053627
AB - Lapatinib, a dual tyrosine kinase inhibitor targeting the epidermal growth factor receptor (EGFR) and human epidermal growth factor receptor 2 (HER-2), is prescribed for the treatment of patients with metastatic breast cancer overexpressing HER-2. Involvement of this drug in pulmonary carcinogenesis has been poorly investigated. We used murine models suitable to evaluate cigarette smoke-related molecular and histopathological alterations. A total of 481 Swiss H mice were used. The mice were exposed to mainstream cigarette smoke (MCS) during the first four months of life. After 10 weeks, MCS caused an elevation of bulky DNA adducts, oxidative DNA damage and an extensive downregulation of microRNAs in lung. After four months, an increase in micronucleus frequency was observed in peripheral blood erythrocytes. After 7.5 months, histopathological alterations were detected in the lung, also including benign tumors and malignant tumors, and in the urinary tract. A subchronic toxicity study assessed the non-toxic doses of lapatinib, administered daily with the diet after weaning. After 10 weeks, lapatinib significantly attenuated the MCS-related nucleotide changes and upregulated several low-intensity microRNAs in lung. The drug poorly affected the MCS systemic genotoxicity and had modest protective effects on MCS-induced preneoplastic lesions in lung and kidney, when administered under conditions that temporarily mimicked interventions either in current smokers or ex-smokers. On the other hand, it caused some toxicity to the liver. Thus, on the whole, lapatinib appears to have a low impact in the smoke-related lung carcinogenesis models used, especially in terms of tumorigenic response. © The Author 2014. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.
JF - Carcinogenesis
AU - Balansky, Roumen
AU - Izzotti, Alberto
AU - D'Agostini, Francesco
AU - Longobardi, Mariagrazia
AU - Micale, Rosanna T
AU - La Maestra, Sebastiano
AU - Camoirano, Anna
AU - Ganchev, Gancho
AU - Iltcheva, Marietta
AU - Steele, Vernon E
AU - De Flora, Silvio
AD - Department of Health Sciences, University of Genoa, Via A. Pastore 1, 16132 Genoa, Italy, National Center of Oncology, Sofia-1756, Bulgaria. ; Department of Health Sciences, University of Genoa, Via A. Pastore 1, 16132 Genoa, Italy, IRCCS AOU San Martino - IST, 16132 Genoa, Italy and. ; Department of Health Sciences, University of Genoa, Via A. Pastore 1, 16132 Genoa, Italy. ; National Center of Oncology, Sofia-1756, Bulgaria. ; Division of Cancer Prevention, National Cancer Institute, Rockville, MD 20892, USA. ; Department of Health Sciences, University of Genoa, Via A. Pastore 1, 16132 Genoa, Italy, sdf@unige.it.
Y1 - 2014/10//
PY - 2014
DA - October 2014
SP - 2300
EP - 2307
VL - 35
IS - 10
KW - Antineoplastic Agents
KW - 0
KW - DNA Adducts
KW - MicroRNAs
KW - Protein Kinase Inhibitors
KW - Quinazolines
KW - Tobacco Smoke Pollution
KW - lapatinib
KW - 0VUA21238F
KW - Index Medicus
KW - Erythrocytes -- drug effects
KW - Animals
KW - Toxicity Tests, Subchronic
KW - Protein Kinase Inhibitors -- pharmacology
KW - Body Weight -- drug effects
KW - Disease Models, Animal
KW - Mice
KW - Gene Expression Regulation -- drug effects
KW - DNA Damage -- drug effects
KW - Lung Neoplasms -- drug therapy
KW - Tobacco Smoke Pollution -- adverse effects
KW - Lung -- drug effects
KW - Lung Neoplasms -- mortality
KW - Lung Neoplasms -- chemically induced
KW - Lung -- pathology
KW - Lung -- metabolism
KW - Antineoplastic Agents -- pharmacology
KW - Quinazolines -- pharmacology
KW - Lung Neoplasms -- pathology
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1566821174?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Assay+of+lapatinib+in+murine+models+of+cigarette+smoke+carcinogenesis.&rft.au=Balansky%2C+Roumen%3BIzzotti%2C+Alberto%3BD%27Agostini%2C+Francesco%3BLongobardi%2C+Mariagrazia%3BMicale%2C+Rosanna+T%3BLa+Maestra%2C+Sebastiano%3BCamoirano%2C+Anna%3BGanchev%2C+Gancho%3BIltcheva%2C+Marietta%3BSteele%2C+Vernon+E%3BDe+Flora%2C+Silvio&rft.aulast=Balansky&rft.aufirst=Roumen&rft.date=2014-10-01&rft.volume=35&rft.issue=10&rft.spage=2300&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgu154
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-05-11
N1 - Date created - 2014-09-30
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Mutat Res. 2011 Dec 1;717(1-2):9-16 [21185844]
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J Clin Oncol. 2011 Sep 10;29(26):3529-34 [21825264]
Mutat Res. 2011 Dec 1;717(1-2):17-24 [20974155]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/carcin/bgu154
ER -
TY - JOUR
T1 - An improved recombinant Fab-immunotoxin targeting CD22 expressing malignancies.
AN - 1566820524; 25127689
AB - Moxetumomab pasudotox (HA22) is a recombinant immunotoxin, now in clinical trials, that combines an anti-CD22-Fv with a 38-kDa fragment of Pseudomonas exotoxin A. To produce a less immunogenic molecule without reducing the half-life in circulation, we constructed LMB11 combining an anti-CD22 Fab with a less immunogenic version of PE38. We found that LMB11 retains full activity toward CD22-expressing cells. In mice, the half-life of LMB11 is 29 min and the antitumor activity of LMB11 is better than that of HA22. Because it can be safely given at much higher doses, LMB11 produced complete tumor remissions in 7/7 mice.
Published by Elsevier Ltd.
JF - Leukemia research
AU - Bera, Tapan K
AU - Onda, Masanori
AU - Kreitman, Robert J
AU - Pastan, Ira
AD - Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Room 5106, Bethesda, MD 20892-4264, USA. ; Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Room 5106, Bethesda, MD 20892-4264, USA. Electronic address: pastani@mail.nih.gov.
Y1 - 2014/10//
PY - 2014
DA - October 2014
SP - 1224
EP - 1229
VL - 38
IS - 10
KW - Bacterial Toxins
KW - 0
KW - Exotoxins
KW - Immunoglobulin Fab Fragments
KW - Immunotoxins
KW - Sialic Acid Binding Ig-like Lectin 2
KW - immunotoxin HA22
KW - Index Medicus
KW - B-cell malignancies
KW - Less immunogenic PE38
KW - Moxetumomab pasudotox
KW - Animals
KW - Half-Life
KW - Humans
KW - Xenograft Model Antitumor Assays
KW - Mice
KW - Mice, Inbred BALB C
KW - Female
KW - Leukemia
KW - Sialic Acid Binding Ig-like Lectin 2 -- immunology
KW - Immunotoxins -- pharmacology
KW - Immunoglobulin Fab Fragments -- pharmacology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Leukemia+research&rft.atitle=An+improved+recombinant+Fab-immunotoxin+targeting+CD22+expressing+malignancies.&rft.au=Bera%2C+Tapan+K%3BOnda%2C+Masanori%3BKreitman%2C+Robert+J%3BPastan%2C+Ira&rft.aulast=Bera&rft.aufirst=Tapan&rft.date=2014-10-01&rft.volume=38&rft.issue=10&rft.spage=1224&rft.isbn=&rft.btitle=&rft.title=Leukemia+research&rft.issn=1873-5835&rft_id=info:doi/10.1016%2Fj.leukres.2014.06.014
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-11-18
N1 - Date created - 2014-09-30
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Methods Mol Biol. 2004;248:503-18 [14970517]
Br Med Bull. 2012;104:41-59 [23118261]
Bioconjug Chem. 1998 Nov-Dec;9(6):736-43 [9815167]
Int J Cancer. 1999 Mar 31;81(1):148-55 [10077166]
Clin Cancer Res. 2005 Feb 15;11(4):1545-50 [15746059]
Annu Rev Med. 2007;58:221-37 [17059365]
Blood. 2009 Apr 16;113(16):3792-800 [18988862]
J Clin Oncol. 2009 Jun 20;27(18):2983-90 [19414673]
Clin Cancer Res. 2010 Mar 15;16(6):1894-903 [20215554]
J Immunother. 2010 Apr;33(3):297-304 [20445350]
Proc Natl Acad Sci U S A. 2011 Apr 5;108(14):5742-7 [21436054]
Cancer Res. 2011 Oct 15;71(20):6300-9 [21998010]
J Clin Oncol. 2012 May 20;30(15):1822-8 [22355053]
Proc Natl Acad Sci U S A. 2012 Jul 17;109(29):11782-7 [22753489]
Cancer Immun. 2012;12:14 [22896759]
Nature. 1989 Jun 1;339(6223):394-7 [2498664]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.leukres.2014.06.014
ER -
TY - JOUR
T1 - Activation of invariant natural killer T cells impedes liver regeneration by way of both IFN-γ- and IL-4-dependent mechanisms.
AN - 1566107791; 24623351
AB - Invariant natural killer T (iNKT) cells are a major subset of lymphocytes found in the liver. These cells mediate various functions, including hepatic injury, fibrogenesis, and carcinogenesis. However, the function of iNKT cells in liver regeneration remains unclear. In the present study, partial hepatectomy (PHx) was used to study liver regeneration. α-Galactosylceramide (α-GalCer), a specific ligand for iNKT cells, was used to induce iNKT cell activation. After PHx, two strains of iNKT cell-deficient mice, CD1d(-/-) and Jα281(-/-) mice, showed normal liver regeneration. Injection of α-GalCer before or after PHx, which rapidly stimulated interferon-gamma (IFN-γ) and interleukin (IL)-4 production by iNKT cells, markedly inhibited liver regeneration. In vitro treatment with IFN-γ inhibited hepatocyte proliferation. In agreement with this in vitro finding, genetic disruption of IFN-γ or its downstream signaling molecule signal transducer and activator of transcription (STAT)1 significantly abolished the α-GalCer-mediated inhibition of liver regeneration. In vitro exposure to IL-4 did not affect hepatocyte proliferation, but surprisingly, genetic ablation of IL-4 or its downstream signaling molecule STAT6 partially eliminated the inhibitory effect of α-GalCer on liver regeneration. Further studies revealed that IL-4 contributed to α-GalCer-induced iNKT cell expansion and IFN-γ production, thereby inhibiting liver regeneration.
iNKT cells play a minor role in controlling liver regeneration after PHx under healthy conditions. Activation of iNKT cells by α-GalCer induces the production of IFN-γ, which directly inhibits liver regeneration, and IL-4, which indirectly attenuates liver regeneration by stimulating iNKT cell expansion and IFN-γ production. © 2014 by the American Association for the Study of Liver Diseases. This article has been contributed to by U.S. Government employees and their work is in the public domain in the USA.
JF - Hepatology (Baltimore, Md.)
AU - Yin, Shi
AU - Wang, Hua
AU - Bertola, Adeline
AU - Feng, Dechun
AU - Xu, Ming-Jiang
AU - Wang, Yan
AU - Gao, Bin
AD - Laboratory of Liver Diseases, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA; Department of Geriatrics, Affiliated Provincial Hospital of Anhui Medical University, Hefei, China.
Y1 - 2014/10//
PY - 2014
DA - October 2014
SP - 1356
EP - 1366
VL - 60
IS - 4
KW - Antigens, CD1d
KW - 0
KW - CD1d antigen, mouse
KW - Galactosylceramides
KW - STAT6 Transcription Factor
KW - Stat6 protein, mouse
KW - alpha-galactosylceramide
KW - Interleukin-4
KW - 207137-56-2
KW - Interferon-gamma
KW - 82115-62-6
KW - Index Medicus
KW - Models, Animal
KW - Cell Proliferation -- drug effects
KW - Animals
KW - Galactosylceramides -- pharmacology
KW - Antigens, CD1d -- genetics
KW - Hepatocytes -- drug effects
KW - STAT6 Transcription Factor -- physiology
KW - Mice
KW - Hepatocytes -- pathology
KW - Mice, Knockout
KW - Antigens, CD1d -- physiology
KW - STAT6 Transcription Factor -- genetics
KW - STAT6 Transcription Factor -- deficiency
KW - Hepatectomy
KW - In Vitro Techniques
KW - Mice, Inbred C57BL
KW - Male
KW - Interleukin-4 -- genetics
KW - Liver Regeneration -- drug effects
KW - Interferon-gamma -- genetics
KW - Liver -- surgery
KW - Liver -- drug effects
KW - Interferon-gamma -- deficiency
KW - Interleukin-4 -- deficiency
KW - Natural Killer T-Cells -- physiology
KW - Interferon-gamma -- physiology
KW - Natural Killer T-Cells -- pathology
KW - Liver Regeneration -- physiology
KW - Interleukin-4 -- physiology
KW - Liver -- physiology
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1566107791?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Hepatology+%28Baltimore%2C+Md.%29&rft.atitle=Activation+of+invariant+natural+killer+T+cells+impedes+liver+regeneration+by+way+of+both+IFN-%CE%B3-+and+IL-4-dependent+mechanisms.&rft.au=Yin%2C+Shi%3BWang%2C+Hua%3BBertola%2C+Adeline%3BFeng%2C+Dechun%3BXu%2C+Ming-Jiang%3BWang%2C+Yan%3BGao%2C+Bin&rft.aulast=Yin&rft.aufirst=Shi&rft.date=2014-10-01&rft.volume=60&rft.issue=4&rft.spage=1356&rft.isbn=&rft.btitle=&rft.title=Hepatology+%28Baltimore%2C+Md.%29&rft.issn=1527-3350&rft_id=info:doi/10.1002%2Fhep.27128
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-05-11
N1 - Date created - 2014-09-25
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Hepatology. 2003 Nov;38(5):1116-24 [14578850]
Nat Rev Immunol. 2002 Aug;2(8):557-68 [12154375]
J Hepatol. 2006 Sep;45(3):347-9 [16854494]
Hepatology. 2006 Oct;44(4):955-66 [17006930]
Gastroenterology. 2006 Nov;131(5):1573-83 [17064698]
Hepatology. 2007 Jan;45(1):22-30 [17187419]
Hepatology. 2007 Jun;45(6):1400-12 [17523147]
Nat Protoc. 2008;3(7):1167-70 [18600221]
Curr Mol Med. 2008 Aug;8(5):384-92 [18691065]
J Leukoc Biol. 2009 Sep;86(3):513-28 [19542050]
Am J Pathol. 2010 Jan;176(1):2-13 [20019184]
Hepatology. 2010 Apr;51(4):1354-62 [20041412]
Cytokine Growth Factor Rev. 2011 Feb;22(1):35-43 [21334249]
Expert Opin Ther Targets. 2011 Aug;15(8):973-88 [21564001]
Clin Immunol. 2011 Aug;140(2):130-41 [21169066]
Hepatology. 2011 Oct;54(4):1445-53 [21626524]
Autoimmun Rev. 2011 Oct;10(12):793-800 [21740985]
J Immunol. 2012 Jan 15;188(2):641-8 [22184721]
J Hepatol. 2012 Aug;57(2):430-41 [22504331]
J Hepatol. 2012 Sep;57(3):692-4 [22613006]
Am J Physiol Gastrointest Liver Physiol. 2013 Feb 1;304(3):G293-9 [23086918]
Hepatology. 2013 Apr;57(4):1575-84 [23150232]
Hepatology. 2013 May;57(5):1969-79 [22898900]
Hepatology. 2013 May;57(5):1688-90 [23390033]
Compr Physiol. 2013 Jan;3(1):485-513 [23720294]
Proc Natl Acad Sci U S A. 2013 Jun 11;110(24):9914-9 [23716700]
Hepatology. 2013 Oct;58(4):1474-85 [23686838]
Gastroenterology. 2004 Nov;127(5):1525-39 [15521020]
Hepatology. 2000 Apr;31(4):907-15 [10733547]
J Exp Med. 2000 Oct 2;192(7):921-30 [11015434]
Comment In:
Hepatology. 2014 Oct;60(4):1133-5 [24824434]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1002/hep.27128
ER -
TY - JOUR
T1 - The effect of the UGT1A1*28 allele on survival after irinotecan-based chemotherapy: a collaborative meta-analysis.
AN - 1565502104; 24709690
AB - To date, studies of irinotecan pharmacogenetics have mostly focused on the effect of the UGT1A1*28 allele on irinotecan-related toxicity. However, the clinical utility of routine UGT1A1*28 genotyping to pre-emptively adjust irinotecan dosage is dependent upon whether UGT1A1*28 also affects patient survival following irinotecan therapy. Previous observational studies evaluating the influence of UGT1A1*28 on survival have shown contradictory results. A systematic review and meta-analysis of both published and unpublished data were performed to summarize the available evidence of the relationship between the UGT1A1*28 allele and patient survival related to irinotecan therapy. Overall and progression-free survival meta-analysis data were available for 1524 patients and 1494 patients, respectively. The difference in the survival between patients of different UGT1A1*28 genotypes (homozygous, heterozygous or wild-type) who had received irinotecan was not found to be statistically significant. There was also no evidence of irinotecan dose, regimen or line of therapy having an impact on this association.
JF - The pharmacogenomics journal
AU - Dias, M M
AU - Pignon, J-P
AU - Karapetis, C S
AU - Boige, V
AU - Glimelius, B
AU - Kweekel, D M
AU - Lara, P N
AU - Laurent-Puig, P
AU - Martinez-Balibrea, E
AU - Páez, D
AU - Punt, C J A
AU - Redman, M W
AU - Toffoli, G
AU - Wadelius, M
AU - McKinnon, R A
AU - Sorich, M J
AD - School of Pharmacy and Medical Sciences, University of South Australia, Adelaide, South Australia, Australia. ; Meta-analysis Unit, Department of Biostatistics and Epidemiology, Gustave-Roussy, Villejuif, France. ; Flinders Centre for Innovation in Cancer, School of Medicine, Flinders University, Adelaide, South Australia, Australia. ; Department of Oncologic Medicine, Gustave-Roussy, Villejuif, France. ; Section of Oncology, Department of Radiology, Oncology and Radiation Science, Uppsala University, Uppsala, Sweden. ; Department of Clinical Pharmacy and Toxicology, Leiden University Medical Centre, Leiden, The Netherlands. ; Davis Comprehensive Cancer Center, University of California, Sacramento, CA, USA. ; Unité Mixte de Recherche S775, Institut National de la Santé et de la Recherche Médicale, Université Paris Descartes, Paris, France. ; Laboratori Biologia Molecular del Càncer, Institut Català d'Oncologia, Fundació Institut IGTP, Badalona, Spain. ; Medical Oncology Department, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain. ; Department of Medical Oncology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. ; Lung and Cancer Control Committees, Fred Hutchinson Cancer Research Center, Statistical Center: SWOG, Seattle, WA, USA. ; Experimental and Clinical Pharmacology Unit, CRO-National Cancer Institute, Aviano, Italy. ; Department of Medical Sciences, Clinical Pharmacology, Uppsala University, Uppsala, Sweden. ; 1] School of Pharmacy and Medical Sciences, University of South Australia, Adelaide, South Australia, Australia [2] Department of Clinical Pharmacology, School of Medicine, Flinders University, Adelaide, South Australia, Australia.
Y1 - 2014/10//
PY - 2014
DA - October 2014
SP - 424
EP - 431
VL - 14
IS - 5
KW - irinotecan
KW - 0H43101T0J
KW - UGT1A1 enzyme
KW - EC 2.4.1.-
KW - Glucuronosyltransferase
KW - EC 2.4.1.17
KW - Camptothecin
KW - XT3Z54Z28A
KW - Index Medicus
KW - Genotype
KW - Humans
KW - Disease Progression
KW - Antineoplastic Combined Chemotherapy Protocols -- administration & dosage
KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use
KW - Survival Analysis
KW - Neoplasms -- drug therapy
KW - Glucuronosyltransferase -- genetics
KW - Alleles
KW - Camptothecin -- analogs & derivatives
KW - Camptothecin -- therapeutic use
KW - Neoplasms -- genetics
KW - Camptothecin -- administration & dosage
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+pharmacogenomics+journal&rft.atitle=The+effect+of+the+UGT1A1*28+allele+on+survival+after+irinotecan-based+chemotherapy%3A+a+collaborative+meta-analysis.&rft.au=Dias%2C+M+M%3BPignon%2C+J-P%3BKarapetis%2C+C+S%3BBoige%2C+V%3BGlimelius%2C+B%3BKweekel%2C+D+M%3BLara%2C+P+N%3BLaurent-Puig%2C+P%3BMartinez-Balibrea%2C+E%3BP%C3%A1ez%2C+D%3BPunt%2C+C+J+A%3BRedman%2C+M+W%3BToffoli%2C+G%3BWadelius%2C+M%3BMcKinnon%2C+R+A%3BSorich%2C+M+J&rft.aulast=Dias&rft.aufirst=M&rft.date=2014-10-01&rft.volume=14&rft.issue=5&rft.spage=424&rft.isbn=&rft.btitle=&rft.title=The+pharmacogenomics+journal&rft.issn=1473-1150&rft_id=info:doi/10.1038%2Ftpj.2014.16
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-10-12
N1 - Date created - 2014-09-24
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1038/tpj.2014.16
ER -
TY - JOUR
T1 - Effects of deep hypothermic circulatory arrest on the blood brain barrier in a cardiopulmonary bypass model--a pilot study.
AN - 1565500341; 24931068
AB - Neurologic injury is common after cardiac surgery and disruption of the blood brain barrier (BBB) has been proposed as a contributing factor. We sought to study BBB characteristics in a rodent model of cardiopulmonary bypass (CPB) and deep hypothermic circulatory arrest (DHCA).
Adult rats were subjected to CPB/DHCA or to sham surgery. Analysis included Western blotting of relevant BBB proteins in addition to in vivo brain magnetic resonance imaging (MRI) with a clinically used low-molecular contrast agent. While quantitative analysis of BBB proteins revealed similar expression levels, MRI showed evidence of BBB disruption after CPB/DHCA compared to sham surgery.
Combining molecular BBB analysis and MRI technology in a rodent model is a highly translatable approach to study adverse neurologic outcomes following CPB/DHCA. Copyright © 2014 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). All rights reserved.
JF - Heart, lung & circulation
AU - Bartels, Karsten
AU - Ma, Qing
AU - Venkatraman, Talaignair N
AU - Campos, Christopher R
AU - Smith, Lindsay
AU - Cannon, Ronald E
AU - Podgoreanu, Mihai V
AU - Lascola, Christopher D
AU - Miller, David S
AU - Mathew, Joseph P
AD - Department of Anesthesiology, Duke University Medical Center, Durham, NC, USA. ; Department of Radiology, Duke University Medical Center, Durham, NC, USA. ; Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, USA. ; Department of Anesthesiology, Duke University Medical Center, Durham, NC, USA. Electronic address: joseph.mathew@duke.edu.
Y1 - 2014/10//
PY - 2014
DA - October 2014
SP - 981
EP - 984
VL - 23
IS - 10
KW - Claudin-5
KW - 0
KW - Contrast Media
KW - Occludin
KW - Organometallic Compounds
KW - P-Glycoprotein
KW - gadobutrol
KW - 1BJ477IO2L
KW - Index Medicus
KW - Blood brain barrier
KW - Cardiac surgery
KW - Neurologic injury
KW - Deep hypothermic circulatory arrest
KW - Cardiopulmonary bypass
KW - Rats
KW - Models, Animal
KW - Animals
KW - Rats, Sprague-Dawley
KW - P-Glycoprotein -- metabolism
KW - Claudin-5 -- metabolism
KW - Occludin -- metabolism
KW - Pilot Projects
KW - Male
KW - Magnetic Resonance Imaging
KW - Circulatory Arrest, Deep Hypothermia Induced -- adverse effects
KW - Cardiopulmonary Bypass -- adverse effects
KW - Blood-Brain Barrier -- metabolism
KW - Blood-Brain Barrier -- physiopathology
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1565500341?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Heart%2C+lung+%26+circulation&rft.atitle=Effects+of+deep+hypothermic+circulatory+arrest+on+the+blood+brain+barrier+in+a+cardiopulmonary+bypass+model--a+pilot+study.&rft.au=Bartels%2C+Karsten%3BMa%2C+Qing%3BVenkatraman%2C+Talaignair+N%3BCampos%2C+Christopher+R%3BSmith%2C+Lindsay%3BCannon%2C+Ronald+E%3BPodgoreanu%2C+Mihai+V%3BLascola%2C+Christopher+D%3BMiller%2C+David+S%3BMathew%2C+Joseph+P&rft.aulast=Bartels&rft.aufirst=Karsten&rft.date=2014-10-01&rft.volume=23&rft.issue=10&rft.spage=981&rft.isbn=&rft.btitle=&rft.title=Heart%2C+lung+%26+circulation&rft.issn=1444-2892&rft_id=info:doi/10.1016%2Fj.hlc.2014.04.131
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-06-24
N1 - Date created - 2014-09-24
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Ann Thorac Surg. 2004 Oct;78(4):1418-25 [15464507]
Eur J Cardiothorac Surg. 1989;3(6):539-43 [2635941]
Mol Pharmacol. 2006 Feb;69(2):462-70 [16278373]
J Thorac Cardiovasc Surg. 2006 Apr;131(4):805-12 [16580438]
Curr Opin Anaesthesiol. 2013 Feb;26(1):91-7 [23235523]
Pharmacol Rev. 2008 Jun;60(2):196-209 [18560012]
Neurobiol Dis. 2010 Jan;37(1):13-25 [19664713]
Trends Pharmacol Sci. 2010 Jun;31(6):246-54 [20417575]
Ann Thorac Surg. 2010 Dec;90(6):2001-8 [21095352]
Stroke. 2008 May;39(5):1427-33 [18323490]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.hlc.2014.04.131
ER -
TY - JOUR
T1 - Role of alpha-1 antitrypsin in human health and disease.
AN - 1564602676; 24661570
AB - Alpha-1 antitrypsin (AAT) deficiency is an under-recognized hereditary disorder associated with the premature onset of chronic obstructive pulmonary disease, liver cirrhosis in children and adults, and less frequently, relapsing panniculitis, systemic vasculitis and other inflammatory, autoimmune and neoplastic diseases. Severe AAT deficiency mainly affects Caucasian individuals and has its highest prevalence (1 : 2000-1 : 5000 individuals) in Northern, Western and Central Europe. In the USA and Canada, the prevalence is 1: 5000-10 000. Prevalence is five times lower in Latin American countries and is rare or nonexistent in African and Asian individuals. The key to successful diagnosis is by measuring serum AAT, followed by the determination of the phenotype or genotype if low concentrations are found. Case detection allows implementation of genetic counselling and, in selected cases, the application of augmentation therapy. Over the past decade, it has been demonstrated that AAT is a broad-spectrum anti-inflammatory, immunomodulatory, anti-infective and tissue-repair molecule. These new capacities are promoting an increasing number of clinical studies, new pharmacological formulations, new patent applications and the search for alternative sources of AAT (including transgenic and recombinant AAT) to meet the expected demand for treating a large number of diseases, inside and outside the context of AAT deficiency. © 2014 The Association for the Publication of the Journal of Internal Medicine.
JF - Journal of internal medicine
AU - de Serres, F
AU - Blanco, I
AD - Center for the Evaluation of Risks to Human Reproduction, National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA.
Y1 - 2014/10//
PY - 2014
DA - October 2014
SP - 311
EP - 335
VL - 276
IS - 4
KW - alpha 1-Antitrypsin
KW - 0
KW - Index Medicus
KW - hereditary disorder
KW - alpha-1 antitrypsin
KW - AAT deficiency
KW - therapy
KW - Genotype
KW - Animals
KW - Injections, Intravenous
KW - Humans
KW - Genetic Therapy
KW - Prevalence
KW - alpha 1-Antitrypsin Deficiency -- drug therapy
KW - alpha 1-Antitrypsin Deficiency -- complications
KW - alpha 1-Antitrypsin -- blood
KW - alpha 1-Antitrypsin Deficiency -- diagnosis
KW - alpha 1-Antitrypsin -- therapeutic use
KW - alpha 1-Antitrypsin -- physiology
KW - alpha 1-Antitrypsin Deficiency -- epidemiology
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1564602676?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+internal+medicine&rft.atitle=Role+of+alpha-1+antitrypsin+in+human+health+and+disease.&rft.au=de+Serres%2C+F%3BBlanco%2C+I&rft.aulast=de+Serres&rft.aufirst=F&rft.date=2014-10-01&rft.volume=276&rft.issue=4&rft.spage=311&rft.isbn=&rft.btitle=&rft.title=Journal+of+internal+medicine&rft.issn=1365-2796&rft_id=info:doi/10.1111%2Fjoim.12239
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-01-19
N1 - Date created - 2014-09-23
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1111/joim.12239
ER -
TY - JOUR
T1 - Crucial role of macrophage selenoproteins in experimental colitis.
AN - 1563993583; 25187657
AB - Inflammation is a hallmark of inflammatory bowel disease (IBD) that involves macrophages. Given the inverse link between selenium (Se) status and IBD-induced inflammation, our objective was to demonstrate that selenoproteins in macrophages were essential to suppress proinflammatory mediators, in part, by the modulation of arachidonic acid metabolism. Acute colitis was induced using 4% dextran sodium sulfate in wild-type mice maintained on Se-deficient (<0.01 ppm Se), Se-adequate (0.08 ppm; sodium selenite), and two supraphysiological levels in the form of Se-supplemented (0.4 ppm; sodium selenite) and high Se (1.0 ppm; sodium selenite) diets. Selenocysteinyl transfer RNA knockout mice (Trsp(fl/fl)LysM(Cre)) were used to examine the role of selenoproteins in macrophages on disease progression and severity using histopathological evaluation, expression of proinflammatory and anti-inflammatory genes, and modulation of PG metabolites in urine and plasma. Whereas Se-deficient and Se-adequate mice showed increased colitis and exhibited poor survival, Se supplementation at 0.4 and 1.0 ppm increased survival of mice and decreased colitis-associated inflammation with an upregulation of expression of proinflammatory and anti-inflammatory genes. Metabolomic profiling of urine suggested increased oxidation of PGE2 at supraphysiological levels of Se that also correlated well with Se-dependent upregulation of 15-hydroxy-PG dehydrogenase (15-PGDH) in macrophages. Pharmacological inhibition of 15-PGDH, lack of selenoprotein expression in macrophages, and depletion of infiltrating macrophages indicated that macrophage-specific selenoproteins and upregulation of 15-PGDH expression were key for Se-dependent anti-inflammatory and proresolving effects. Selenoproteins in macrophages protect mice from dextran sodium sulfate-colitis by enhancing 15-PGDH-dependent oxidation of PGE2 to alleviate inflammation, suggesting a therapeutic role for Se in IBD.
Copyright © 2014 by The American Association of Immunologists, Inc.
JF - Journal of immunology (Baltimore, Md. : 1950)
AU - Kaushal, Naveen
AU - Kudva, Avinash K
AU - Patterson, Andrew D
AU - Chiaro, Christopher
AU - Kennett, Mary J
AU - Desai, Dhimant
AU - Amin, Shantu
AU - Carlson, Bradley A
AU - Cantorna, Margherita T
AU - Prabhu, K Sandeep
AD - Center for Molecular Immunology and Infectious Disease and Center for Molecular Toxicology and Carcinogenesis, Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, PA 16802; ; Department of Pharmacology, Penn State College of Medicine, Hershey, PA 17033; and. ; Molecular Biology of Selenium Section, Mouse Cancer Genetics Program, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. ; Center for Molecular Immunology and Infectious Disease and Center for Molecular Toxicology and Carcinogenesis, Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, PA 16802; ksprabhu@psu.edu.
Y1 - 2014/10/01/
PY - 2014
DA - 2014 Oct 01
SP - 3683
EP - 3692
VL - 193
IS - 7
KW - RNA, Transfer, Amino Acyl
KW - 0
KW - Selenoproteins
KW - selenocysteinyl-tRNA
KW - Dextran Sulfate
KW - 9042-14-2
KW - Hydroxyprostaglandin Dehydrogenases
KW - EC 1.1.1.-
KW - 15-hydroxyprostaglandin dehydrogenase
KW - EC 1.1.1.141
KW - Selenium
KW - H6241UJ22B
KW - Dinoprostone
KW - K7Q1JQR04M
KW - Abridged Index Medicus
KW - Index Medicus
KW - Dinoprostone -- immunology
KW - Animals
KW - Selenium -- pharmacology
KW - RNA, Transfer, Amino Acyl -- genetics
KW - Inflammation -- genetics
KW - Mice
KW - Dextran Sulfate -- toxicity
KW - Mice, Knockout
KW - Hydroxyprostaglandin Dehydrogenases -- genetics
KW - Hydroxyprostaglandin Dehydrogenases -- immunology
KW - RNA, Transfer, Amino Acyl -- immunology
KW - Dietary Supplements
KW - Inflammation -- immunology
KW - Dinoprostone -- genetics
KW - Cell Line
KW - Macrophages -- pathology
KW - Macrophages -- immunology
KW - Colitis -- immunology
KW - Selenoproteins -- genetics
KW - Selenoproteins -- immunology
KW - Colitis -- pathology
KW - Colitis -- chemically induced
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1563993583?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.atitle=Crucial+role+of+macrophage+selenoproteins+in+experimental+colitis.&rft.au=Kaushal%2C+Naveen%3BKudva%2C+Avinash+K%3BPatterson%2C+Andrew+D%3BChiaro%2C+Christopher%3BKennett%2C+Mary+J%3BDesai%2C+Dhimant%3BAmin%2C+Shantu%3BCarlson%2C+Bradley+A%3BCantorna%2C+Margherita+T%3BPrabhu%2C+K+Sandeep&rft.aulast=Kaushal&rft.aufirst=Naveen&rft.date=2014-10-01&rft.volume=193&rft.issue=7&rft.spage=3683&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.issn=1550-6606&rft_id=info:doi/10.4049%2Fjimmunol.1400347
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-11-14
N1 - Date created - 2014-09-20
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Cancer Metastasis Rev. 2011 Dec;30(3-4):409-17 [22020925]
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J Biol Chem. 2013 Jul 5;288(27):19484-502 [23687300]
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Eur J Clin Nutr. 2000 Jun;54(6):514-21 [10878655]
Am J Physiol Gastrointest Liver Physiol. 2000 Jul;279(1):G238-44 [10898767]
Acta Gastroenterol Belg. 2001 Jan-Mar;64(1):1-5 [11322060]
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Rocz Akad Med Bialymst. 2001;46:60-8 [11780581]
Methods. 2001 Dec;25(4):402-8 [11846609]
J Clin Invest. 2002 Apr;109(7):883-93 [11927615]
Prostaglandins Other Lipid Mediat. 2002 Aug;68-69:483-93 [12432938]
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Gut. 1984 Nov;25(11):1271-8 [6149981]
Gut. 1987 Aug;28(8):1002-7 [3117625]
Gastroenterology. 1990 Mar;98(3):694-702 [1688816]
Annu Rev Med. 1992;43:125-33 [1580577]
Gastroenterology. 1993 Jun;104(6):1832-47 [8500743]
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Nutrition. 2005 May;21(5):574-9 [15850963]
Prostaglandins Other Lipid Mediat. 2005 Dec;78(1-4):160-8 [16303613]
Am J Physiol Gastrointest Liver Physiol. 2006 Feb;290(2):G361-8 [16195422]
Curr Pharm Des. 2006;12(8):943-54 [16533161]
ScientificWorldJournal. 2006;6:577-88 [16752007]
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Br J Pharmacol. 2006 Nov;149(6):611-23 [17016496]
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J Immunol. 2007 Jun 15;178(12):8138-47 [17548652]
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Mol Nutr Food Res. 2008 Nov;52(11):1273-80 [18384097]
BMC Immunol. 2009;10:57 [19863805]
Inflamm Bowel Dis. 2010 Jan;16(1):87-95 [19572372]
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PLoS Pathog. 2010 May;6(5):e1000902 [20485566]
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BMC Gastroenterol. 2010;10:82 [20637112]
Gastroenterology. 2010 Dec;139(6):1912-7 [20950616]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.4049/jimmunol.1400347
ER -
TY - JOUR
T1 - A microRNA 221- and 222-mediated feedback loop maintains constitutive activation of NFκB and STAT3 in colorectal cancer cells.
AN - 1563991779; 24931456
AB - Constitutive activation of the transcription factors nuclear factor κB (NF-κB) and STAT3 is involved in the development and progression of human colorectal cancer (CRC). Little is known about how these factors become activated in cancer cells. We investigated whether microRNA miR-221 and miR-222 regulate NF-κB and signal transducer and activator of transcription 3 (STAT3) activation in human CRC cell lines.
CRC cell lines (HCT116 and RKO) were transfected with miR-221 or miR-222 mimics or inhibitors. The activity levels of NF-κB and STAT3 were measured in dual luciferase reporter assays. We used immunoblot and real-time polymerase chain reaction analyses to measure protein and messenger RNA (mRNA) levels. Cells were analyzed by proliferation, viability, and flow cytometry analyses. Mice were given injections of azoxymethane, followed by dextran sodium sulfate, along with control lentivirus or those expressing mRNAs that bind miR-221 and miR-222 (miR-221/miR-222 sponge). The levels of miR-221 and miR-222 as well as RelA, STAT3, and PDLIM2 mRNAs were measured in 57 paired CRC and adjacent nontumor tissues from patients. In CRC cell lines, mimics of miR-221 and miR-222 activated NF-κB and STAT3, further increasing expression of miR-221 and miR-222. miR-221 and miR-222 bound directly to the coding region of RelA mRNA, increasing its stability. miR-221 and miR-222 also reduced the ubiquitination and degradation of the RelA and STAT3 proteins by binding to the 3' untranslated region of PDLIM2 mRNA (PDLIM2 is a nuclear ubiquitin E3 ligase for RelA and STAT3). Incubation of CRC cells with miR-221 and miR-222 inhibitors reduced their proliferation and colony formation compared with control cells. In mice with colitis, injection of lentiviruses expressing miR-221/miR-222 sponges led to formation of fewer tumors than injection of control lentiviruses. Human CRC tissues had higher levels of miR-221 and miR-222 than nontumor colon tissues; increases correlated with increased levels of RelA and STAT3 mRNAs. Levels of PDLIM2 mRNA were lower in CRC than nontumor tissues.
In human CRC cells, miR-221 and miR-222 act in a positive feedback loop to increase expression levels of RelA and STAT3. Antagonism of miR-221 and miR-222 reduces growth of colon tumors in mice with colitis. Copyright © 2014 AGA Institute. Published by Elsevier Inc. All rights reserved.
JF - Gastroenterology
AU - Liu, Sanhong
AU - Sun, Xiaohua
AU - Wang, Mingliang
AU - Hou, Yingyong
AU - Zhan, Yu
AU - Jiang, Yuhang
AU - Liu, Zhanjie
AU - Cao, Xinwei
AU - Chen, Pengfei
AU - Liu, Zhi
AU - Chen, Xi
AU - Tao, Yu
AU - Xu, Chen
AU - Mao, Jie
AU - Cheng, Chunyan
AU - Li, Cuifeng
AU - Hu, Yiming
AU - Wang, Lunshan
AU - Chin, Y Eugene
AU - Shi, Yufang
AU - Siebenlist, Ulrich
AU - Zhang, Xiaoren
AD - Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences and Shanghai Jiao Tong University School of Medicine, Shanghai, China. ; General Surgery Department, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. ; Department of Pathology, Zhongshan Hospital, Fudan University, Shanghai, China. ; Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland. ; Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences and Shanghai Jiao Tong University School of Medicine, Shanghai, China. Electronic address: xrzhang@sibs.ac.cn.
Y1 - 2014/10//
PY - 2014
DA - October 2014
SP - 847
EP - 859.e11
VL - 147
IS - 4
KW - 3' Untranslated Regions
KW - 0
KW - LIM Domain Proteins
KW - MIRN221 microRNA, human
KW - MIRN222 microRNA, human
KW - MicroRNAs
KW - Microfilament Proteins
KW - NF-kappa B
KW - PDLIM2 protein, human
KW - RELA protein, human
KW - RNA, Messenger
KW - STAT3 Transcription Factor
KW - STAT3 protein, human
KW - Transcription Factor RelA
KW - Abridged Index Medicus
KW - Index Medicus
KW - Carcinogenesis
KW - microRNA 221
KW - microRNA 222
KW - Colon Cancer
KW - Animals
KW - Microfilament Proteins -- metabolism
KW - LIM Domain Proteins -- genetics
KW - Open Reading Frames
KW - Humans
KW - Tumor Burden
KW - Disease Models, Animal
KW - Colitis -- pathology
KW - Mice, Nude
KW - Feedback, Physiological
KW - Cell Proliferation
KW - Mice, Inbred BALB C
KW - Colitis -- metabolism
KW - Cell Survival
KW - Gene Expression Regulation, Neoplastic
KW - Genes, Reporter
KW - Xenograft Model Antitumor Assays
KW - HT29 Cells
KW - RNA Interference
KW - Time Factors
KW - Signal Transduction
KW - Male
KW - Transcription Factor RelA -- metabolism
KW - LIM Domain Proteins -- metabolism
KW - Microfilament Proteins -- genetics
KW - Mice
KW - HCT116 Cells
KW - Colitis -- genetics
KW - Binding Sites
KW - RNA, Messenger -- metabolism
KW - Transfection
KW - Colitis -- therapy
KW - Mice, Inbred C57BL
KW - MicroRNAs -- metabolism
KW - Colorectal Neoplasms -- pathology
KW - Colorectal Neoplasms -- metabolism
KW - STAT3 Transcription Factor -- genetics
KW - STAT3 Transcription Factor -- metabolism
KW - Colorectal Neoplasms -- genetics
KW - Colorectal Neoplasms -- prevention & control
KW - NF-kappa B -- genetics
KW - NF-kappa B -- metabolism
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1563991779?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gastroenterology&rft.atitle=A+microRNA+221-+and+222-mediated+feedback+loop+maintains+constitutive+activation+of+NF%CE%BAB+and+STAT3+in+colorectal+cancer+cells.&rft.au=Liu%2C+Sanhong%3BSun%2C+Xiaohua%3BWang%2C+Mingliang%3BHou%2C+Yingyong%3BZhan%2C+Yu%3BJiang%2C+Yuhang%3BLiu%2C+Zhanjie%3BCao%2C+Xinwei%3BChen%2C+Pengfei%3BLiu%2C+Zhi%3BChen%2C+Xi%3BTao%2C+Yu%3BXu%2C+Chen%3BMao%2C+Jie%3BCheng%2C+Chunyan%3BLi%2C+Cuifeng%3BHu%2C+Yiming%3BWang%2C+Lunshan%3BChin%2C+Y+Eugene%3BShi%2C+Yufang%3BSiebenlist%2C+Ulrich%3BZhang%2C+Xiaoren&rft.aulast=Liu&rft.aufirst=Sanhong&rft.date=2014-10-01&rft.volume=147&rft.issue=4&rft.spage=847&rft.isbn=&rft.btitle=&rft.title=Gastroenterology&rft.issn=1528-0012&rft_id=info:doi/10.1053%2Fj.gastro.2014.06.006
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-11-25
N1 - Date created - 2014-09-20
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Carcinogenesis. 2006 Jun;27(6):1285-91 [16497702]
Oncogene. 2004 Mar 18;23(12):2138-45 [14676835]
J Biol Chem. 2007 Aug 10;282(32):23716-24 [17569667]
EMBO J. 2007 Aug 8;26(15):3699-708 [17627278]
Nat Methods. 2007 Sep;4(9):721-6 [17694064]
Cancer Cell. 2008 Jan;13(1):7-9 [18167335]
Proc Natl Acad Sci U S A. 2008 Feb 5;105(5):1608-13 [18227514]
Int J Colorectal Dis. 2004 Jan;19(1):18-22 [12827408]
Oncology. 2003;65(1):37-45 [12837981]
Anticancer Res. 2004 Mar-Apr;24(2B):675-81 [15161011]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1053/j.gastro.2014.06.006
ER -
TY - JOUR
T1 - Docetaxel, oxaliplatin, and capecitabine combination chemotherapy for metastatic gastric cancer.
AN - 1563991337; 24318671
AB - The incorporation of docetaxel into the cisplatin and fluorouracil backbone has been demonstrated to be an active combination in metastatic gastric cancer. Nevertheless, this regimen is burdened by nonnegligible toxicity. We hypothesized that replacing cisplatin and fluorouracil with oxaliplatin and capecitabine should be an active and safe option for metastatic gastric cancer patients.
In this phase II study, we tested the activity of docetaxel in combination with oxaliplatin and capecitabine (DOC) as a first-line treatment. DOC was administered as follows: docetaxel (60 mg/m(2)) and oxaliplatin (100 mg/m(2)) on day 1, and capecitabine (500 mg/m(2)) was administered orally twice daily given continuously, with cycles repeated every 3 weeks. The primary endpoint was the overall response rate. Forty-eight patients entered the study. All patients had metastatic disease (stage IV). None of the patients had previously received chemotherapy for advanced disease. Performance status was 0, 1, and 2 in 25, 58, and 17 % of patients, respectively; 13 patients (27 %) had adenocarcinoma of the gastroesophageal junction, and 29 patients (60.5 %) had two or more metastatic sites. The overall response rate was 52.1 %. Progression-free survival and overall survival were 6.9 and 12.6 months, respectively. The treatment was well tolerated with no treatment-related deaths. The most common grade 3-4 toxicity was neutropenia (41 %).
DOC is an effective and tolerated first-line treatment, and the lower dose of docetaxel and oxaliplatin used in this study compared with other similar regimens does not seem to hamper the antitumor activity.
JF - Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association
AU - Di Lauro, Luigi
AU - Vici, Patrizia
AU - Belli, Franca
AU - Tomao, Silverio
AU - Fattoruso, Silvia Ileana
AU - Arena, Maria Grazia
AU - Pizzuti, Laura
AU - Giannarelli, Diana
AU - Paoletti, Giancarlo
AU - Barba, Maddalena
AU - Sergi, Domenico
AU - Maugeri-Saccà, Marcello
AD - Division of Medical Oncology B, "Regina Elena" National Cancer Institute, Via Elio Chianesi 53, 00144, Rome, Italy, dilauro@ifo.it.
Y1 - 2014/10//
PY - 2014
DA - October 2014
SP - 718
EP - 724
VL - 17
IS - 4
KW - Organoplatinum Compounds
KW - 0
KW - Taxoids
KW - oxaliplatin
KW - 04ZR38536J
KW - Deoxycytidine
KW - 0W860991D6
KW - docetaxel
KW - 15H5577CQD
KW - Capecitabine
KW - 6804DJ8Z9U
KW - Fluorouracil
KW - U3P01618RT
KW - Index Medicus
KW - Organoplatinum Compounds -- administration & dosage
KW - Humans
KW - Deoxycytidine -- analogs & derivatives
KW - Adenocarcinoma -- mortality
KW - Neutropenia -- chemically induced
KW - Aged
KW - Taxoids -- administration & dosage
KW - Adenocarcinoma -- pathology
KW - Esophageal Neoplasms -- mortality
KW - Esophageal Neoplasms -- pathology
KW - Fluorouracil -- administration & dosage
KW - Fluorouracil -- analogs & derivatives
KW - Adult
KW - Treatment Outcome
KW - Deoxycytidine -- administration & dosage
KW - Middle Aged
KW - Adenocarcinoma -- drug therapy
KW - Male
KW - Female
KW - Esophageal Neoplasms -- drug therapy
KW - Stomach Neoplasms -- drug therapy
KW - Stomach Neoplasms -- pathology
KW - Stomach Neoplasms -- mortality
KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects
KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1563991337?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gastric+cancer+%3A+official+journal+of+the+International+Gastric+Cancer+Association+and+the+Japanese+Gastric+Cancer+Association&rft.atitle=Docetaxel%2C+oxaliplatin%2C+and+capecitabine+combination+chemotherapy+for+metastatic+gastric+cancer.&rft.au=Di+Lauro%2C+Luigi%3BVici%2C+Patrizia%3BBelli%2C+Franca%3BTomao%2C+Silverio%3BFattoruso%2C+Silvia+Ileana%3BArena%2C+Maria+Grazia%3BPizzuti%2C+Laura%3BGiannarelli%2C+Diana%3BPaoletti%2C+Giancarlo%3BBarba%2C+Maddalena%3BSergi%2C+Domenico%3BMaugeri-Sacc%C3%A0%2C+Marcello&rft.aulast=Di+Lauro&rft.aufirst=Luigi&rft.date=2014-10-01&rft.volume=17&rft.issue=4&rft.spage=718&rft.isbn=&rft.btitle=&rft.title=Gastric+cancer+%3A+official+journal+of+the+International+Gastric+Cancer+Association+and+the+Japanese+Gastric+Cancer+Association&rft.issn=1436-3305&rft_id=info:doi/10.1007%2Fs10120-013-0321-3
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-06-23
N1 - Date created - 2014-09-20
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1007/s10120-013-0321-3
ER -
TY - JOUR
T1 - Chemoprevention of head and neck squamous cell carcinoma through inhibition of NF-κB signaling.
AN - 1562430931; 24177052
AB - Nuclear factor-kappa B (NF-κB) transcription factors regulate cellular processes such as inflammation and cell survival. The NF-κB pathway is often activated with development and progression of head and neck squamous cell carcinoma (HNSCC). As such, NF-κB represents an attractive target for chemoprevention. HNSCC involves progression of lesions from premalignant to malignant, providing a window of opportunity for intervention with chemopreventive agents. Appropriate chemopreventive agents should be inexpensive, nontoxic, and target important pathways involved in the development of HNSCC. Several such agents that inhibit the NF-κB pathway have been investigated in HNSCC. Retinoids have been studied most extensively but have shown limited potential in human trials. Epidermal growth factor receptor inhibitors and PI3K-mTOR inhibitors may benefit a subset of patients. Other agents such as green tea extract and curcumin are appealing because they are generally regarded as safe. In contrast, there is evidence that Vitamin E supplementation may actually increase mortality of cancer patients. Repurposed drugs such as cyclooxygenase (COX) inhibitors and antidiabetic drugs are an emerging area of interest. Future research to develop agents with lower toxicity and higher specificity for the NF-κB pathway, and to target these therapies to individual patient genetic signatures should help to increase the utility of chemoprevention in HSNCC.
Published by Elsevier Ltd.
JF - Oral oncology
AU - Vander Broek, Robert
AU - Snow, Grace E
AU - Chen, Zhong
AU - Van Waes, Carter
AD - Tumor Biology Section, Head and Neck Surgery Branch, National Institute on Deafness and Other Communication Disorders, NIH, Bethesda, Maryland, United States; Medical Research Scholars Program, NIH, Bethesda, Maryland, United States. ; Tumor Biology Section, Head and Neck Surgery Branch, National Institute on Deafness and Other Communication Disorders, NIH, Bethesda, Maryland, United States. ; Tumor Biology Section, Head and Neck Surgery Branch, National Institute on Deafness and Other Communication Disorders, NIH, Bethesda, Maryland, United States. Electronic address: vanwaesc@nidcd.nih.gov.
Y1 - 2014/10//
PY - 2014
DA - October 2014
SP - 930
EP - 941
VL - 50
IS - 10
KW - Anticarcinogenic Agents
KW - 0
KW - NF-kappa B
KW - Index Medicus
KW - Cyclooxygenase (COX) inhibitors
KW - Green tea extract (GTE)
KW - Curcumin
KW - Nuclear factor-kappa B (NF-κB)
KW - Epidermal growth factor receptor (EGFR)
KW - Head and neck cancer
KW - Mammalian target of rapamycin (mTOR)
KW - Chemoprevention
KW - Retinoids
KW - Phosphatidylinositol 3-kinase (PI3K)
KW - Humans
KW - Disease Progression
KW - Head and Neck Neoplasms -- prevention & control
KW - Head and Neck Neoplasms -- metabolism
KW - Anticarcinogenic Agents -- pharmacology
KW - Carcinoma, Squamous Cell -- prevention & control
KW - Carcinoma, Squamous Cell -- metabolism
KW - Signal Transduction
KW - NF-kappa B -- metabolism
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1562430931?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oral+oncology&rft.atitle=Chemoprevention+of+head+and+neck+squamous+cell+carcinoma+through+inhibition+of+NF-%CE%BAB+signaling.&rft.au=Vander+Broek%2C+Robert%3BSnow%2C+Grace+E%3BChen%2C+Zhong%3BVan+Waes%2C+Carter&rft.aulast=Vander+Broek&rft.aufirst=Robert&rft.date=2014-10-01&rft.volume=50&rft.issue=10&rft.spage=930&rft.isbn=&rft.btitle=&rft.title=Oral+oncology&rft.issn=1879-0593&rft_id=info:doi/10.1016%2Fj.oraloncology.2013.10.005
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-05-26
N1 - Date created - 2014-09-15
N1 - Date revised - 2017-01-14
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Mutat Res. 2001 Sep 20;496(1-2):181-90 [11551494]
J Biol Chem. 2001 Sep 28;276(39):36530-4 [11479302]
Anticancer Res. 2001 Jul-Aug;21(4B):2895-900 [11712783]
Annu Rev Pharmacol Toxicol. 2002;42:25-54 [11807163]
Nutr Cancer. 2001;40(2):125-33 [11962247]
Int J Cancer. 2002 Jun 1;99(4):538-48 [11992543]
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Carcinogenesis. 2002 Sep;23(9):1511-8 [12189195]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.oraloncology.2013.10.005
ER -
TY - JOUR
T1 - Chronic treatment with novel brain-penetrating selective NOP receptor agonist MT-7716 reduces alcohol drinking and seeking in the rat.
AN - 1562430826; 24863033
AB - Since its discovery, the nociceptin/orphanin FQ (N/OFQ)-NOP receptor system has been extensively investigated as a promising target to treat alcoholism. Encouraging results obtained with the endogenous ligand N/OFQ stimulated research towards the development of novel brain-penetrating NOP receptor agonists with a pharmacological and toxicological profile compatible with clinical development. Here we describe the biochemical and alcohol-related behavioral effects of the novel NOP receptor agonist MT-7716. MT-7716 has high affinity for human NOP receptors expressed in HEK293 cells with a Ki value of 0.21 nM. MT-7716 concentration-dependently stimulated GTPγ(35)S binding with an EC50 value of 0.30 nM and its efficacy was similar to N/OFQ, suggesting that MT7716 is a full agonist at NOP receptors. In the two bottle choice test MT-7716 (0, 0.3, 1, and 3 mg/kg, bid) given orally for 14 days dose-dependently decreased voluntary alcohol intake in Marchigian Sardinian rats. The effect became gradually stronger following repeated administration, and was still significant 1 week after discontinuation of the drug. Oral naltrexone (30 mg/kg, bid) for 14 days also reduced ethanol intake; however, the effect decreased over the treatment period and rapidly disappeared when drug treatment was discontinued. MT-7716 is also effective for preventing reinstatement caused by both ethanol-associated environmental stimuli and stress. Finally, to investigate the effect of MT-7716 on alcohol withdrawal symptoms, Wistar rats were withdrawn from a 7-day alcohol liquid diet. MT-7716 significantly attenuated somatic alcohol withdrawal symptoms. Together these findings indicate that MT-7716 is a promising candidate for alcoholism treatment remaining effective with chronic administration.
JF - Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology
AU - Ciccocioppo, Roberto
AU - Stopponi, Serena
AU - Economidou, Daina
AU - Kuriyama, Makoto
AU - Kinoshita, Hiroshi
AU - Heilig, Markus
AU - Roberto, Marisa
AU - Weiss, Friedbert
AU - Teshima, Koji
AD - Pharmacology Unit, School of Pharmacy, University of Camerino, Camerino, Italy. ; Department II (CNS), Pharmacology Research Laboratories I, Research Division, Mitsubishi Tanabe Pharma Corporation, Yokohama, Japan. ; Laboratory of Clinical and Translational Studies, National Institute of Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA. ; Committee on the Neurobiology of Addictive Disorders, The Scripps Research Institute, La Jolla, CA, USA. ; Department of Molecular and Cellular Neuroscience, The Scripps Research Institute, La Jolla, CA, USA.
Y1 - 2014/10//
PY - 2014
DA - October 2014
SP - 2601
EP - 2610
VL - 39
IS - 11
KW - 2-(3-(1-(acenaphthen-1-yl)piperidin-4-yl)-2-oxo-2,3-dihydro-1H-benzimidazol-1-yl)-N-methylacetamide
KW - 0
KW - Acenaphthenes
KW - Alcohol Deterrents
KW - Benzimidazoles
KW - Narcotic Antagonists
KW - Opioid Peptides
KW - Receptors, Opioid
KW - nociceptin receptor
KW - Naltrexone
KW - 5S6W795CQM
KW - nociceptin
KW - 7AYI9N34FF
KW - Index Medicus
KW - Animals
KW - Substance Withdrawal Syndrome -- physiopathology
KW - Dose-Response Relationship, Drug
KW - HEK293 Cells
KW - Humans
KW - Rats
KW - Choice Behavior -- drug effects
KW - Choice Behavior -- physiology
KW - Naltrexone -- pharmacology
KW - Rats, Wistar
KW - Substance Withdrawal Syndrome -- drug therapy
KW - Narcotic Antagonists -- pharmacology
KW - Male
KW - Opioid Peptides -- metabolism
KW - Stress, Psychological -- complications
KW - Receptors, Opioid -- agonists
KW - Drug-Seeking Behavior -- drug effects
KW - Acenaphthenes -- pharmacology
KW - Alcohol Drinking -- drug therapy
KW - Receptors, Opioid -- metabolism
KW - Benzimidazoles -- pharmacology
KW - Alcohol Drinking -- physiopathology
KW - Alcohol Deterrents -- pharmacology
KW - Drug-Seeking Behavior -- physiology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuropsychopharmacology+%3A+official+publication+of+the+American+College+of+Neuropsychopharmacology&rft.atitle=Chronic+treatment+with+novel+brain-penetrating+selective+NOP+receptor+agonist+MT-7716+reduces+alcohol+drinking+and+seeking+in+the+rat.&rft.au=Ciccocioppo%2C+Roberto%3BStopponi%2C+Serena%3BEconomidou%2C+Daina%3BKuriyama%2C+Makoto%3BKinoshita%2C+Hiroshi%3BHeilig%2C+Markus%3BRoberto%2C+Marisa%3BWeiss%2C+Friedbert%3BTeshima%2C+Koji&rft.aulast=Ciccocioppo&rft.aufirst=Roberto&rft.date=2014-10-01&rft.volume=39&rft.issue=11&rft.spage=2601&rft.isbn=&rft.btitle=&rft.title=Neuropsychopharmacology+%3A+official+publication+of+the+American+College+of+Neuropsychopharmacology&rft.issn=1740-634X&rft_id=info:doi/10.1038%2Fnpp.2014.113
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-06-15
N1 - Date created - 2014-09-15
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1038/npp.2014.113
ER -
TY - JOUR
T1 - PPARγ in head and neck cancer prevention.
AN - 1562430628; 24434068
AB - Head and neck cancer is a major source of morbidity and mortality worldwide. Intervention during the early phases of carcinogenesis represents a promising new strategy for curbing the devastating effects of this disease and its primary treatment modalities, surgery and radiation with or without concomitant chemotherapy. This review focuses on the peroxisome proliferator-activated receptor gamma (PPARγ) as a target for chemoprevention of oral cancer. Accumulating data suggest that ligands of PPARγ, which include the thiazolidinedione class of agents approved for the treatment of diabetes, inhibit cancer cell growth in vitro and in animal carcinogenesis models, providing the rationale for testing this approach in populations at risk for head and neck cancer.
Published by Elsevier Ltd.
JF - Oral oncology
AU - Burotto, Mauricio
AU - Szabo, Eva
AD - Medical Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, United States. ; Lung and Upper Aerodigestive Cancer Research Group, Division of Cancer Prevention, National Cancer Institute, National Institutes of Health, United States. Electronic address: szaboe@mail.nih.gov.
Y1 - 2014/10//
PY - 2014
DA - October 2014
SP - 924
EP - 929
VL - 50
IS - 10
KW - PPAR gamma
KW - 0
KW - Thiazolidinediones
KW - pioglitazone
KW - X4OV71U42S
KW - Index Medicus
KW - Pioglitazone
KW - Head and neck cancer
KW - PPARγ (peroxisome proliferator-activated receptor γ)
KW - Oral carcinoma
KW - Evidence-Based Medicine
KW - Humans
KW - Thiazolidinediones -- pharmacology
KW - Disease Progression
KW - Clinical Trials as Topic
KW - Head and Neck Neoplasms -- prevention & control
KW - PPAR gamma -- drug effects
KW - Head and Neck Neoplasms -- pathology
KW - PPAR gamma -- physiology
KW - Precancerous Conditions -- pathology
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1562430628?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oral+oncology&rft.atitle=PPAR%CE%B3+in+head+and+neck+cancer+prevention.&rft.au=Burotto%2C+Mauricio%3BSzabo%2C+Eva&rft.aulast=Burotto&rft.aufirst=Mauricio&rft.date=2014-10-01&rft.volume=50&rft.issue=10&rft.spage=924&rft.isbn=&rft.btitle=&rft.title=Oral+oncology&rft.issn=1879-0593&rft_id=info:doi/10.1016%2Fj.oraloncology.2013.12.020
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-05-26
N1 - Date created - 2014-09-15
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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Lancet Oncol. 2004 Jul;5(7):419-29 [15231248]
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Cancer Epidemiol Biomarkers Prev. 2009 Feb;18(2):541-50 [19190158]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.oraloncology.2013.12.020
ER -
TY - JOUR
T1 - 2-[5-Selenocyanato-pentyl]-6-amino-benzo[de]isoquinoline-1,3-dione inhibits angiogenesis, induces p53 dependent mitochondrial apoptosis and enhances therapeutic efficacy of cyclophosphamide.
AN - 1562426638; 25038569
AB - The present study embodies a detailed investigation of the chemoenhancement property of a synthetic organoselenium compound, 2-[5-selenocyanato-pentyl]-7-amino benzo[de]isoquinoline-1,3-dione (ANOS) in tumor bearing Swiss albino mice. The results accumulated from this study illustrated that the administration of ANOS significantly potentiated the therapeutic efficacy of cyclophosphamide by reducing the tumor burden and chemotherapy induced toxicity in the host. Ability of ANOS in inducing apoptosis and inhibiting angiogenesis was thought to be the crucial effecter for enhancing the therapeutic efficacy of cyclophosphamide. Fluorescence microscopic study revealed that ANOS was capable of penetrating tumor cells and distributed in the subcellular compartments. We showed that ANOS-induced apoptosis, as evidenced by the TUNEL assay and cleavage of poly(ADP-ribose) polymerase (PARP), involved ROS production and DNA damage in tumor cells. ROS production subsequently activated p53 phosphorylation at Ser-15. This in turn activated cytochrome c (cyt c) release from mitochondria via Bcl-2 and Bax. Finally activation of caspase 3 led to PARP cleavage and apoptosis. These results suggested that p53 dependent mitochondrial pathway was playing an important role in ANOS induced apoptosis of tumor cells. Administration of ANOS also resulted in significant improvement of tumor vasculature and sprouting of the peritoneal cavity along with the normalization of MMP-9 level in serum and ascites fluid of tumor bearing mice. This potential antiangiogenic activity of ANOS also facilitated the therapeutic efficacy of the combination therapy. Furthermore, ANOS significantly suppressed cyclophosphamide-induced liver, hematopoietic and genetic damages. A concomitant decrease in drug-induced toxicity by ANOS might also have enhanced the efficacy of cyclophosphamide by improving the intrinsic defense machineries of the host. Copyright © 2014 Elsevier Masson SAS. All rights reserved.
JF - Biochimie
AU - Roy, Somnath Singha
AU - Chakraborty, Pramita
AU - Biswas, Jaydip
AU - Bhattacharya, Sudin
AD - Chittaranjan National Cancer Institute, Department of Cancer Chemoprevention, 37, S.P. Mukherjee Road, Kolkata 700 026, West Bengal, India. ; Chittaranjan National Cancer Institute, Department of Translational Research, 37, S.P. Mukherjee Road, Kolkata 700 026, West Bengal, India. ; Chittaranjan National Cancer Institute, Department of Cancer Chemoprevention, 37, S.P. Mukherjee Road, Kolkata 700 026, West Bengal, India. Electronic address: sudinb19572004@yahoo.co.in.
Y1 - 2014/10//
PY - 2014
DA - October 2014
SP - 137
EP - 148
VL - 105
KW - 2-(5-selenocyanato-pentyl)-6-amino-benzo(de)isoquinoline-1,3-dione
KW - 0
KW - Isoquinolines
KW - Organoselenium Compounds
KW - Proto-Oncogene Proteins c-bcl-2
KW - Reactive Oxygen Species
KW - Tumor Suppressor Protein p53
KW - Cyclophosphamide
KW - 8N3DW7272P
KW - isoquinoline
KW - JGX76Y85M6
KW - Index Medicus
KW - Apoptosis
KW - Mitochondrial pathway
KW - Angiogenesis
KW - Organoselenocyanate
KW - Reactive Oxygen Species -- metabolism
KW - Animals
KW - Humans
KW - Mitochondria -- drug effects
KW - Apoptosis -- drug effects
KW - Mice
KW - Drug Synergism
KW - DNA Damage -- drug effects
KW - Cyclophosphamide -- administration & dosage
KW - Cyclophosphamide -- chemistry
KW - Organoselenium Compounds -- administration & dosage
KW - Neovascularization, Pathologic -- metabolism
KW - Neoplasms, Experimental -- metabolism
KW - Neoplasms, Experimental -- pathology
KW - Tumor Suppressor Protein p53 -- metabolism
KW - Neovascularization, Pathologic -- pathology
KW - Isoquinolines -- chemistry
KW - Neovascularization, Pathologic -- drug therapy
KW - Neoplasms, Experimental -- drug therapy
KW - Isoquinolines -- administration & dosage
KW - Organoselenium Compounds -- chemistry
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochimie&rft.atitle=2-%5B5-Selenocyanato-pentyl%5D-6-amino-benzo%5Bde%5Disoquinoline-1%2C3-dione+inhibits+angiogenesis%2C+induces+p53+dependent+mitochondrial+apoptosis+and+enhances+therapeutic+efficacy+of+cyclophosphamide.&rft.au=Roy%2C+Somnath+Singha%3BChakraborty%2C+Pramita%3BBiswas%2C+Jaydip%3BBhattacharya%2C+Sudin&rft.aulast=Roy&rft.aufirst=Somnath&rft.date=2014-10-01&rft.volume=105&rft.issue=&rft.spage=137&rft.isbn=&rft.btitle=&rft.title=Biochimie&rft.issn=1638-6183&rft_id=info:doi/10.1016%2Fj.biochi.2014.07.010
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-05-29
N1 - Date created - 2014-09-13
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.biochi.2014.07.010
ER -
TY - JOUR
T1 - Methamphetamine and amphetamine isomer concentrations in human urine following controlled Vicks VapoInhaler administration.
AN - 1561978911; 25217541
AB - Legitimate use of legal intranasal decongestants containing l-methamphetamine may complicate interpretation of urine drug tests positive for amphetamines. Our study hypotheses were that commonly used immunoassays would produce no false-positive results and a recently developed enantiomer-specific gas chromatography-mass spectrometry (GC-MS) procedure would find no d-amphetamine or d-methamphetamine in urine following controlled Vicks VapoInhaler administration at manufacturer's recommended doses. To evaluate these hypotheses, 22 healthy adults were each administered one dose (two inhalations in each nostril) of a Vicks VapoInhaler every 2 h for 10 h on Day 1 (six doses), followed by a single dose on Day 2. Every urine specimen was collected as an individual void for 32 h after the first dose and assayed for d- and l-amphetamines specific isomers with a GC-MS method with >99% purity of R-(-)-α-methoxy-α-(trifluoromethyl)phenylacetyl derivatives and 10 µg/L lower limits of quantification. No d-methamphetamine or d-amphetamine was detected in any urine specimen by GC-MS. The median l-methamphetamine maximum concentration was 62.8 µg/L (range: 11.0-1,440). Only two subjects had detectable l-amphetamine, with maximum concentrations coinciding with l-methamphetamine peak levels, and always ≤ 4% of the parent's maximum. Three commercial immunoassays for amphetamines EMIT(®) II Plus, KIMS(®) II and DRI(®) had sensitivities, specificities and efficiencies of 100, 97.8, 97.8; 100, 99.6, 99.6 and 100, 100, 100%, respectively. The immunoassays had high efficiencies, but our first hypothesis was not affirmed. The EMIT(®) II Plus assay produced 2.2% false-positive results, requiring an enantiomer-specific confirmation.
Published by Oxford University Press 2014. This work is written by (a) US Government employee(s) and is in the public domain in the US.
JF - Journal of analytical toxicology
AU - Smith, Michael L
AU - Nichols, Daniel C
AU - Underwood, Paula
AU - Fuller, Zachary
AU - Moser, Matthew A
AU - Flegel, Ron
AU - Gorelick, David A
AU - Newmeyer, Matthew N
AU - Concheiro, Marta
AU - Huestis, Marilyn A
AD - U.S. Army Forensic Toxicology Drug Testing Laboratory, Fort Meade, MD, USA. ; Division of Workplace Programs, Department of Health and Human Services, Substance Abuse Mental Health Services Administration, Rockville, MD, USA. ; Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, 251 Bayview Blvd., Suite 200 Room 05A-721, Baltimore, MD 21224, USA Department of Psychiatry, University of Maryland School of Medicine, Baltimore, MD, USA. ; Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, 251 Bayview Blvd., Suite 200 Room 05A-721, Baltimore, MD 21224, USA Program in Toxicology, University of Maryland Baltimore, Baltimore, MD, USA. ; Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, 251 Bayview Blvd., Suite 200 Room 05A-721, Baltimore, MD 21224, USA. ; Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, 251 Bayview Blvd., Suite 200 Room 05A-721, Baltimore, MD 21224, USA mhuestis@intra.nida.nih.gov.
Y1 - 2014/10//
PY - 2014
DA - October 2014
SP - 524
EP - 527
VL - 38
IS - 8
KW - Methamphetamine
KW - 44RAL3456C
KW - Creatinine
KW - AYI8EX34EU
KW - Amphetamine
KW - CK833KGX7E
KW - Index Medicus
KW - Sensitivity and Specificity
KW - Young Adult
KW - Stereoisomerism
KW - Creatinine -- urine
KW - Dose-Response Relationship, Drug
KW - Humans
KW - Specimen Handling
KW - Aged
KW - Substance Abuse Detection -- methods
KW - False Positive Reactions
KW - Immunoassay -- methods
KW - Adult
KW - Gas Chromatography-Mass Spectrometry
KW - Middle Aged
KW - Healthy Volunteers
KW - Administration, Inhalation
KW - Adolescent
KW - Male
KW - Female
KW - Methamphetamine -- urine
KW - Amphetamine -- urine
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-06-05
N1 - Date created - 2014-09-13
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Clin Chem. 1977 Aug;23(8):1504 [872410]
BMC Clin Pharmacol. 2008;8:4 [18644153]
J Anal Toxicol. 2004 Sep;28(6):449-55 [15516295]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/jat/bku077
ER -
TY - JOUR
T1 - A case-control study of occupational exposure to metalworking fluids and bladder cancer risk among men.
AN - 1561130152; 25201311
AB - Metalworking has been associated with an excess risk of bladder cancer in over 20 studies. Metalworking fluids (MWFs) are suspected as the responsible exposure, but epidemiological data are limited. We investigated this association among men in the New England Bladder Cancer Study using state-of-the-art, quantitative exposure assessment methods.
Cases (n=895) and population controls (n=1031) provided occupational histories during personal interviews. For selected jobs, exposure-oriented modules were administered to collect information on use of three MWF types: (1) straight (mineral oil, additives), (2) soluble (mineral oil, water, additives) and (3) synthetic (water, organics, additives) or semisynthetic (hybrid of soluble and synthetic). We computed ORs and 95% CIs relating bladder cancer risk to a variety of exposure metrics, adjusting for smoking and other factors. Non-metalworkers who had held jobs with possible exposure to mineral oil were analysed separately. Bladder cancer risk was elevated among men who reported using straight MWFs (OR=1.7, 95% CI 1.1 to 2.8); risk increased monotonically with increasing cumulative exposure (p=0.041). Use of soluble MWFs was associated with a 50% increased risk (95% CI 0.96 to 2.5). ORs were non-significantly elevated for synthetic/semisynthetic MWFs based on a small number of exposed men. Non-metalworkers holding jobs with possible exposure to mineral oil had a 40% increased risk (95% CI 1.1 to 1.8).
Exposure to straight MWFs was associated with a significantly increased bladder cancer risk, as was employment in non-metalworking jobs with possible exposure to mineral oil. These findings strengthen prior evidence for mineral oil as a bladder carcinogen. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
JF - Occupational and environmental medicine
AU - Colt, Joanne S
AU - Friesen, Melissa C
AU - Stewart, Patricia A
AU - Donguk, Park
AU - Johnson, Alison
AU - Schwenn, Molly
AU - Karagas, Margaret R
AU - Armenti, Karla
AU - Waddell, Richard
AU - Verrill, Castine
AU - Ward, Mary H
AU - Freeman, Laura E Beane
AU - Moore, Lee E
AU - Koutros, Stella
AU - Baris, Dalsu
AU - Silverman, Debra T
AD - Department of Health and Human Services, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA. ; Department of Health and Human Services, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA Stewart Exposure Assessments, LLC, Arlington, Virginia, USA. ; Korea National Open University, Seoul, Korea. ; Vermont Cancer Registry, Burlington, Vermont, USA. ; Maine Cancer Registry, Augusta, Maine, USA. ; Geisel School of Medicine at Dartmouth, Hanover, New Hampshire, USA. ; New Hampshire Department of Health and Human Services, Concord, New Hampshire, USA.
Y1 - 2014/10//
PY - 2014
DA - October 2014
SP - 667
EP - 674
VL - 71
IS - 10
KW - Index Medicus
KW - Risk Factors
KW - Humans
KW - Adult
KW - Case-Control Studies
KW - Aged
KW - Middle Aged
KW - New England -- epidemiology
KW - Male
KW - Occupational Exposure
KW - Urinary Bladder Neoplasms -- epidemiology
KW - Metallurgy
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Occupational+and+environmental+medicine&rft.atitle=A+case-control+study+of+occupational+exposure+to+metalworking+fluids+and+bladder+cancer+risk+among+men.&rft.au=Colt%2C+Joanne+S%3BFriesen%2C+Melissa+C%3BStewart%2C+Patricia+A%3BDonguk%2C+Park%3BJohnson%2C+Alison%3BSchwenn%2C+Molly%3BKaragas%2C+Margaret+R%3BArmenti%2C+Karla%3BWaddell%2C+Richard%3BVerrill%2C+Castine%3BWard%2C+Mary+H%3BFreeman%2C+Laura+E+Beane%3BMoore%2C+Lee+E%3BKoutros%2C+Stella%3BBaris%2C+Dalsu%3BSilverman%2C+Debra+T&rft.aulast=Colt&rft.aufirst=Joanne&rft.date=2014-10-01&rft.volume=71&rft.issue=10&rft.spage=667&rft.isbn=&rft.btitle=&rft.title=Occupational+and+environmental+medicine&rft.issn=1470-7926&rft_id=info:doi/10.1136%2Foemed-2013-102056
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-12-29
N1 - Date created - 2014-09-09
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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Am J Ind Med. 2011 Jun;54(6):450-60 [21328414]
IARC Monogr Eval Carcinog Risks Hum. 2013;101:9-549 [24772663]
Am J Ind Med. 2014 Aug;57(8):915-27 [25060071]
J Occup Environ Hyg. 2014;11(11):757-70 [25256317]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1136/oemed-2013-102056
ER -
TY - JOUR
T1 - Functional selectivity of allosteric interactions within G protein-coupled receptor oligomers: the dopamine D1-D3 receptor heterotetramer.
AN - 1561035527; 25097189
AB - The dopamine D1 receptor-D3 receptor (D1R-D3R) heteromer is being considered as a potential therapeutic target for neuropsychiatric disorders. Previous studies suggested that this heteromer could be involved in the ability of D3R agonists to potentiate locomotor activation induced by D1R agonists. It has also been postulated that its overexpression plays a role in L-dopa-induced dyskinesia and in drug addiction. However, little is known about its biochemical properties. By combining bioluminescence resonance energy transfer, bimolecular complementation techniques, and cell-signaling experiments in transfected cells, evidence was obtained for a tetrameric stoichiometry of the D1R-D3R heteromer, constituted by two interacting D1R and D3R homodimers coupled to Gs and Gi proteins, respectively. Coactivation of both receptors led to the canonical negative interaction at the level of adenylyl cyclase signaling, to a strong recruitment of β-arrestin-1, and to a positive cross talk of D1R and D3R agonists at the level of mitogen-activated protein kinase (MAPK) signaling. Furthermore, D1R or D3R antagonists counteracted β-arrestin-1 recruitment and MAPK activation induced by D3R and D1R agonists, respectively (cross-antagonism). Positive cross talk and cross-antagonism at the MAPK level were counteracted by specific synthetic peptides with amino acid sequences corresponding to D1R transmembrane (TM) domains TM5 and TM6, which also selectively modified the quaternary structure of the D1R-D3R heteromer, as demonstrated by complementation of hemiproteins of yellow fluorescence protein fused to D1R and D3R. These results demonstrate functional selectivity of allosteric modulations within the D1R-D3R heteromer, which can be involved with the reported behavioral synergism of D1R and D3R agonists. U.S. Government work not protected by U.S. copyright.
JF - Molecular pharmacology
AU - Guitart, Xavier
AU - Navarro, Gemma
AU - Moreno, Estefania
AU - Yano, Hideaki
AU - Cai, Ning-Sheng
AU - Sánchez-Soto, Marta
AU - Kumar-Barodia, Sandeep
AU - Naidu, Yamini T
AU - Mallol, Josefa
AU - Cortés, Antoni
AU - Lluís, Carme
AU - Canela, Enric I
AU - Casadó, Vicent
AU - McCormick, Peter J
AU - Ferré, Sergi
AD - National Institute on Drug Abuse, Intramural Research Program, National Institutes of Health, Department of Health and Human Services, Baltimore, Maryland (X.G., H.Y., N.-S.C., M.S.-S., S.K.-B., Y.T.N., S.F.); Centro de Investigación Biomédica en Red Sobre Enfermedades Neurodegenerativas and Department of Biochemistry and Molecular Biology, Faculty of Biology, University of Barcelona, Barcelona, Spain (G.N., E.M., J.M., A.C., C.L., E.I.C., V.C., P.J.M.); and School of Pharmacy, University of East Anglia, Norwich, United Kingdom (P.J.M.). ; National Institute on Drug Abuse, Intramural Research Program, National Institutes of Health, Department of Health and Human Services, Baltimore, Maryland (X.G., H.Y., N.-S.C., M.S.-S., S.K.-B., Y.T.N., S.F.); Centro de Investigación Biomédica en Red Sobre Enfermedades Neurodegenerativas and Department of Biochemistry and Molecular Biology, Faculty of Biology, University of Barcelona, Barcelona, Spain (G.N., E.M., J.M., A.C., C.L., E.I.C., V.C., P.J.M.); and School of Pharmacy, University of East Anglia, Norwich, United Kingdom (P.J.M.) sferre@intra.nida.nih.gov.
Y1 - 2014/10//
PY - 2014
DA - October 2014
SP - 417
EP - 429
VL - 86
IS - 4
KW - ARRB1 protein, human
KW - 0
KW - Arrestins
KW - DRD1 protein, human
KW - DRD3 protein, human
KW - Dopamine Agonists
KW - Receptors, Dopamine D1
KW - Receptors, Dopamine D3
KW - beta-Arrestin 1
KW - beta-Arrestins
KW - GTP-Binding Protein alpha Subunits, Gi-Go
KW - EC 3.6.5.1
KW - GTP-Binding Protein alpha Subunits, Gs
KW - Adenylyl Cyclases
KW - EC 4.6.1.1
KW - Index Medicus
KW - GTP-Binding Protein alpha Subunits, Gi-Go -- metabolism
KW - MAP Kinase Signaling System
KW - Dopamine Agonists -- pharmacology
KW - Humans
KW - HEK293 Cells
KW - Adenylyl Cyclases -- metabolism
KW - Allosteric Regulation
KW - GTP-Binding Protein alpha Subunits, Gs -- metabolism
KW - Protein Multimerization
KW - Protein Binding
KW - Arrestins -- metabolism
KW - Receptors, Dopamine D3 -- agonists
KW - Receptors, Dopamine D3 -- metabolism
KW - Receptors, Dopamine D1 -- agonists
KW - Receptors, Dopamine D1 -- chemistry
KW - Receptors, Dopamine D3 -- chemistry
KW - Allosteric Site
KW - Receptors, Dopamine D1 -- metabolism
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-11-07
N1 - Date created - 2014-09-06
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
J Neurosci. 2002 Sep 15;22(18):7931-40 [12223546]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1124/mol.114.093096
ER -
TY - JOUR
T1 - Promiscuous and specific recognition among ephrins and Eph receptors.
AN - 1561032653; 25017878
AB - Eph-ephrin interactions control the signal transduction between cells and play an important role in carcinogenesis and other diseases. The interactions between Eph receptors and ephrins of the same subclass are promiscuous; there are cross-interactions between some subclasses, but not all. To understand how Eph-ephrin interactions can be both promiscuous and specific, we investigated sixteen energy landscapes of four Eph receptors (A2, A4, B2, and B4) interacting with four ephrin ligands (A1, A2, A5, and B2). We generated conformational ensembles and recognition energy landscapes starting from separated Eph and ephrin molecules and proceeding up to the formation of Eph-ephrin complexes. Analysis of the Eph-ephrin recognition trajectories and the co-evolution entropy of 400 ligand binding domains of Eph receptor and 241 ephrin ligands identified conserved residues during the recognition process. Our study correctly predicted the promiscuity and specificity of the interactions and provided insights into their recognition. The dynamic conformational changes during Eph-ephrin recognition can be described by progressive conformational selection and population shift events, with two dynamic salt bridges between EphB4 and ephrin-B2 contributing to the specific recognition. EphA3 cancer-related mutations lowered the binding energies. The specificity is not only controlled by the final stage of the interaction across the protein-protein interface, but also has large contributions from binding kinetics with the help of dynamic intermediates along the pathway from the separated Eph and ephrin to the Eph-ephrin complex.
Copyright © 2014 Elsevier B.V. All rights reserved.
JF - Biochimica et biophysica acta
AU - Dai, Dandan
AU - Huang, Qiang
AU - Nussinov, Ruth
AU - Ma, Buyong
AD - State Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai 200433, China. ; State Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai 200433, China. Electronic address: huangqiang@fudan.edu.cn. ; Basic Science Program, Leidos Biomedical Research, Inc., Cancer and Inflammation Program, National Cancer Institute, Frederick, MD 21702, USA; Sackler Inst. of Molecular Medicine, Department of Human Genetics and Molecular Medicine, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel. ; Basic Science Program, Leidos Biomedical Research, Inc., Cancer and Inflammation Program, National Cancer Institute, Frederick, MD 21702, USA. Electronic address: mabuyong@mail.nih.gov.
Y1 - 2014/10//
PY - 2014
DA - October 2014
SP - 1729
EP - 1740
VL - 1844
IS - 10
SN - 0006-3002, 0006-3002
KW - Index Medicus
KW - Energy landscape
KW - Protein–protein interaction
KW - Induced fit
KW - Conformational selection
KW - Eph receptor tyrosine kinase
KW - Conformational dynamics
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date created - 2014-09-08
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.bbapap.2014.07.002
ER -
TY - JOUR
T1 - Gcn5 and PCAF regulate PPARγ and Prdm16 expression to facilitate brown adipogenesis.
AN - 1560584330; 25071153
AB - The acetyltransferase Gcn5 is critical for embryogenesis and shows partial functional redundancy with its homolog PCAF. However, the tissue- and cell lineage-specific functions of Gcn5 and PCAF are still not well defined. Here we probe the functions of Gcn5 and PCAF in adipogenesis. We found that the double knockout (DKO) of Gcn5/PCAF inhibits expression of the master adipogenic transcription factor gene PPARγ, thereby preventing adipocyte differentiation. The adipogenesis defects in Gcn5/PCAF DKO cells are rescued by ectopic expression of peroxisome proliferator-activated receptor γ (PPARγ), suggesting Gcn5/PCAF act upstream of PPARγ to facilitate adipogenesis. The requirement of Gcn5/PCAF for PPARγ expression was unexpectedly bypassed by prolonged treatment with an adipogenic inducer, 3-isobutyl-1-methylxanthine (IBMX). However, neither PPARγ ectopic expression nor prolonged IBMX treatment rescued defects in Prdm16 expression in DKO cells, indicating that Gcn5/PCAF are essential for normal Prdm16 expression. Gcn5/PCAF regulate PPARγ and Prdm16 expression at different steps in the transcription process, facilitating RNA polymerase II recruitment to Prdm16 and elongation of PPARγ transcripts. Overall, our study reveals that Gcn5/PCAF facilitate adipogenesis through regulation of PPARγ expression and regulate brown adipogenesis by influencing Prdm16 expression.
Copyright © 2014, American Society for Microbiology. All Rights Reserved.
JF - Molecular and cellular biology
AU - Jin, Qihuang
AU - Wang, Chaochen
AU - Kuang, Xianghong
AU - Feng, Xuesong
AU - Sartorelli, Vittorio
AU - Ying, Hao
AU - Ge, Kai
AU - Dent, Sharon Y R
AD - Department of Molecular Carcinogenesis, Center for Cancer Epigenetics, The University of Texas M. D. Anderson Cancer Center, Smithville, Texas, USA Laboratory of Endocrinology and Receptor Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA. ; Laboratory of Endocrinology and Receptor Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA. ; Department of Molecular Carcinogenesis, Center for Cancer Epigenetics, The University of Texas M. D. Anderson Cancer Center, Smithville, Texas, USA. ; Laboratory of Muscle Stem Cells and Gene Regulation, National Institute of Arthritis, Musculoskeletal, and Skin Diseases, National Institutes of Health, Bethesda, Maryland, USA. ; Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China. ; Laboratory of Endocrinology and Receptor Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA kaig@niddk.nih.gov sroth@mdanderson.org. ; Department of Molecular Carcinogenesis, Center for Cancer Epigenetics, The University of Texas M. D. Anderson Cancer Center, Smithville, Texas, USA kaig@niddk.nih.gov sroth@mdanderson.org.
Y1 - 2014/10/01/
PY - 2014
DA - 2014 Oct 01
SP - 3746
EP - 3753
VL - 34
IS - 19
KW - DNA-Binding Proteins
KW - 0
KW - PPAR gamma
KW - Phosphodiesterase Inhibitors
KW - Prdm16 protein, mouse
KW - Transcription Factors
KW - p300-CBP Transcription Factors
KW - EC 2.3.1.48
KW - RNA Polymerase III
KW - EC 2.7.7.6
KW - 1-Methyl-3-isobutylxanthine
KW - TBT296U68M
KW - Index Medicus
KW - Phosphodiesterase Inhibitors -- pharmacology
KW - Animals
KW - RNA Polymerase III -- physiology
KW - Catalytic Domain
KW - Mice
KW - Gene Expression Regulation
KW - 1-Methyl-3-isobutylxanthine -- pharmacology
KW - Models, Biological
KW - Adipocytes, Brown -- drug effects
KW - Transcription Factors -- metabolism
KW - p300-CBP Transcription Factors -- metabolism
KW - DNA-Binding Proteins -- genetics
KW - p300-CBP Transcription Factors -- genetics
KW - PPAR gamma -- metabolism
KW - Transcription Factors -- genetics
KW - Adipogenesis -- drug effects
KW - PPAR gamma -- genetics
KW - DNA-Binding Proteins -- metabolism
KW - Adipocytes, Brown -- metabolism
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1560584330?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+and+cellular+biology&rft.atitle=Gcn5+and+PCAF+regulate+PPAR%CE%B3+and+Prdm16+expression+to+facilitate+brown+adipogenesis.&rft.au=Jin%2C+Qihuang%3BWang%2C+Chaochen%3BKuang%2C+Xianghong%3BFeng%2C+Xuesong%3BSartorelli%2C+Vittorio%3BYing%2C+Hao%3BGe%2C+Kai%3BDent%2C+Sharon+Y+R&rft.aulast=Jin&rft.aufirst=Qihuang&rft.date=2014-10-01&rft.volume=34&rft.issue=19&rft.spage=3746&rft.isbn=&rft.btitle=&rft.title=Molecular+and+cellular+biology&rft.issn=1098-5549&rft_id=info:doi/10.1128%2FMCB.00622-14
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-11-11
N1 - Date created - 2014-09-06
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
EMBO Rep. 2009 Sep;10(9):1009-14 [19633696]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1128/MCB.00622-14
ER -
TY - JOUR
T1 - Cholinergic immunotoxin 192 IgG-SAPORIN alters subicular theta-gamma activity and impairs spatial learning in rats.
AN - 1556290320; 24907423
AB - Subiculum is an important structure of hippocampal formation and is a part of intra hippocampal network involved in spatial information processing. However, relatively very few studies are available in literature demonstrating the explicit role of subiculum in spatial information processing. The present study investigated the cholinergic modulation of subicular theta-gamma activity on spatial learning and memory functions in rats. The cholinergic projections to ventral subiculum were selectively eliminated using 192 IgG-SAPORIN. Eliminations of cholinergic inputs to ventral subiculum significantly reduced the subicular theta and enhanced the gamma activity during active wake and REM sleep states. In addition, the spatial learning was severely impaired following cholinergic elimination of ventral subiculum. The ChAT immunocytochemical studies showed sparse distribution of cholinergic fibers in the ventral subiculum confirming the cholinergic elimination to ventral subiculum. Cholinotoxic infusions to ventral subiculum did not alter the hippocampal cholinergic innervations and retained the hippocampal theta and gamma activities. The present findings support that cholinergic modulation of subicular theta-gamma oscillations is crucial for spatial information processing.
Copyright © 2014 Elsevier Inc. All rights reserved.
JF - Neurobiology of learning and memory
AU - Rastogi, Shweta
AU - Unni, Sumithra
AU - Sharma, Sumit
AU - Laxmi, T Rao
AU - Kutty, Bindu M
AD - Department of Neurophysiology, National Institute of Mental Health and Neurosciences (NIMHANS), Bangalore, India. ; Forensic and Medical Systems, Axxonet Systems Technologies Pvt. Ltd., Bangalore, India. ; Department of Neurophysiology, National Institute of Mental Health and Neurosciences (NIMHANS), Bangalore, India. Electronic address: bindu.nimhans@gmail.com.
Y1 - 2014/10//
PY - 2014
DA - October 2014
SP - 117
EP - 126
VL - 114
KW - 192 IgG-saporin
KW - 0
KW - Antibodies, Monoclonal
KW - Immunotoxins
KW - Ribosome Inactivating Proteins, Type 1
KW - Choline O-Acetyltransferase
KW - EC 2.3.1.6
KW - Index Medicus
KW - Cholinotoxin
KW - Theta–gamma oscillations
KW - Cholinergic projections
KW - Spatial memory
KW - Ventral subiculum
KW - REM sleep
KW - Rats
KW - Animals
KW - Rats, Wistar
KW - Cholinergic Fibers -- drug effects
KW - Choline O-Acetyltransferase -- metabolism
KW - Male
KW - Cholinergic Fibers -- metabolism
KW - Spatial Learning -- drug effects
KW - Hippocampus -- metabolism
KW - Ribosome Inactivating Proteins, Type 1 -- pharmacology
KW - Antibodies, Monoclonal -- pharmacology
KW - Immunotoxins -- pharmacology
KW - Theta Rhythm -- drug effects
KW - Hippocampus -- drug effects
KW - Gamma Rhythm -- drug effects
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurobiology+of+learning+and+memory&rft.atitle=Cholinergic+immunotoxin+192+IgG-SAPORIN+alters+subicular+theta-gamma+activity+and+impairs+spatial+learning+in+rats.&rft.au=Rastogi%2C+Shweta%3BUnni%2C+Sumithra%3BSharma%2C+Sumit%3BLaxmi%2C+T+Rao%3BKutty%2C+Bindu+M&rft.aulast=Rastogi&rft.aufirst=Shweta&rft.date=2014-10-01&rft.volume=114&rft.issue=&rft.spage=117&rft.isbn=&rft.btitle=&rft.title=Neurobiology+of+learning+and+memory&rft.issn=1095-9564&rft_id=info:doi/10.1016%2Fj.nlm.2014.05.008
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-05-22
N1 - Date created - 2014-08-25
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.nlm.2014.05.008
ER -
TY - JOUR
T1 - The risk of amyotrophic lateral sclerosis after cancer in U.S. elderly adults: A population-based prospective study
AN - 1551622049; 20290577
AB - Although epidemiologic studies have examined the risk of amyotrophic lateral sclerosis (ALS) in relation to cancer, none have been large population-based studies using incident ALS and adjusting for medical surveillance. Addressing those limitations, all first primary cancer cases from the Surveillance, Epidemiology and End Results (SEER) Program (1992-2005), linked to Medicare claims data were used. Cases were followed from cancer diagnosis until the earliest date of ALS diagnosis, a break in Medicare claims data, death, age 85 or December 31, 2005. A comparison group from a 5% random Medicare sample in the SEER areas who were cancer-free and censored as above, or until a cancer diagnosis were selected. ALS outcomes were derived from medical claims. The proportional hazards models to estimate ALS hazard ratios (HRs), using age as the time scale, adjusting for sex, race and physician visits, and stratifying the baseline hazard on birth year and SEER registry were used. A total of 303 ALS cases were ascertained in cancer patients (2,154,062 person-years) compared with 246 ALS cases (2,467,634 person-years) in the reference population. There was no overall relationship between cancer and ALS (HR = 0.99; 95% CI = 0.81-1.22), nor by gender or race. Except for an elevated ALS risk in the first year after a leukemia diagnosis, the relationship between site-specific cancers and ALS was null after correcting for multiple comparisons. Having a cancer diagnosis was not associated with an overall risk of incident ALS. The short-term ALS risk after leukemia may reflect screening or reporting errors. What's new? Studies suggest that incident Parkinson's disease and Alzheimer's disease are inversely associated with cancer, but whether the same is true for amyotrophic lateral sclerosis (ALS), another neurodegenerative disease, remains unclear. Here, following examination of incident ALS risk after cancer in a large population-based study that controlled for medical surveillance, no overall association was found to exist between cancer and ALS risk. Heightened screening or reporting errors may be responsible for the detection of elevated ALS risk in the first year following leukemia diagnosis.
JF - International Journal of Cancer
AU - Freedman, DMichal
AU - Wu, Jincao
AU - Daugherty, Sarah E
AU - Kuncl, Ralph W
AU - Enewold, Lindsey R
AU - Pfeiffer, Ruth M
AD - U.S. Department of Health and Human Services, National Institutes of Health, National Cancer Institute, Division of Cancer Epidemiology and Genetics, 9609 Medical Center Drive, Rockville, MD.
Y1 - 2014/10//
PY - 2014
DA - Oct 2014
SP - 1745
EP - 1750
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 135
IS - 7
SN - 0020-7136, 0020-7136
KW - Risk Abstracts
KW - Health risks
KW - Leukemia
KW - Mortality
KW - Age
KW - Parkinson's disease
KW - Alzheimer's disease
KW - Gender
KW - Elderly
KW - Cancer
KW - R2 23060:Medical and environmental health
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551622049?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Cancer&rft.atitle=The+risk+of+amyotrophic+lateral+sclerosis+after+cancer+in+U.S.+elderly+adults%3A+A+population-based+prospective+study&rft.au=Freedman%2C+DMichal%3BWu%2C+Jincao%3BDaugherty%2C+Sarah+E%3BKuncl%2C+Ralph+W%3BEnewold%2C+Lindsey+R%3BPfeiffer%2C+Ruth+M&rft.aulast=Freedman&rft.aufirst=DMichal&rft.date=2014-10-01&rft.volume=135&rft.issue=7&rft.spage=1745&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.28795
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-08-01
N1 - Last updated - 2014-08-21
N1 - SubjectsTermNotLitGenreText - Mortality; Leukemia; Health risks; Age; Parkinson's disease; Gender; Alzheimer's disease; Elderly; Cancer
DO - http://dx.doi.org/10.1002/ijc.28795
ER -
TY - JOUR
T1 - Maternal smoking during pregnancy and infant stress response: test of a prenatal programming hypothesis.
AN - 1551025049; 24999830
AB - Maternal smoking during pregnancy (MSDP) is associated with early and long-term neurobehavioral deficits; however mechanisms remain unknown. We tested the hypothesis that MSDP programs the hypothalamic pituitary adrenocortical (HPA) axis of the offspring leading to adverse outcomes. In an intensive, prospective study, we investigated associations between MSDP and infant cortisol stress response and explored whether alterations in cortisol response were mediated by epigenetic modulation of the placental glucocorticoid receptor gene (NR3C1).
Participants were 100 healthy mother-infant pairs (53% MSDP-exposed; 42% female) from a low income, racially/ethnically diverse sample (55% minorities). MSDP was assessed by timeline followback interview verified by saliva and meconium cotinine. Infant cortisol responses to a neurobehavioral exam were assessed seven times over the first postnatal month. Methylation of placental NR3C1 promoter exon 1F was assessed using bisulfite pyrosequencing in a subsample (n=45). MSDP-exposed infants showed significantly and persistently attenuated basal and reactive cortisol levels over the first postnatal month vs. unexposed infants. Exploratory analyses revealed that MSDP was associated with altered methylation of the placental NR3C1 promoter; degree of methylation of the placental NR3C1 was associated with infant basal and reactive cortisol over the first postnatal month and mediated effects of MSDP on infant basal cortisol.
Results provide initial support for our hypothesis that MSDP programs offspring HPA (dys)regulation. Epigenetic regulation of placental GR may serve as a novel underlying mechanism. Results may have implications for delineating pathways to adverse outcomes from MSDP. Copyright © 2014 Elsevier Ltd. All rights reserved.
JF - Psychoneuroendocrinology
AU - Stroud, Laura R
AU - Papandonatos, George D
AU - Rodriguez, Daniel
AU - McCallum, Meaghan
AU - Salisbury, Amy L
AU - Phipps, Maureen G
AU - Lester, Barry
AU - Huestis, Marilyn A
AU - Niaura, Raymond
AU - Padbury, James F
AU - Marsit, Carmen J
AD - Department of Psychiatry and Human Behavior, Warren Alpert Medical School, Brown University, Providence, RI 02906, United States; Centers for Behavioral and Preventive Medicine, The Miriam Hospital, Providence, RI 02906, United States. Electronic address: Laura_Stroud@brown.edu. ; Department of Biostatistics, School of Public Health, Brown University, Providence, RI 02903, United States. ; Department of Public Health and Nutrition, School of Nursing and Health Sciences, La Salle University, Philadelphia, PA 19141, United States. ; Department of Psychology, Emory University, Atlanta, GA 30322, United States. ; Department of Psychiatry and Human Behavior, Warren Alpert Medical School, Brown University, Providence, RI 02906, United States; Department of Pediatrics, Warren Alpert Medical School, Brown University, Providence, RI 02903, United States; Women & Infants' Hospital of Rhode Island, Providence, RI 02905, United States. ; Women & Infants' Hospital of Rhode Island, Providence, RI 02905, United States; Department of Obstetrics and Gynecology, Warren Alpert Medical School, Brown University, Providence, RI 02905, United States. ; Chemistry and Drug Metabolism, Intramural Research Branch, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD 21224, United States. ; Schroeder Institute for Tobacco Research and Policy Studies, American Legacy Foundation, Washington, DC 20036, United States. ; Department of Pediatrics, Warren Alpert Medical School, Brown University, Providence, RI 02903, United States; Women & Infants' Hospital of Rhode Island, Providence, RI 02905, United States. ; Department of Pharmacology and Toxicology, Dartmouth University, Hanover, NH 03755, United States.
Y1 - 2014/10//
PY - 2014
DA - October 2014
SP - 29
EP - 40
VL - 48
KW - NR3C1 protein, human
KW - 0
KW - Receptors, Glucocorticoid
KW - Hydrocortisone
KW - WI4X0X7BPJ
KW - Index Medicus
KW - Infant
KW - Smoking
KW - Programming
KW - Placenta
KW - Cortisol
KW - Tobacco
KW - Stress
KW - NR3C1
KW - Epigenetic
KW - Pregnancy
KW - Young Adult
KW - Epigenesis, Genetic -- physiology
KW - DNA Methylation
KW - Humans
KW - Adult
KW - Infant, Newborn
KW - Case-Control Studies
KW - Hydrocortisone -- metabolism
KW - Placenta -- metabolism
KW - Adolescent
KW - Receptors, Glucocorticoid -- metabolism
KW - Receptors, Glucocorticoid -- genetics
KW - Female
KW - Smoking -- physiopathology
KW - Prenatal Exposure Delayed Effects -- metabolism
KW - Pregnancy Complications -- metabolism
KW - Prenatal Exposure Delayed Effects -- psychology
KW - Pregnancy Complications -- psychology
KW - Smoking -- metabolism
KW - Stress, Physiological -- genetics
KW - Smoking -- adverse effects
KW - Prenatal Exposure Delayed Effects -- physiopathology
KW - Pregnancy Complications -- physiopathology
KW - Embryonic Development -- genetics
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551025049?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Psychoneuroendocrinology&rft.atitle=Maternal+smoking+during+pregnancy+and+infant+stress+response%3A+test+of+a+prenatal+programming+hypothesis.&rft.au=Stroud%2C+Laura+R%3BPapandonatos%2C+George+D%3BRodriguez%2C+Daniel%3BMcCallum%2C+Meaghan%3BSalisbury%2C+Amy+L%3BPhipps%2C+Maureen+G%3BLester%2C+Barry%3BHuestis%2C+Marilyn+A%3BNiaura%2C+Raymond%3BPadbury%2C+James+F%3BMarsit%2C+Carmen+J&rft.aulast=Stroud&rft.aufirst=Laura&rft.date=2014-10-01&rft.volume=48&rft.issue=&rft.spage=29&rft.isbn=&rft.btitle=&rft.title=Psychoneuroendocrinology&rft.issn=1873-3360&rft_id=info:doi/10.1016%2Fj.psyneuen.2014.05.017
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-04-16
N1 - Date created - 2014-08-01
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.psyneuen.2014.05.017
ER -
TY - JOUR
T1 - International Union of Basic and Clinical Pharmacology. XC. multisite pharmacology: recommendations for the nomenclature of receptor allosterism and allosteric ligands.
AN - 1545776692; 25026896
AB - Allosteric interactions play vital roles in metabolic processes and signal transduction and, more recently, have become the focus of numerous pharmacological studies because of the potential for discovering more target-selective chemical probes and therapeutic agents. In addition to classic early studies on enzymes, there are now examples of small molecule allosteric modulators for all superfamilies of receptors encoded by the genome, including ligand- and voltage-gated ion channels, G protein-coupled receptors, nuclear hormone receptors, and receptor tyrosine kinases. As a consequence, a vast array of pharmacologic behaviors has been ascribed to allosteric ligands that can vary in a target-, ligand-, and cell-/tissue-dependent manner. The current article presents an overview of allostery as applied to receptor families and approaches for detecting and validating allosteric interactions and gives recommendations for the nomenclature of allosteric ligands and their properties. U.S. Government work not protected by U.S. copyright.
JF - Pharmacological reviews
AU - Christopoulos, Arthur
AU - Changeux, Jean-Pierre
AU - Catterall, William A
AU - Fabbro, Doriano
AU - Burris, Thomas P
AU - Cidlowski, John A
AU - Olsen, Richard W
AU - Peters, John A
AU - Neubig, Richard R
AU - Pin, Jean-Philippe
AU - Sexton, Patrick M
AU - Kenakin, Terry P
AU - Ehlert, Frederick J
AU - Spedding, Michael
AU - Langmead, Christopher J
AD - Drug Discovery Biology and Department of Pharmacology, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, Victoria, Australia (A.C., P.M.S., C.J.L.); Collège de France and CNRS URA 2182, Institut Pasteur, Paris, France (J.-P.C.); Department of Pharmacology, School of Medicine, University of Washington, Seattle, Washington (W.A.C.); PIQUR Therapeutics AG, Basel, Switzerland (D.F.); Department of Pharmacological & Physiological Science, Saint Louis University School of Medicine, St. Louis, Louisiana (T.P.B.); Signal Transduction Laboratory, Molecular Endocrinology Group, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina (J.A.C.); Department of Molecular and Medical Pharmacology, University of California, Los Angeles, California (R.W.O.); Division of Neuroscience, School of Medicine, University of Dundee, Scotland, United Kingdom (J.A.P.); Department of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan (R.R.N.); Institut de Genomique Fonctionelle, CNRS, Montpellier, France (J.-P.P.); Department of Pharmacology, University of North Carolina, Chapel Hill, North Carolina (T.P.K.); Department of Pharmacology, University of California, Irvine, California (F.J.E.); and Research Solutions SARL, Paris, France (M.S.) arthur.christopoulos@monash.edu. ; Drug Discovery Biology and Department of Pharmacology, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, Victoria, Australia (A.C., P.M.S., C.J.L.); Collège de France and CNRS URA 2182, Institut Pasteur, Paris, France (J.-P.C.); Department of Pharmacology, School of Medicine, University of Washington, Seattle, Washington (W.A.C.); PIQUR Therapeutics AG, Basel, Switzerland (D.F.); Department of Pharmacological & Physiological Science, Saint Louis University School of Medicine, St. Louis, Louisiana (T.P.B.); Signal Transduction Laboratory, Molecular Endocrinology Group, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina (J.A.C.); Department of Molecular and Medical Pharmacology, University of California, Los Angeles, California (R.W.O.); Division of Neuroscience, School of Medicine, University of Dundee, Scotland, United Kingdom (J.A.P.); Department of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan (R.R.N.); Institut de Genomique Fonctionelle, CNRS, Montpellier, France (J.-P.P.); Department of Pharmacology, University of North Carolina, Chapel Hill, North Carolina (T.P.K.); Department of Pharmacology, University of California, Irvine, California (F.J.E.); and Research Solutions SARL, Paris, France (M.S.).
Y1 - 2014/10//
PY - 2014
DA - October 2014
SP - 918
EP - 947
VL - 66
IS - 4
KW - Ion Channels
KW - 0
KW - Ligands
KW - Receptors, Cytoplasmic and Nuclear
KW - Receptors, G-Protein-Coupled
KW - Protein-Tyrosine Kinases
KW - EC 2.7.10.1
KW - Index Medicus
KW - Receptors, G-Protein-Coupled -- chemistry
KW - Receptors, Cytoplasmic and Nuclear -- metabolism
KW - Receptors, Cytoplasmic and Nuclear -- chemistry
KW - Humans
KW - Receptors, G-Protein-Coupled -- metabolism
KW - Models, Chemical
KW - Protein-Tyrosine Kinases -- metabolism
KW - Protein-Tyrosine Kinases -- chemistry
KW - Ion Channels -- metabolism
KW - Allosteric Regulation -- drug effects
KW - Terminology as Topic
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1545776692?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacological+reviews&rft.atitle=International+Union+of+Basic+and+Clinical+Pharmacology.+XC.+multisite+pharmacology%3A+recommendations+for+the+nomenclature+of+receptor+allosterism+and+allosteric+ligands.&rft.au=Christopoulos%2C+Arthur%3BChangeux%2C+Jean-Pierre%3BCatterall%2C+William+A%3BFabbro%2C+Doriano%3BBurris%2C+Thomas+P%3BCidlowski%2C+John+A%3BOlsen%2C+Richard+W%3BPeters%2C+John+A%3BNeubig%2C+Richard+R%3BPin%2C+Jean-Philippe%3BSexton%2C+Patrick+M%3BKenakin%2C+Terry+P%3BEhlert%2C+Frederick+J%3BSpedding%2C+Michael%3BLangmead%2C+Christopher+J&rft.aulast=Christopoulos&rft.aufirst=Arthur&rft.date=2014-10-01&rft.volume=66&rft.issue=4&rft.spage=918&rft.isbn=&rft.btitle=&rft.title=Pharmacological+reviews&rft.issn=1521-0081&rft_id=info:doi/10.1124%2Fpr.114.008862
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-03-30
N1 - Date created - 2014-07-16
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1124/pr.114.008862
ER -
TY - JOUR
T1 - Quantitative high-throughput profiling of environmental chemicals and drugs that modulate farnesoid X receptor.
AN - 1566408416; 25257666
AB - The farnesoid X receptor (FXR) regulates the homeostasis of bile acids, lipids, and glucose. Because endogenous chemicals bind and activate FXR, it is important to examine which xenobiotic compounds would disrupt normal receptor function. We used a cell-based human FXR β-lactamase (Bla) reporter gene assay to profile the Tox21 10K compound collection of environmental chemicals and drugs. Structure-activity relationships of FXR-active compounds revealed by this screening were then compared against the androgen receptor, estrogen receptor α, peroxisome proliferator-activated receptors δ and γ, and the vitamin D receptor. We identified several FXR-active structural classes including anthracyclines, benzimidazoles, dihydropyridines, pyrethroids, retinoic acids, and vinca alkaloids. Microtubule inhibitors potently decreased FXR reporter gene activity. Pyrethroids specifically antagonized FXR transactivation. Anthracyclines affected reporter activity in all tested assays, suggesting non-specific activity. These results provide important information to prioritize chemicals for further investigation, and suggest possible modes of action of compounds in FXR signaling.
JF - Scientific reports
AU - Hsu, Chia-Wen
AU - Zhao, Jinghua
AU - Huang, Ruili
AU - Hsieh, Jui-Hua
AU - Hamm, Jon
AU - Chang, Xiaoqing
AU - Houck, Keith
AU - Xia, Menghang
AD - National Center for Advancing Translational Sciences, National Institutes of Health, Bethesda, MD. ; Division of the National Toxicology Program, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC. ; Integrated Laboratory Systems, Inc., Morrisville, NC. ; U.S. Environmental Protection Agency, Research Triangle Park, NC.
Y1 - 2014/09/26/
PY - 2014
DA - 2014 Sep 26
SP - 6437
VL - 4
KW - Bile Acids and Salts
KW - 0
KW - DNA-Binding Proteins
KW - Receptors, Cytoplasmic and Nuclear
KW - Xenobiotics
KW - farnesoid X-activated receptor
KW - beta-Lactamases
KW - EC 3.5.2.6
KW - Glucose
KW - IY9XDZ35W2
KW - Index Medicus
KW - Lipid Metabolism -- drug effects
KW - Promoter Regions, Genetic -- drug effects
KW - Humans
KW - HEK293 Cells
KW - Glucose -- metabolism
KW - Genes, Reporter
KW - DNA-Binding Proteins -- genetics
KW - Bile Acids and Salts -- metabolism
KW - Signal Transduction
KW - Binding Sites
KW - beta-Lactamases -- biosynthesis
KW - Xenobiotics -- pharmacology
KW - Receptors, Cytoplasmic and Nuclear -- genetics
KW - Xenobiotics -- toxicity
KW - Receptors, Cytoplasmic and Nuclear -- biosynthesis
KW - beta-Lactamases -- genetics
KW - Structure-Activity Relationship
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Scientific+reports&rft.atitle=Quantitative+high-throughput+profiling+of+environmental+chemicals+and+drugs+that+modulate+farnesoid+X+receptor.&rft.au=Hsu%2C+Chia-Wen%3BZhao%2C+Jinghua%3BHuang%2C+Ruili%3BHsieh%2C+Jui-Hua%3BHamm%2C+Jon%3BChang%2C+Xiaoqing%3BHouck%2C+Keith%3BXia%2C+Menghang&rft.aulast=Hsu&rft.aufirst=Chia-Wen&rft.date=2014-09-26&rft.volume=4&rft.issue=&rft.spage=6437&rft.isbn=&rft.btitle=&rft.title=Scientific+reports&rft.issn=2045-2322&rft_id=info:doi/10.1038%2Fsrep06437
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2016-03-21
N1 - Date created - 2014-09-26
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1038/srep06437
ER -
TY - JOUR
T1 - Di-(2-ethylhexyl) phthalate inhibits DNA replication leading to hyperPARylation, SIRT1 attenuation, and mitochondrial dysfunction in the testis.
AN - 1564354749; 25242624
AB - Di-(2-ethylhexyl)-phthalate (DEHP) is a ubiquitously used endocrine disruptor.There is widespread exposure to DEHP in the general population which has raised substantial public concern due to its potential detrimental health effects. It is particularly pertinent to investigate the molecular mechanisms of its testicular toxicity which are largely unknown. By feeding male rats DEHP for 2 weeks, rat spermatogenesis became disrupted, resulting in a decreased number of spermatocytes and spermatids. Since rapidly dividing tissues appeared to be particularly vulnerable to DEHP toxicity we investigated the effect of DEHP on DNA replication. Intriguingly, DEHP appeared to inhibit DNA replication as evidenced by results of fiber tract analysis. This led to induction of the mitochondrial apoptotic pathways and increased ROS production. Furthermore, the toxicity of DEHP led to respiratory chain defects and attenuation of ATP level probably brought about by hyperPARylation and undermined SIRT1 activity. Our findings reveal a previously unknown mitochondrial dysfunction in DEHP-induced testicular toxicity and highlight the importance of SIRT1 in male reproduction.
JF - Scientific reports
AU - Li, Xiaolin
AU - Fang, Evandro Fei
AU - Scheibye-Knudsen, Morten
AU - Cui, Honghua
AU - Qiu, Lu
AU - Li, Jian
AU - He, Yuping
AU - Huang, Jing
AU - Bohr, Vilhelm A
AU - Ng, Tzi Bun
AU - Guo, Hongwei
AD - 1] School of Public Health, Fudan University, Shanghai, 200032, China [2] Shanghai Entry-Exit Inspection and Quarantine Bureau, Shanghai, 200135, China [3]. ; 1] Laboratory of Molecular Gerontology, National Institute on Ageing, National Institutes of Health, Baltimore, MD USA [2] School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, Shatin, New Territories, Hong Kong [3]. ; Laboratory of Molecular Gerontology, National Institute on Ageing, National Institutes of Health, Baltimore, MD USA. ; Shanghai Stomatological Disease Centre. Shanghai, 200001, PR China. ; Shanghai Entry-Exit Inspection and Quarantine Bureau, Shanghai, 200135, China. ; School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, Shatin, New Territories, Hong Kong. ; School of Public Health, Fudan University, Shanghai, 200032, China.
Y1 - 2014/09/22/
PY - 2014
DA - 2014 Sep 22
SP - 6434
VL - 4
KW - Sirt1 protein, rat
KW - EC 3.5.1.-
KW - Sirtuin 1
KW - Index Medicus
KW - Rats
KW - Animals
KW - Testis -- drug effects
KW - Reproduction -- drug effects
KW - Reproduction -- genetics
KW - Humans
KW - Male
KW - Spermatogenesis -- genetics
KW - Sirtuin 1 -- biosynthesis
KW - DNA Replication -- genetics
KW - Mitochondria -- pathology
KW - Mitochondria -- drug effects
KW - Spermatogenesis -- drug effects
KW - DNA Replication -- drug effects
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1564354749?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Scientific+reports&rft.atitle=Di-%282-ethylhexyl%29+phthalate+inhibits+DNA+replication+leading+to+hyperPARylation%2C+SIRT1+attenuation%2C+and+mitochondrial+dysfunction+in+the+testis.&rft.au=Li%2C+Xiaolin%3BFang%2C+Evandro+Fei%3BScheibye-Knudsen%2C+Morten%3BCui%2C+Honghua%3BQiu%2C+Lu%3BLi%2C+Jian%3BHe%2C+Yuping%3BHuang%2C+Jing%3BBohr%2C+Vilhelm+A%3BNg%2C+Tzi+Bun%3BGuo%2C+Hongwei&rft.aulast=Li&rft.aufirst=Xiaolin&rft.date=2014-09-22&rft.volume=4&rft.issue=&rft.spage=6434&rft.isbn=&rft.btitle=&rft.title=Scientific+reports&rft.issn=2045-2322&rft_id=info:doi/10.1038%2Fsrep06434
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-11-06
N1 - Date created - 2014-09-22
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
J Occup Health. 2008;50(2):169-80 [18403868]
Int J Hyg Environ Health. 2007 Oct;210(5):623-34 [17889607]
Nat Rev Cancer. 2009 Feb;9(2):123-8 [19132007]
NTP CERHR MON. 2006 Nov;(18):v, vii-7, II-iii-xiii passim [19407857]
Diabetes. 2010 Apr;59(4):829-35 [20107110]
Nucleic Acids Res. 2010 Nov;38(21):7458-71 [20660480]
Environ Res. 2011 Apr;111(3):329-36 [21315328]
Cancer Prev Res (Phila). 2012 Jan;5(1):109-21 [21933914]
FASEB J. 2012 Feb;26(2):555-66 [22006156]
Endocr Regul. 2012 Jan;46(1):37-46 [22329821]
Arch Environ Contam Toxicol. 2012 Apr;62(3):539-47 [22002783]
J Exp Med. 2012 Apr 9;209(4):855-69 [22473955]
Biol Res. 2012;45(1):5-14 [22688978]
Food Chem Toxicol. 2012 Jul;50(7):2424-31 [22542555]
PLoS One. 2012;7(11):e50465 [23226291]
Annu Rev Public Health. 2013;34:139-58 [23514318]
Arch Toxicol. 2013 Apr;87(4):735-51 [23192238]
Int J Hyg Environ Health. 2013 Jul;216(4):472-80 [23394848]
Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2013;30(4):735-42 [23641808]
Food Chem Toxicol. 2013 Aug;58:362-8 [23684997]
Mol Cell. 2013 Nov 7;52(3):434-46 [24207054]
Cell. 2014 May 8;157(4):882-96 [24813611]
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Autophagy. 2014 Aug;10(8):1468-9 [24991831]
Toxicol Sci. 2001 Aug;62(2):236-49 [11452136]
Toxicology. 2002 Feb 28;171(2-3):105-15 [11836017]
Environ Health Perspect. 2003 Jul;111(9):1164-9 [12842768]
Proc Natl Acad Sci U S A. 2004 Jan 20;101(3):775-80 [14715905]
Proc Natl Acad Sci U S A. 2004 Apr 27;101(17):6570-5 [15100410]
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Int J Androl. 2006 Feb;29(1):134-9; discussion 181-5 [16466533]
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Proc Natl Acad Sci U S A. 2006 Oct 10;103(41):15148-53 [17005726]
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Hum Reprod. 2007 Mar;22(3):688-95 [17090632]
Environ Res. 2008 Oct;108(2):177-84 [18949837]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1038/srep06434
ER -
TY - JOUR
T1 - Single-molecule sequencing to track plasmid diversity of hospital-associated carbapenemase-producing Enterobacteriaceae
AN - 1727695220; PQ0002040669
AB - Public health officials have raised concerns that plasmid transfer between Enterobacteriaceae species may spread resistance to carbapenems, an antibiotic class of last resort, thereby rendering common health care-associated infections nearly impossible to treat. To determine the diversity of carbapenemase-encoding plasmids and assess their mobility among bacterial species, we performed comprehensive surveillance and genomic sequencing of carbapenem-resistant Enterobacteriaceae in the National Institutes of Health (NIH) Clinical Center patient population and hospital environment. We isolated a repertoire of carbapenemase-encoding Enterobacteriaceae, including multiple strains of Klebsiella pneumoniae, Klebsiella oxytoca, Escherichia coli, Enterobacter cloacae, Citrobacter freundii, and Pantoea species. Long-read genome sequencing with full end-to-end assembly revealed that these organisms carry the carbapenem resistance genes on a wide array of plasmids. K. pneumoniae and E. cloacae isolated simultaneously from a single patient harbored two different carbapenemase-encoding plasmids, indicating that plasmid transfer between organisms was unlikely within this patient. We did, however, find evidence of horizontal transfer of carbapenemase-encoding plasmids between K. pneumoniae, E. cloacae, and C. freundii in the hospital environment. Our data, including full plasmid identification, challenge assumptions about horizontal gene transfer events within patients and identify possible connections between patients and the hospital environment. In addition, we identified a new carbapenemase-encoding plasmid of potentially high clinical impact carried by K. pneumoniae, E. coli, E. cloacae, and Pantoea species, in unrelated patients and in the hospital environment.
JF - Science Translational Medicine
AU - Conlan, Sean
AU - Thomas, Pamela J
AU - Deming, Clayton
AU - Park, Morgan
AU - Lau, Anna F
AU - Dekker, John P
AU - Snitkin, Evan S
AU - Clark, Tyson A
AU - Luong, Khai
AU - Song, Yi
AD - National Human Genome Research Institute, Bethesda, MD 20892, USA
Y1 - 2014/09/17/
PY - 2014
DA - 2014 Sep 17
PB - American Association for the Advancement of Science, 1200 New York Avenue, NW Washington DC 20005 United States
VL - 6
IS - 254
SN - 1946-6234, 1946-6234
KW - Genetics Abstracts; Microbiology Abstracts B: Bacteriology
KW - Genomes
KW - Translation
KW - Data processing
KW - Mobility
KW - Citrobacter freundii
KW - Carbapenems
KW - Antibiotics
KW - Plasmids
KW - Infection
KW - Horizontal transfer
KW - Public health
KW - Enterobacter cloacae
KW - Escherichia coli
KW - Klebsiella oxytoca
KW - genomics
KW - Enterobacteriaceae
KW - Klebsiella pneumoniae
KW - Hospitals
KW - J 02400:Human Diseases
KW - G 07770:Bacteria
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-10-01
N1 - Last updated - 2016-03-17
N1 - SubjectsTermNotLitGenreText - Genomes; Translation; Data processing; Mobility; Carbapenems; Antibiotics; genomics; Infection; Plasmids; Horizontal transfer; Public health; Hospitals; Enterobacter cloacae; Citrobacter freundii; Escherichia coli; Klebsiella oxytoca; Enterobacteriaceae; Klebsiella pneumoniae
DO - http://dx.doi.org/10.1126/scitranslmed.3009845
ER -
TY - JOUR
T1 - The Role of Age on Dose-Limiting Toxicities in Phase I Dose-Escalation Trials
AN - 1808635150; PQ0003448822
AB - Purpose: Elderly oncology patients are not enrolled in early-phase trials in proportion to the numbers of geriatric patients with cancer. There may be concern that elderly patients will not tolerate investigational agents as well as younger patients, resulting in a disproportionate number of dose-limiting toxicities (DLT). Recent single-institution studies provide conflicting data on the relationship between age and DLT.Experimental Design: We retrospectively reviewed data about patients treated on single-agent, dose-escalation, phase I clinical trials sponsored by the Cancer Therapy Evaluation Program (CTEP) of the National Cancer Institute. Patients' dose levels were described as a percentage of maximum tolerated dose, the highest dose level at which <33% of patients had a DLT, or recommended phase II dose (RP2D). Mixed-effect logistic regression models were used to analyze relationships between the probability of a DLT and age and other explanatory variables.Results: Increasing dose, increasing age, and worsening performance status (PS) were significantly related to an increased probability of a DLT in this model (P < 0.05). There was no association between dose level administered and age (P = 0.57).Conclusions: This analysis of phase I dose-escalation trials, involving more than 500 patients older than 70 years of age, is the largest reported. As age and dose level increased and PS worsened, the probability of a DLT increased. Although increasing age was associated with occurrence of DLT, this risk remained within accepted thresholds of risk for phase I trials. There was no evidence of age bias on enrollment of patients on low or high dose levels. Clin Cancer Res; 20(18); 4768-75. copyright 2014 AACR.
JF - Clinical Cancer Research
AU - Schwandt, A
AU - Harris, P J
AU - Hunsberger, S
AU - Deleporte, A
AU - Smith, G L
AU - Vulih, D
AU - Anderson, B D
AU - Ivy, S P
AD - Case Western Reserve School of Medicine, Cleveland, Ohio, ivyp@ctep.nci.nih.gov
Y1 - 2014/09/15/
PY - 2014
DA - 2014 Sep 15
SP - 4768
EP - 4775
PB - American Association for Cancer Research, 615 Chestnut St., 17th Floor Philadelphia PA 19106-4404 United States
VL - 20
IS - 18
SN - 1078-0432, 1078-0432
KW - Biotechnology and Bioengineering Abstracts
KW - Age
KW - Data processing
KW - Geriatrics
KW - Regression analysis
KW - Oncology
KW - Toxicity
KW - Clinical trials
KW - Cancer
KW - Models
KW - W 30965:Miscellaneous, Reviews
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2016-07-01
N1 - Last updated - 2016-08-17
N1 - SubjectsTermNotLitGenreText - Age; Data processing; Regression analysis; Geriatrics; Oncology; Toxicity; Clinical trials; Cancer; Models
DO - http://dx.doi.org/10.1158/1078-0432.CCR-14-0866
ER -
TY - JOUR
T1 - Is the "3+3" dose-escalation phase I clinical trial design suitable for therapeutic cancer vaccine development? A recommendation for alternative design.
AN - 1562663788; 25037736
AB - Phase I clinical trials are generally conducted to identify the maximum tolerated dose (MTD) or the biologically active dose (BAD) using a traditional dose-escalation design. This design may not be applied to cancer vaccines, given their unique mechanism of action. The FDA recently published "Guidance for Industry: Clinical Considerations for Therapeutic Cancer Vaccines." However, many questions about the design of cancer vaccine studies remain unanswered.
We analyzed the toxicity profile in 239 phase I therapeutic cancer vaccine trials. We addressed the ability of dose escalation to determine the MTD or the BAD in trials that used a dose-escalation design. The rate of grade 3/4 vaccine-related systemic toxicities was 1.25 adverse events per 100 patients and 2 per 1,000 vaccines. Only two of the 127 dose-escalation trials reported vaccine-related dose limiting toxicities, both of which used bacterial vector vaccines. Out of the 116 trials analyzed for the dose-immune response relationship, we found a statistically significant dose-immune response correlation only when the immune response was measured by antibodies (P < 0.001) or delayed type hypersensitivity (P < 0.05). However, the increase in cellular immune response did not appear further sustainable with the continued increase in dose.
Our analysis suggests that the risks of serious toxicities with therapeutic cancer vaccines are extremely low and that toxicities do not correlate with dose levels. Accordingly, the conventional dose-escalation design is not suitable for cancer vaccines with few exceptions. Here, we propose an alternative design for therapeutic cancer vaccine development. ©2014 American Association for Cancer Research.
JF - Clinical cancer research : an official journal of the American Association for Cancer Research
AU - Rahma, Osama E
AU - Gammoh, Emily
AU - Simon, Richard M
AU - Khleif, Samir N
AD - Vaccine Branch, National Cancer Institute, Bethesda, Maryland. Division of Hematology/Oncology, University of Virginia, Charlottesville, Virginia. ; Vaccine Branch, National Cancer Institute, Bethesda, Maryland. ; Biometric Research Branch, National Cancer Institute, Rockville, Maryland. ; Vaccine Branch, National Cancer Institute, Bethesda, Maryland. Georgia Health Sciences Cancer Center, Augusta, Georgia. skhleif@gru.edu.
Y1 - 2014/09/15/
PY - 2014
DA - 2014 Sep 15
SP - 4758
EP - 4767
VL - 20
IS - 18
SN - 1078-0432, 1078-0432
KW - Cancer Vaccines
KW - 0
KW - Index Medicus
KW - Humans
KW - Clinical Trials, Phase I as Topic -- methods
KW - Neoplasms -- drug therapy
KW - Cancer Vaccines -- administration & dosage
KW - Clinical Trials, Phase I as Topic -- standards
KW - Research Design -- standards
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-07-31
N1 - Date created - 2014-09-16
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1158/1078-0432.CCR-13-2671
ER -
TY - JOUR
T1 - Mitochondrial topoisomerase I (top1mt) is a novel limiting factor of doxorubicin cardiotoxicity.
AN - 1562663778; 24714774
AB - Doxorubicin is one of the most effective chemotherapeutic agents. However, up to 30% of the patients treated with doxorubicin suffer from congestive heart failure. The mechanism of doxorubicin cardiotoxicity is likely multifactorial and most importantly, the genetic factors predisposing to doxorubicin cardiotoxicity are unknown. On the basis of the fact that mtDNA lesions and mitochondrial dysfunctions have been found in human hearts exposed to doxorubicin and that mitochondrial topoisomerase 1 (Top1mt) specifically controls mtDNA homeostasis, we hypothesized that Top1mt knockout (KO) mice might exhibit hypersensitivity to doxorubicin.
Wild-type (WT) and KO Top1mt mice were treated once a week with 4 mg/kg doxorubicin for 8 weeks. Heart tissues were analyzed one week after the last treatment. Genetic inactivation of Top1mt in mice accentuates mtDNA copy number loss and mtDNA damage in heart tissue following doxorubicin treatment. Top1mt KO mice also fail to maintain respiratory chain protein production and mitochondrial cristae ultrastructure organization. These mitochondrial defects result in decreased O2 consumption, increased reactive oxygen species production, and enhanced heart muscle damage in animals treated with doxorubicin. Accordingly, Top1mt KO mice die within 45 days after the last doxorubicin injection, whereas the WT mice survive.
Our results provide evidence that Top1mt, which is conserved across vertebrates, is critical for cardiac tolerance to doxorubicin and adaptive response to doxorubicin cardiotoxicity. They also suggest the potential of Top1mt single-nucleotide polymorphisms testing to investigate patient susceptibility to doxorubicin-induced cardiotoxicity. ©2014 American Association for Cancer Research.
JF - Clinical cancer research : an official journal of the American Association for Cancer Research
AU - Khiati, Salim
AU - Dalla Rosa, Ilaria
AU - Sourbier, Carole
AU - Ma, Xuefei
AU - Rao, V Ashutosh
AU - Neckers, Leonard M
AU - Zhang, Hongliang
AU - Pommier, Yves
AD - Developmental Therapeutics Branch and Laboratory of Molecular Pharmacology; ; Urologic Oncology Branch, Center for Cancer Research, National Cancer Institute; ; Laboratory of Molecular Cardiology, National Heart, Lung, and Blood Institute, NIH; and. ; Center for Drug Evaluation and Research, Food and Drug Administration, Bethesda, Maryland. ; Developmental Therapeutics Branch and Laboratory of Molecular Pharmacology; pommier@nih.gov.
Y1 - 2014/09/15/
PY - 2014
DA - 2014 Sep 15
SP - 4873
EP - 4881
VL - 20
IS - 18
SN - 1078-0432, 1078-0432
KW - Antibiotics, Antineoplastic
KW - 0
KW - DNA, Mitochondrial
KW - Doxorubicin
KW - 80168379AG
KW - DNA Topoisomerases, Type I
KW - EC 5.99.1.2
KW - Index Medicus
KW - Animals
KW - DNA, Mitochondrial -- drug effects
KW - Blotting, Western
KW - DNA, Mitochondrial -- metabolism
KW - Mice
KW - Fluorescent Antibody Technique
KW - Mice, Knockout
KW - Mitochondria, Heart -- enzymology
KW - Mitochondria, Heart -- drug effects
KW - Doxorubicin -- toxicity
KW - Cardiotoxicity -- enzymology
KW - DNA Topoisomerases, Type I -- metabolism
KW - Antibiotics, Antineoplastic -- toxicity
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-07-31
N1 - Date created - 2014-09-16
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Cell Biol Toxicol. 2007 Jan;23(1):15-25 [17009097]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1158/1078-0432.CCR-13-3373
ER -
TY - CPAPER
T1 - Mitigation of Radiation Induced Pulmonary Injury with Systemic Delivery of Mesenchymal Stem Cells
T2 - 56th Annual Meeting of the American Society for Therapeutic Radiology and Oncology (ASTRO 2014)
AN - 1645181593; 6319308
JF - 56th Annual Meeting of the American Society for Therapeutic Radiology and Oncology (ASTRO 2014)
AU - Scroggins, Bradley
Y1 - 2014/09/14/
PY - 2014
DA - 2014 Sep 14
KW - Stem cells
KW - Mitigation
KW - Injuries
KW - Radiation
KW - Lung
KW - Mesenchyme
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L2 - http://online.myiwf.com/astro2014/Abstract.aspx
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-11-30
N1 - Last updated - 2015-01-14
ER -
TY - CPAPER
T1 - Radiation Enhancement of Head and Neck Squamous Cell Carcinoma by the Dual PI3K/mTOR Inhibitor PF-05212384
T2 - 56th Annual Meeting of the American Society for Therapeutic Radiology and Oncology (ASTRO 2014)
AN - 1645181412; 6319419
JF - 56th Annual Meeting of the American Society for Therapeutic Radiology and Oncology (ASTRO 2014)
AU - Leiker, Andrew
Y1 - 2014/09/14/
PY - 2014
DA - 2014 Sep 14
KW - 1-Phosphatidylinositol 3-kinase
KW - Radiation
KW - Head and neck cancer
KW - Inhibitors
KW - squamous cell carcinoma
KW - Tumors
KW - TOR protein
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L2 - http://online.myiwf.com/astro2014/Abstract.aspx
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-11-30
N1 - Last updated - 2015-01-14
ER -
TY - CPAPER
T1 - Il-13 is a Critical Mediator of Radiation-Induced Pulmonary Fibrosis
T2 - 56th Annual Meeting of the American Society for Therapeutic Radiology and Oncology (ASTRO 2014)
AN - 1645179122; 6319310
JF - 56th Annual Meeting of the American Society for Therapeutic Radiology and Oncology (ASTRO 2014)
AU - Citrin, Deborah
Y1 - 2014/09/14/
PY - 2014
DA - 2014 Sep 14
KW - Interleukin 13
KW - Fibrosis
KW - Lung diseases
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=56th+Annual+Meeting+of+the+American+Society+for+Therapeutic+Radiology+and+Oncology+%28ASTRO+2014%29&rft.atitle=Il-13+is+a+Critical+Mediator+of+Radiation-Induced+Pulmonary+Fibrosis&rft.au=Citrin%2C+Deborah&rft.aulast=Citrin&rft.aufirst=Deborah&rft.date=2014-09-14&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=56th+Annual+Meeting+of+the+American+Society+for+Therapeutic+Radiology+and+Oncology+%28ASTRO+2014%29&rft.issn=&rft_id=info:doi/
L2 - http://online.myiwf.com/astro2014/Abstract.aspx
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-11-30
N1 - Last updated - 2015-01-14
ER -
TY - CPAPER
T1 - Interim Analysis Results Of A Phase II Trial Of Low Dose Radiotherapy For Palliation Of Diffuse Large B Cell Lymphoma
T2 - 56th Annual Meeting of the American Society for Therapeutic Radiology and Oncology (ASTRO 2014)
AN - 1645168132; 6319148
JF - 56th Annual Meeting of the American Society for Therapeutic Radiology and Oncology (ASTRO 2014)
AU - Furlan, Carlo
Y1 - 2014/09/14/
PY - 2014
DA - 2014 Sep 14
KW - B-cell lymphoma
KW - Radiotherapy
KW - Lymphoma
KW - Palliation
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L2 - http://online.myiwf.com/astro2014/Abstract.aspx
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-11-30
N1 - Last updated - 2015-01-14
ER -
TY - JOUR
T1 - Rates of HIV-1 superinfection and primary HIV-1 infection are similar in female sex workers in Uganda
AN - 1765969978; PQ0002559486
AB - Objective: To determine and compare the rates of HIV superinfection and primary HIV infection in high-risk female sex workers (FSWs) in Kampala, Uganda. Design: A retrospective analysis of individuals who participated in a clinical cohort study among high-risk FSWs in Kampala, Uganda. Methods: Plasma samples from HIV-infected FSWs in Kampala, Uganda were examined with next-generation sequencing of the p24 and gp41HIV genomic regions for the occurrence of superinfection. Primary HIV incidence was determined from initially HIV-uninfected FSWs from the same cohort, and incidence rate ratios were compared. Results: The rate of superinfection in these women (7/85; 3.4/100 person-years) was not significantly different from the rate of primary infection in the same population (3.7/ 100 person-years; incidence rate ratio = 0.91, P = 0.42). Seven women also entered the study dual-infected (16.5% either dual or superinfected). The women with any presence of dual infection were more likely to report sex work as their only source of income (P = 0.05), and trended to be older and more likely to be widowed (P = 0.07). Conclusions: In this cohort of FSWs, HIV superinfection occurred at a high rate and was similar to that of primary HIV infection. These results differ from a similar study of high-risk female bar workers in Kenya that found the rate of superinfection to be significantly lower than the rate of primary HIV infection.
JF - AIDS
AU - Redd, Andrew D
AU - Ssemwanga, Deogratius
AU - Vandepitte, Judith
AU - Wendel, Sarah K
AU - Ndembi, Nicaise
AU - Bukenya, Justine
AU - Nakubulwa, Susan
AU - Grosskurth, Heiner
AU - Parry, Chris M
AU - Martens, Craig
AU - Bruno, Daniel
AU - Porcella, Stephen F
AU - Quinn, Thomas C
AU - Kaleebu, Pontiano
AD - Laboratory of Immunoregulation, Division of Intramural Research, NIAID, NIH, Bethesda, aredd2@jhmi.edu
Y1 - 2014/09/10/
PY - 2014
DA - 2014 Sep 10
SP - 2147
EP - 2152
PB - Lippincott Williams & Wilkins, Inc, 530 Walnut Street Philadelphia PA 19106-3621 United States
VL - 28
IS - 14
SN - 0269-9370, 0269-9370
KW - Health & Safety Science Abstracts; Immunology Abstracts; Virology & AIDS Abstracts
KW - Africa
KW - female sex workers
KW - HIV
KW - superinfection
KW - Uganda
KW - Acquired immune deficiency syndrome
KW - Uganda, Kampala
KW - Prostitution
KW - Infection
KW - Superinfection
KW - Income
KW - Workers
KW - Kenya
KW - Human immunodeficiency virus
KW - Human immunodeficiency virus 1
KW - Risk groups
KW - Females
KW - genomics
KW - Sex
KW - V 22360:AIDS and HIV
KW - H 1000:Occupational Safety and Health
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2016-02-01
N1 - Last updated - 2016-03-17
N1 - SubjectsTermNotLitGenreText - Workers; Risk groups; Prostitution; genomics; Superinfection; Sex; Acquired immune deficiency syndrome; Human immunodeficiency virus; Females; Infection; Income; Human immunodeficiency virus 1; Kenya; Uganda, Kampala; Uganda
DO - http://dx.doi.org/10.1097/QAD.0000000000000365
ER -
TY - JOUR
T1 - Substance P exacerbates dopaminergic neurodegeneration through neurokinin-1 receptor-independent activation of microglial NADPH oxidase.
AN - 1561974409; 25209287
AB - Although dysregulated substance P (SP) has been implicated in the pathophysiology of Parkinson's disease (PD), how SP affects the survival of dopaminergic neurons remains unclear. Here, we found that mice lacking endogenous SP (TAC1(-/-)), but not those deficient in the SP receptor (neurokinin-1 receptor, NK1R), were more resistant to lipopolysaccharide (LPS)- and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced nigral dopaminergic neurodegeneration than wild-type controls, suggesting a NK1R-independent toxic action of SP. In vitro dose-response studies revealed that exogenous SP enhanced LPS- and 1-methyl-4-phenylpyridinium (MPP(+))-induced dopaminergic neurodegeneration in a bimodal manner, peaking at submicromolar and subpicomolar concentrations, but was substantially less effective at intermediate concentrations. Mechanistically, the actions of submicromolar levels of SP were NK1R-dependent, whereas subpicomolar SP-elicited actions required microglial NADPH oxidase (NOX2), the key superoxide-producing enzyme, but not NK1R. Subpicomolar concentrations of SP activated NOX2 by binding to the catalytic subunit gp91(phox) and inducing membrane translocation of the cytosolic subunits p47(phox) and p67(phox). The importance of NOX2 was further corroborated by showing that inhibition or disruption of NOX2 blocked subpicomolar SP-exacerbated neurotoxicity. Together, our findings revealed a critical role of microglial NOX2 in mediating the neuroinflammatory and dopaminergic neurodegenerative effects of SP, which may provide new insights into the pathogenesis of PD.
Copyright © 2014 the authors 0270-6474/14/3412490-14$15.00/0.
JF - The Journal of neuroscience : the official journal of the Society for Neuroscience
AU - Wang, Qingshan
AU - Chu, Chun-Hsien
AU - Qian, Li
AU - Chen, Shih-Heng
AU - Wilson, Belinda
AU - Oyarzabal, Esteban
AU - Jiang, Lulu
AU - Ali, Syed
AU - Robinson, Bonnie
AU - Kim, Hyoung-Chun
AU - Hong, Jau-Shyong
AD - Neuropharmacology Section, Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, wangq4@niehs.nih.gov hong3@niehs.nih.gov. ; Neuropharmacology Section, Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. ; Neurochemistry Laboratory, Division of Neurotoxicology, National Center for Toxicological Research/Food and Drug Administration, Jefferson, Arkansas 72079, and. ; Neuropsychopharmacology and Toxicology Program, College of Pharmacy, Kangwon National University, Chunchon 200-701, Korea.
Y1 - 2014/09/10/
PY - 2014
DA - 2014 Sep 10
SP - 12490
EP - 12503
VL - 34
IS - 37
KW - Lipopolysaccharides
KW - 0
KW - Receptors, Neurokinin-1
KW - Substance P
KW - 33507-63-0
KW - NADPH Oxidase
KW - EC 1.6.3.1
KW - Dopamine
KW - VTD58H1Z2X
KW - Index Medicus
KW - Parkinson's disease
KW - substance P
KW - GPCR independence
KW - neuroinflammation
KW - NADPH oxidase
KW - Animals
KW - Enzyme Activation
KW - Mice, Inbred C57BL
KW - Mice
KW - Male
KW - Mice, Knockout
KW - NADPH Oxidase -- metabolism
KW - Parkinsonian Disorders -- chemically induced
KW - Substance P -- metabolism
KW - Receptors, Neurokinin-1 -- metabolism
KW - Dopaminergic Neurons -- metabolism
KW - Dopamine -- metabolism
KW - Parkinsonian Disorders -- pathology
KW - Parkinsonian Disorders -- metabolism
KW - Microglia -- metabolism
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-01-07
N1 - Date created - 2014-09-11
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1523/JNEUROSCI.2238-14.2014
ER -
TY - JOUR
T1 - Synthesis and Structure-Activity Relationship Studies of N-Benzyl-2-phenylpyrimidin-4-amine Derivatives as Potent USP1/UAF1 Deubiquitinase Inhibitors with Anticancer Activity against Nonsmall Cell Lung Cancer
AN - 1753465124; PQ0002067543
AB - Deregulation of ubiquitin conjugation or deconjugation has been implicated in the pathogenesis of many human diseases including cancer. The deubiquitinating enzyme USP1 (ubiquitin-specific protease 1), in association with UAF1 (USP1-associated factor 1), is a known regulator of DNA damage response and has been shown as a promising anticancer target. To further evaluate USP1/UAF1 as a therapeutic target, we conducted a quantitative high throughput screen of >400000 compounds and subsequent medicinal chemistry optimization of small molecules that inhibit the deubiquitinating activity of USP1/UAF1. Ultimately, these efforts led to the identification of ML323 (70) and related N-benzyl-2-phenylpyrimidin-4-amine derivatives, which possess nanomolar USP1/UAF1 inhibitory potency. Moreover, we demonstrate a strong correlation between compound IC50 values for USP1/UAF1 inhibition and activity in nonsmall cell lung cancer cells, specifically increased monoubiquitinated PCNA (Ub-PCNA) levels and decreased cell survival. Our results establish the druggability of the USP1/UAF1 deubiquitinase complex and its potential as a molecular target for anticancer therapies.
JF - Journal of Medicinal Chemistry
AU - Dexheimer, Thomas S
AU - Rosenthal, Andrew S
AU - Luci, Diane K
AU - Liang, Qin
AU - Villamil, Mark A
AU - Chen, Junjun
AU - Sun, Hongmao
AU - Kerns, Edward H
AU - Simeonov, Anton
AU - Jadhav, Ajit
AU - Zhuang, Zhihao
AU - Maloney, David J
AD - National Center for Advancing Translational Sciences, National Institutes of Health, 9800 Medical Center Drive, Rockville, Maryland 20850, United States
PY - 2014
SP - 8099
EP - 8110
PB - American Chemical Society, P.O. Box 182426 Columbus OH 43218-2426 United States
VL - 57
IS - 19
SN - 0022-2623, 0022-2623
KW - Biotechnology and Bioengineering Abstracts
KW - Cell survival
KW - DNA damage
KW - Enzymes
KW - ubiquitin-specific proteinase
KW - Proliferating cell nuclear antigen
KW - Structure-activity relationships
KW - Lung cancer
KW - Ubiquitin
KW - Antitumor activity
KW - W 30915:Pharmaceuticals & Vaccines
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1753465124?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Medicinal+Chemistry&rft.atitle=Synthesis+and+Structure-Activity+Relationship+Studies+of+N-Benzyl-2-phenylpyrimidin-4-amine+Derivatives+as+Potent+USP1%2FUAF1+Deubiquitinase+Inhibitors+with+Anticancer+Activity+against+Nonsmall+Cell+Lung+Cancer&rft.au=Dexheimer%2C+Thomas+S%3BRosenthal%2C+Andrew+S%3BLuci%2C+Diane+K%3BLiang%2C+Qin%3BVillamil%2C+Mark+A%3BChen%2C+Junjun%3BSun%2C+Hongmao%3BKerns%2C+Edward+H%3BSimeonov%2C+Anton%3BJadhav%2C+Ajit%3BZhuang%2C+Zhihao%3BMaloney%2C+David+J&rft.aulast=Dexheimer&rft.aufirst=Thomas&rft.date=2014-09-07&rft.volume=57&rft.issue=19&rft.spage=8099&rft.isbn=&rft.btitle=&rft.title=Journal+of+Medicinal+Chemistry&rft.issn=00222623&rft_id=info:doi/10.1021%2Fjm5010495
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2016-01-01
N1 - Last updated - 2016-01-21
N1 - SubjectsTermNotLitGenreText - Cell survival; DNA damage; Enzymes; ubiquitin-specific proteinase; Proliferating cell nuclear antigen; Structure-activity relationships; Antitumor activity; Ubiquitin; Lung cancer
DO - http://dx.doi.org/10.1021/jm5010495
ER -
TY - JOUR
T1 - Evaluation of the Murine Immune Response to Xenopsylla cheopis Flea Saliva and Its Effect on Transmission of Yersinia pestis
AN - 1618149286; 20801535
AB - The saliva of blood-feeding arthropods contains a variety of components that prevent blood clotting and interfere with the immune system of the vertebrate host. These properties have been shown to enhance or inhibit the transmission of different pathogens transmitted by arthropods. Yersinia pestis, the bacterial agent of plague, is maintained in nature by flea to rodent transmission cycles. Most rodents live in close association with fleas and are constantly being bitten by them, but the influence this has on plague transmission is unknown - previous studies used laboratory animals which have never experienced a flea bite. We found that flea bites caused a mild inflammatory response in mice, and eventually an antibody response to components of flea saliva, but did not significantly affect pathogenesis. The transmission of Y. pestis by infected fleas and the incidence rate of bubonic plague mortality were the same in mice that had been exposed to frequent uninfected flea bites and mice with no prior exposure to fleas. Therefore, in contrast to what has been shown for many other arthropod-borne disease systems, vector saliva did not enhance or inhibit Y. pestis infection in mice, regardless of the immune status of the host to flea saliva.
JF - PLoS Neglected Tropical Diseases
AU - Bosio, Christopher F
AU - Viall, Austin K
AU - Jarrett, Clayton O
AU - Gardner, Donald
AU - Rood, Michael P
AU - Hinnebusch, BJoseph
AD - Laboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana
PY - 2014
PB - Public Library of Science, 185 Berry Street San Francisco CA 94107 United States
VL - 8
IS - 9
SN - 1935-2727, 1935-2727
KW - Immunology Abstracts; Microbiology Abstracts B: Bacteriology
KW - Immune status
KW - Mortality
KW - Bites
KW - Laboratory animals
KW - Yersinia pestis
KW - Vectors
KW - Pathogens
KW - Antibody response
KW - Infection
KW - Inflammation
KW - Disease transmission
KW - Xenopsylla cheopis
KW - Blood coagulation
KW - Arthropoda
KW - Immune response
KW - Plague
KW - Saliva
KW - J 02350:Immunology
KW - F 06910:Microorganisms & Parasites
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PLoS+Neglected+Tropical+Diseases&rft.atitle=Evaluation+of+the+Murine+Immune+Response+to+Xenopsylla+cheopis+Flea+Saliva+and+Its+Effect+on+Transmission+of+Yersinia+pestis&rft.au=Bosio%2C+Christopher+F%3BViall%2C+Austin+K%3BJarrett%2C+Clayton+O%3BGardner%2C+Donald%3BRood%2C+Michael+P%3BHinnebusch%2C+BJoseph&rft.aulast=Bosio&rft.aufirst=Christopher&rft.date=2014-09-05&rft.volume=8&rft.issue=9&rft.spage=&rft.isbn=&rft.btitle=&rft.title=PLoS+Neglected+Tropical+Diseases&rft.issn=19352727&rft_id=info:doi/10.1371%2Fjournal.pntd.0003196
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-10-01
N1 - Last updated - 2016-01-21
N1 - SubjectsTermNotLitGenreText - Immune status; Mortality; Bites; Laboratory animals; Vectors; Antibody response; Pathogens; Infection; Disease transmission; Inflammation; Blood coagulation; Saliva; Plague; Immune response; Xenopsylla cheopis; Arthropoda; Yersinia pestis
DO - http://dx.doi.org/10.1371/journal.pntd.0003196
ER -
TY - CPAPER
T1 - Southern Tick Associated Rash Illness (STARI)
T2 - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014)
AN - 1611579609; 6306169
JF - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014)
AU - Marques, Adriana
Y1 - 2014/09/05/
PY - 2014
DA - 2014 Sep 05
KW - Exanthema
KW - Ixodidae
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L2 - http://www.icaac.org/index.php/scientific-program/course-program
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-09-30
N1 - Last updated - 2014-10-15
ER -
TY - CPAPER
T1 - The HOPE Act: Criteria for Transplanting Kidneys or Livers from HIV+ donors to HIV+ recipients
T2 - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014)
AN - 1611579213; 6306325
JF - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014)
AU - Odim Odim, Jonah
Y1 - 2014/09/05/
PY - 2014
DA - 2014 Sep 05
KW - Donors
KW - Transplantation
KW - Liver
KW - Kidneys
KW - Human immunodeficiency virus
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L2 - http://www.icaac.org/index.php/scientific-program/course-program
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-09-30
N1 - Last updated - 2014-10-15
ER -
TY - CPAPER
T1 - Chemokine Receptor Cxcr1 Promotes Candida Killing by Neutrophils and Host Survival After Systemic Candidiasis
T2 - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014)
AN - 1611578620; 6306383
JF - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014)
AU - Swamydas, M
AU - Gao, J-L
AU - Break, T
AU - Green, N
AU - Murphy, P
AU - Lionakis, M
Y1 - 2014/09/05/
PY - 2014
DA - 2014 Sep 05
KW - Cell survival
KW - Candidiasis
KW - Leukocytes (neutrophilic)
KW - Chemokine receptors
KW - Survival
KW - Candida
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L2 - http://www.icaac.org/index.php/scientific-program/course-program
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-09-30
N1 - Last updated - 2014-10-15
ER -
TY - CPAPER
T1 - Effects of Recombinant Human Interleukin 7 on T-Cell Recovery in Patients with Idiopathic CD4 Lymphocytopenia: Results of a Phase I/IIa Study
T2 - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014)
AN - 1611578504; 6306205
JF - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014)
AU - Sheikh, V
AU - Porter, B
AU - DerSimonian, R
AU - Kovacs, S
AU - Freeman, A
AU - Roby, G
AU - Mican, J
AU - Pau, A
AU - Adelsberger, J
AU - Higgins, J
AU - Croughs, T
AU - Estes, J
AU - Yao, M
AU - Sereti, I
Y1 - 2014/09/05/
PY - 2014
DA - 2014 Sep 05
KW - Recombinants
KW - Interleukin 7
KW - CD4 antigen
KW - Lymphocytes T
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L2 - http://www.icaac.org/index.php/scientific-program/course-program
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-09-30
N1 - Last updated - 2014-10-15
ER -
TY - CPAPER
T1 - Development of Animal Models for Pathogenicity and Drug/Vaccine Studies
T2 - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014)
AN - 1611578317; 6306359
JF - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014)
AU - Hensley, Lisa
Y1 - 2014/09/05/
PY - 2014
DA - 2014 Sep 05
KW - Pathogenicity
KW - Disease control
KW - Animal models
KW - Drug development
KW - Vaccines
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L2 - http://www.icaac.org/index.php/scientific-program/course-program
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-09-30
N1 - Last updated - 2014-10-15
ER -
TY - CPAPER
T1 - Pathogenesis of ICL
T2 - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014)
AN - 1611577841; 6306432
JF - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014)
AU - Sereti, Irini
Y1 - 2014/09/05/
PY - 2014
DA - 2014 Sep 05
KW - Chemotherapy
KW - Oncology
KW - Antimicrobial agents
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L2 - http://www.icaac.org/index.php/scientific-program/course-program
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-09-30
N1 - Last updated - 2014-10-15
ER -
TY - CPAPER
T1 - The Role of HIV Reservoirs in HIV Pathogenesis
T2 - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014)
AN - 1611577730; 6306548
JF - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014)
AU - Douek, Daniel
Y1 - 2014/09/05/
PY - 2014
DA - 2014 Sep 05
KW - Human immunodeficiency virus
KW - Reservoirs
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L2 - http://www.icaac.org/index.php/scientific-program/course-program
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-09-30
N1 - Last updated - 2014-10-15
ER -
TY - CPAPER
T1 - Phase I/IIA Clinical Trial of IL-7 for ICL
T2 - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014)
AN - 1611576558; 6306433
JF - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014)
AU - Sheikh, Virginia
Y1 - 2014/09/05/
PY - 2014
DA - 2014 Sep 05
KW - Interleukin 7
KW - Clinical trials
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L2 - http://www.icaac.org/index.php/scientific-program/course-program
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-09-30
N1 - Last updated - 2014-10-15
ER -
TY - CPAPER
T1 - Clinical Consequences of ICL/NIH ICL Cohort
T2 - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014)
AN - 1611576357; 6306430
JF - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014)
AU - Freeman, Alexandra
Y1 - 2014/09/05/
PY - 2014
DA - 2014 Sep 05
KW - Chemotherapy
KW - Oncology
KW - Antimicrobial agents
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L2 - http://www.icaac.org/index.php/scientific-program/course-program
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-09-30
N1 - Last updated - 2014-10-15
ER -
TY - JOUR
T1 - Rapid quantitative chiral amphetamines liquid chromatography-tandem mass spectrometry: method in plasma and oral fluid with a cost-effective chiral derivatizing reagent.
AN - 1553104982; 25065924
AB - Methamphetamine is a widely abused psychostimulant containing a chiral center. Consumption of over-the-counter and prescription medications may yield positive amphetamines results, but chiral separation of l- and d-methamphetamine and its metabolite amphetamine can help determine whether the source was licit or illicit. We present the first LC-MS/MS method with precolumn derivatization for methamphetamine and amphetamine chiral resolution in plasma and oral fluid collected with the Oral-Eze(®) and Quantisal™ devices. To 0.5mL plasma, 0.75mL Oral-Eze, or 1mL Quantisal specimen racemic d11-methamphetamine and amphetamine internal standards were added, followed by protein precipitation. Samples were centrifuged and supernatants loaded onto pre-conditioned Phenomenex(®) Strata™-XC Polymeric Strong Cation solid phase extraction columns. After washing, analytes were eluted with 5% ammonium hydroxide in methanol. The eluate was evaporated to dryness and reconstituted in water. Derivatization was performed with 1-fluoro-2,4-dinitrophenyl-5-l-alanineamide (Marfey's reagent) and heating at 45°C for 1h. Derivatized enantiomer separations were performed under isocratic conditions (methanol:water, 60:40) with a Phenomenex(®) Kinetex(®) 2.6μm C18 column. Analytes were identified and quantified by two MRM transitions and their ratio on a 3200 QTrap (AB Sciex) mass spectrometer in ESI negative mode. In all three matrices, the method was linear for all enantiomers from 1 to 500μg/L, with imprecision and accuracy of ≤11.3% and 85.3-108%, respectively. Extraction efficiencies ranged from 67.4 to 117% and matrix effects from -17.0 to 468%, with variation always ≤19.1%. Authentic plasma and OF specimens were collected from an IRB-approved study that included controlled Vicks(®) VapoInhaler™ administration. The present method is sensitive, selective, economic and rapid (separations accomplished in <10min), and improves methamphetamine result interpretation.
Published by Elsevier B.V.
JF - Journal of chromatography. A
AU - Newmeyer, Matthew N
AU - Concheiro, Marta
AU - Huestis, Marilyn A
AD - Chemistry and Drug Metabolism Section, IRP, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD, USA; Program in Toxicology, University of Maryland Baltimore, Baltimore, MD, USA. ; Chemistry and Drug Metabolism Section, IRP, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD, USA. ; Chemistry and Drug Metabolism Section, IRP, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD, USA. Electronic address: mhuestis@intra.nida.nih.gov.
Y1 - 2014/09/05/
PY - 2014
DA - 2014 Sep 05
SP - 68
EP - 74
VL - 1358
KW - Central Nervous System Stimulants
KW - 0
KW - Dinitrobenzenes
KW - Methamphetamine
KW - 44RAL3456C
KW - Marfey's reagent
KW - 95713-52-3
KW - Alanine
KW - OF5P57N2ZX
KW - Index Medicus
KW - Amphetamines
KW - Plasma
KW - Oral fluid
KW - Chiral analysis
KW - Chromatography, High Pressure Liquid -- standards
KW - Stereoisomerism
KW - Tandem Mass Spectrometry -- standards
KW - Saliva -- chemistry
KW - Humans
KW - Reference Standards
KW - Adult
KW - Limit of Detection
KW - Spectrometry, Mass, Electrospray Ionization -- standards
KW - Male
KW - Methamphetamine -- isolation & purification
KW - Alanine -- analogs & derivatives
KW - Methamphetamine -- blood
KW - Dinitrobenzenes -- chemistry
KW - Central Nervous System Stimulants -- isolation & purification
KW - Central Nervous System Stimulants -- blood
KW - Methamphetamine -- chemistry
KW - Alanine -- chemistry
KW - Central Nervous System Stimulants -- chemistry
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-10-10
N1 - Date created - 2014-08-12
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
J Chromatogr A. 2012 Dec 21;1269:122-35 [22858363]
J Anal Toxicol. 2013 Sep;37(7):452-74 [23934984]
Anal Bioanal Chem. 2012 Nov;404(8):2427-35 [23010844]
J Mass Spectrom. 2011 Jul;46(7):603-14 [21656610]
Br J Clin Pharmacol. 2010 Feb;69(2):187-92 [20233182]
Chirality. 2010 Mar;22(3):320-30 [19544347]
Clin Chem. 2009 Nov;55(11):1910-31 [19745062]
Drug Metab Dispos. 2009 Nov;37(11):2212-20 [19666989]
Anal Bioanal Chem. 2009 Jan;393(2):709-18 [18982317]
Clin Chem. 2007 Apr;53(4):702-10 [17332148]
Clin Pharmacol Ther. 2006 Oct;80(4):403-20 [17015058]
J Anal Toxicol. 1998 Jul-Aug;22(4):265-9 [9681327]
Electrophoresis. 2005 Oct;26(20):3910-20 [16167308]
J Anal Toxicol. 2006 May;30(4):232-7 [16803660]
Drug Metab Rev. 2000 Feb;32(1):15-44 [10711406]
Ther Drug Monit. 2002 Apr;24(2):277-89 [11897973]
Clin Chem. 2002 Sep;48(9):1472-85 [12194924]
Rapid Commun Mass Spectrom. 2003;17(6):569-75 [12621619]
J Anal Toxicol. 2003 Nov-Dec;27(8):552-9 [14670133]
Drug Metab Dispos. 1997 Sep;25(9):1059-64 [9311621]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.chroma.2014.06.096
ER -
TY - JOUR
T1 - Mutant IDH inhibits HNF-4α to block hepatocyte differentiation and promote biliary cancer.
AN - 1560581844; 25043045
AB - Mutations in isocitrate dehydrogenase 1 (IDH1) and IDH2 are among the most common genetic alterations in intrahepatic cholangiocarcinoma (IHCC), a deadly liver cancer. Mutant IDH proteins in IHCC and other malignancies acquire an abnormal enzymatic activity allowing them to convert α-ketoglutarate (αKG) to 2-hydroxyglutarate (2HG), which inhibits the activity of multiple αKG-dependent dioxygenases, and results in alterations in cell differentiation, survival, and extracellular matrix maturation. However, the molecular pathways by which IDH mutations lead to tumour formation remain unclear. Here we show that mutant IDH blocks liver progenitor cells from undergoing hepatocyte differentiation through the production of 2HG and suppression of HNF-4α, a master regulator of hepatocyte identity and quiescence. Correspondingly, genetically engineered mouse models expressing mutant IDH in the adult liver show an aberrant response to hepatic injury, characterized by HNF-4α silencing, impaired hepatocyte differentiation, and markedly elevated levels of cell proliferation. Moreover, IDH and Kras mutations, genetic alterations that co-exist in a subset of human IHCCs, cooperate to drive the expansion of liver progenitor cells, development of premalignant biliary lesions, and progression to metastatic IHCC. These studies provide a functional link between IDH mutations, hepatic cell fate, and IHCC pathogenesis, and present a novel genetically engineered mouse model of IDH-driven malignancy.
JF - Nature
AU - Saha, Supriya K
AU - Parachoniak, Christine A
AU - Ghanta, Krishna S
AU - Fitamant, Julien
AU - Ross, Kenneth N
AU - Najem, Mortada S
AU - Gurumurthy, Sushma
AU - Akbay, Esra A
AU - Sia, Daniela
AU - Cornella, Helena
AU - Miltiadous, Oriana
AU - Walesky, Chad
AU - Deshpande, Vikram
AU - Zhu, Andrew X
AU - Hezel, Aram F
AU - Yen, Katharine E
AU - Straley, Kimberly S
AU - Travins, Jeremy
AU - Popovici-Muller, Janeta
AU - Gliser, Camelia
AU - Ferrone, Cristina R
AU - Apte, Udayan
AU - Llovet, Josep M
AU - Wong, Kwok-Kin
AU - Ramaswamy, Sridhar
AU - Bardeesy, Nabeel
AD - 1] Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, Massachusetts 02114, USA [2]. ; Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, Massachusetts 02114, USA. ; Department of Medical Oncology, Dana-Farber Cancer Institute, Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA. ; 1] HCC Translational Research Laboratory, Barcelona-Clínic Liver Cancer Group, Liver Unit, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Hospital Clínic, University of Barcelona, Catalonia 08036, Spain [2] Mount Sinai Liver Cancer Program, Division of Liver Diseases, Dept of Medicine. Icahn School of Medicine at Mount Sinai, New York 10029, USA [3] Gastrointestinal Surgery and Liver Transplantation Unit, National Cancer Institute, and Department of Experimental Oncology, Milan 20133, Italy. ; HCC Translational Research Laboratory, Barcelona-Clínic Liver Cancer Group, Liver Unit, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Hospital Clínic, University of Barcelona, Catalonia 08036, Spain. ; Mount Sinai Liver Cancer Program, Division of Liver Diseases, Dept of Medicine. Icahn School of Medicine at Mount Sinai, New York 10029, USA. ; Department of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, Kansas 66160, USA. ; University of Rochester Medical Center, Rochester, New York 14642, USA. ; Agios Pharmaceuticals, Cambridge, Massachusetts 02139, USA. ; 1] HCC Translational Research Laboratory, Barcelona-Clínic Liver Cancer Group, Liver Unit, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Hospital Clínic, University of Barcelona, Catalonia 08036, Spain [2] Mount Sinai Liver Cancer Program, Division of Liver Diseases, Dept of Medicine. Icahn School of Medicine at Mount Sinai, New York 10029, USA [3] Institució Catalana de Recerca i Estudis Avançats, Barcelona, Catalonia 08010, Spain [4] University of Barcelona, Catalonia 08036, Spain. ; 1] Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, Massachusetts 02114, USA [2] Broad Institute of Harvard and MIT, Cambridge, Massachusetts 02142, USA.
Y1 - 2014/09/04/
PY - 2014
DA - 2014 Sep 04
SP - 110
EP - 114
VL - 513
IS - 7516
KW - Glutarates
KW - 0
KW - HNF4A protein, human
KW - Hepatocyte Nuclear Factor 4
KW - KRAS protein, human
KW - Mutant Proteins
KW - Proto-Oncogene Proteins
KW - alpha-hydroxyglutarate
KW - 2889-31-8
KW - Isocitrate Dehydrogenase
KW - EC 1.1.1.41
KW - isocitrate dehydrogenase 2, human
KW - IDH1 protein, human
KW - EC 1.1.1.42.
KW - Proto-Oncogene Proteins p21(ras)
KW - EC 3.6.5.2
KW - ras Proteins
KW - Index Medicus
KW - ras Proteins -- genetics
KW - Animals
KW - Glutarates -- metabolism
KW - Humans
KW - Proto-Oncogene Proteins -- metabolism
KW - Stem Cells -- pathology
KW - Disease Models, Animal
KW - Mice
KW - Cell Lineage -- genetics
KW - Mice, Transgenic
KW - Bile Ducts, Intrahepatic -- enzymology
KW - Bile Ducts, Intrahepatic -- pathology
KW - Neoplasm Metastasis
KW - Mutation -- genetics
KW - ras Proteins -- metabolism
KW - Proto-Oncogene Proteins -- genetics
KW - Cell Division -- genetics
KW - Female
KW - Male
KW - Bile Duct Neoplasms -- genetics
KW - Hepatocyte Nuclear Factor 4 -- antagonists & inhibitors
KW - Mutant Proteins -- metabolism
KW - Isocitrate Dehydrogenase -- genetics
KW - Cholangiocarcinoma -- enzymology
KW - Cholangiocarcinoma -- pathology
KW - Hepatocyte Nuclear Factor 4 -- genetics
KW - Cell Differentiation -- genetics
KW - Hepatocytes -- pathology
KW - Bile Duct Neoplasms -- enzymology
KW - Hepatocyte Nuclear Factor 4 -- metabolism
KW - Hepatocytes -- enzymology
KW - Mutant Proteins -- genetics
KW - Cholangiocarcinoma -- genetics
KW - Hepatocyte Nuclear Factor 4 -- biosynthesis
KW - Bile Duct Neoplasms -- pathology
KW - Isocitrate Dehydrogenase -- metabolism
KW - Hepatocytes -- metabolism
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature&rft.atitle=Mutant+IDH+inhibits+HNF-4%CE%B1+to+block+hepatocyte+differentiation+and+promote+biliary+cancer.&rft.au=Saha%2C+Supriya+K%3BParachoniak%2C+Christine+A%3BGhanta%2C+Krishna+S%3BFitamant%2C+Julien%3BRoss%2C+Kenneth+N%3BNajem%2C+Mortada+S%3BGurumurthy%2C+Sushma%3BAkbay%2C+Esra+A%3BSia%2C+Daniela%3BCornella%2C+Helena%3BMiltiadous%2C+Oriana%3BWalesky%2C+Chad%3BDeshpande%2C+Vikram%3BZhu%2C+Andrew+X%3BHezel%2C+Aram+F%3BYen%2C+Katharine+E%3BStraley%2C+Kimberly+S%3BTravins%2C+Jeremy%3BPopovici-Muller%2C+Janeta%3BGliser%2C+Camelia%3BFerrone%2C+Cristina+R%3BApte%2C+Udayan%3BLlovet%2C+Josep+M%3BWong%2C+Kwok-Kin%3BRamaswamy%2C+Sridhar%3BBardeesy%2C+Nabeel&rft.aulast=Saha&rft.aufirst=Supriya&rft.date=2014-09-04&rft.volume=513&rft.issue=7516&rft.spage=110&rft.isbn=&rft.btitle=&rft.title=Nature&rft.issn=1476-4687&rft_id=info:doi/10.1038%2Fnature13441
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-09-24
N1 - Date created - 2014-09-04
N1 - Date revised - 2017-01-14
N1 - Genetic sequence - GSE57002; GEO
N1 - SuppNotes - Cited By:
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Erratum In:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1038/nature13441
ER -
TY - JOUR
T1 - Understanding the Role of mHealth and Other Media Interventions for Behavior Change to Enhance Child Survival and Development in Low- and Middle-Income Countries: An Evidence Review
AN - 1727697830; 20864202
AB - Given the high morbidity and mortality among children in low- and middle-income countries as a result of preventable causes, the U.S. government and the United Nations Children's Fund convened an Evidence Summit on Enhancing Child Survival and Development in Lower- and Middle-Income Countries by Achieving Population-Level Behavior Change on June 3-4, 2013, in Washington, D.C. This article summarizes evidence for technological advances associated with population-level behavior changes necessary to advance child survival and healthy development in children under 5 years of age in low- and middle-income countries. After a rigorous evidence selection process, the authors assessed science, technology, and innovation papers that used mHealth, social/transmedia, multiplatform media, health literacy, and devices for behavior changes supporting child survival and development. Because of an insufficient number of studies on health literacy and devices that supported causal attribution of interventions to outcomes, the review focused on mHealth, social/transmedia, and multiplatform media. Overall, this review found that some mHealth interventions have sufficient evidence to make topic-specific recommendations for broader implementation, scaling, and next research steps (e.g., adherence to HIV/AIDS antiretroviral therapy, uptake and demand of maternal health service, and compliance with malaria treatment guidelines). While some media evidence demonstrates effectiveness in changing cognitive abilities, knowledge, and attitudes, evidence is minimal on behavioral endpoints linked to child survival. Population level behavior change is necessary to end preventable child deaths. Donors and low- and middle-income countries are encouraged to implement recommendations for informing practice, policy, and research decisions to fully maximize the impact potential of mHealth and multimedia for child survival and development.
JF - Journal of Health Communication
AU - Higgs, Elizabeth S
AU - Goldberg, Allison B
AU - Labrique, Alain B
AU - Cook, Stephanie H
AU - Schmid, Carina
AU - Cole, Charlotte F
AU - Obregon, Rafael A
AD - Division of Clinical Research, National Institute for Allergy and Infectious Diseases, Bethesda, Maryland, USA, ehiggs@niaid.nih.gov
Y1 - 2014/09/02/
PY - 2014
DA - 2014 Sep 02
SP - 164
EP - 189
PB - Taylor & Francis Group Ltd., 2 Park Square Oxford OX14 4RN United Kingdom
VL - 19
IS - sup1
SN - 1081-0730, 1081-0730
KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources
KW - Policies
KW - Human diseases
KW - Human immunodeficiency virus
KW - International organizations
KW - Environmental impact
KW - Therapy
KW - Survival
KW - Malaria
KW - INE, USA, Washington
KW - Mortality causes
KW - Ecosystem disturbance
KW - Q1 08604:Stock assessment and management
KW - Q5 08524:Public health, medicines, dangerous organisms
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Health+Communication&rft.atitle=Understanding+the+Role+of+mHealth+and+Other+Media+Interventions+for+Behavior+Change+to+Enhance+Child+Survival+and+Development+in+Low-+and+Middle-Income+Countries%3A+An+Evidence+Review&rft.au=Higgs%2C+Elizabeth+S%3BGoldberg%2C+Allison+B%3BLabrique%2C+Alain+B%3BCook%2C+Stephanie+H%3BSchmid%2C+Carina%3BCole%2C+Charlotte+F%3BObregon%2C+Rafael+A&rft.aulast=Higgs&rft.aufirst=Elizabeth&rft.date=2014-09-02&rft.volume=19&rft.issue=sup1&rft.spage=164&rft.isbn=&rft.btitle=&rft.title=Journal+of+Health+Communication&rft.issn=10810730&rft_id=info:doi/10.1080%2F10810730.2014.929763
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-10-01
N1 - Last updated - 2016-10-12
N1 - SubjectsTermNotLitGenreText - Human diseases; Policies; International organizations; Therapy; Environmental impact; Survival; Malaria; Ecosystem disturbance; Mortality causes; Human immunodeficiency virus; INE, USA, Washington
DO - http://dx.doi.org/10.1080/10810730.2014.929763
ER -
TY - JOUR
T1 - Making Sense of the Undue Burden Interpretation of Minimal Risk
AN - 1611637063; 20660684
JF - American Journal of Bioethics
AU - Resnik, David B
AD - National Institute of Environmental Health Sciences
Y1 - 2014/09/02/
PY - 2014
DA - 2014 Sep 02
SP - 1
EP - 2
PB - Taylor & Francis Group Ltd., 2 Park Square Oxford OX14 4RN United Kingdom
VL - 14
IS - 9
SN - 1526-5161, 1526-5161
KW - Environment Abstracts
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1611637063?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aenvabstractsmodule&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Bioethics&rft.atitle=Making+Sense+of+the+Undue+Burden+Interpretation+of+Minimal+Risk&rft.au=Resnik%2C+David+B&rft.aulast=Resnik&rft.aufirst=David&rft.date=2014-09-02&rft.volume=14&rft.issue=9&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Bioethics&rft.issn=15265161&rft_id=info:doi/10.1080%2F15265161.2014.935880
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-10-01
N1 - Last updated - 2014-10-15
DO - http://dx.doi.org/10.1080/15265161.2014.935880
ER -
TY - JOUR
T1 - Duration and intensity of tobacco smoking and the risk of papillary and non-papillary transitional cell carcinoma of the bladder
AN - 1842507920; 20695225
AB - Purpose: To evaluate the impact of tobacco smoking on specific histological subtypes of transitional cell carcinoma of the bladder (TCC). Methods: Between 2003 and 2009, we conducted a hospital-based case-control study in Italy, enrolling 531 incident TCC cases and 524 cancer-free matched patients. Odds ratios (OR) and corresponding 95% confidence intervals (CI) were estimated through multiple logistic regression models. Results: Compared to never smokers, TCC risk was threefold higher in former smokers (95% CI 2.07-4.18) and more than sixfold higher in current smokers (95% CI 4.54-9.85). TCC risk steadily increased with increasing intensity (OR for greater than or equal to 25 cigarettes/day 8.75; 95% CI 3.40-22.55) and duration of smoking (OR for greater than or equal to 50 years 5.46; 95% CI 2.60-11.49). No heterogeneity emerged between papillary and non-papillary TCCs for smoking intensity and duration, but the risk for those who had smoked for greater than or equal to 50 years was twice for non-papillary TCC (OR 10.88) compared with papillary one (OR 4.76). Among current smokers, the risk for a 10-year increase in duration grew across strata of intensity (p-trend = 0.046). Conversely, the risk for a 5-cigarette/day increase in smoking intensity was quite steady across strata of duration (p-trend = 0.18). Conclusions: Study results suggested that duration of smoking outweighs intensity in determining TCC risk, with limited differences across histological subtypes. Elimination of tobacco smoking may prevent about 65 % of TCCs.
JF - Cancer Causes & Control
AU - Polesel, Jerry
AU - Bosetti, Cristina
AU - di Maso, Matteo
AU - Montella, Maurizio
AU - Libra, Massimo
AU - Garbeglio, Antonio
AU - Zucchetto, Antonella
AU - Turati, Federica
AU - Talamini, Renato
AU - La Vecchia, Carlo
AU - Serraino, Diego
AD - Unit of Epidemiology and Biostatistics, IRCCS - CRO Aviano National Cancer Institute, Via F. Gallini 2, 33081, Aviano, PN, Italy, polesel@cro.it
Y1 - 2014/09//
PY - 2014
DA - September 2014
SP - 1151
EP - 1158
PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL - 25
IS - 9
SN - 0957-5243, 0957-5243
KW - Toxicology Abstracts
KW - Tobacco smoking
KW - Cigarettes
KW - Urinary bladder
KW - Risk factors
KW - Regression analysis
KW - transitional cell carcinoma
KW - X 24380:Social Poisons & Drug Abuse
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Causes+%26+Control&rft.atitle=Duration+and+intensity+of+tobacco+smoking+and+the+risk+of+papillary+and+non-papillary+transitional+cell+carcinoma+of+the+bladder&rft.au=Polesel%2C+Jerry%3BBosetti%2C+Cristina%3Bdi+Maso%2C+Matteo%3BMontella%2C+Maurizio%3BLibra%2C+Massimo%3BGarbeglio%2C+Antonio%3BZucchetto%2C+Antonella%3BTurati%2C+Federica%3BTalamini%2C+Renato%3BLa+Vecchia%2C+Carlo%3BSerraino%2C+Diego&rft.aulast=Polesel&rft.aufirst=Jerry&rft.date=2014-09-01&rft.volume=25&rft.issue=9&rft.spage=1151&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/10.1007%2Fs10552-014-0416-0
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2016-11-01
N1 - Number of references - 27
N1 - Last updated - 2016-12-22
N1 - SubjectsTermNotLitGenreText - Tobacco smoking; Cigarettes; Urinary bladder; Risk factors; Regression analysis; transitional cell carcinoma
DO - http://dx.doi.org/10.1007/s10552-014-0416-0
ER -
TY - JOUR
T1 - State‐Level School Competitive Food and Beverage Laws Are Associated With Children's Weight Status
AN - 1748688066
AB - This study attempted to determine whether state laws regulating low nutrient, high energy‐dense foods and beverages sold outside of the reimbursable school meals program (referred to as “competitive foods”) are associated with children's weight status. We use the Classification of Laws Associated with School Students (CLASS) database of state codified law(s) relevant to school nutrition. States were classified as having strong, weak, or no competitive food laws in 2005 based on strength and comprehensiveness. Parent‐reported height and weight along with demographic, behavioral, family, and household characteristics were obtained from the 2007 National Survey of Children's Health. Bivariate and logistic regression analyses estimated the association between states' competitive food laws and children's overweight and obesity status (body mass index [BMI]‐for‐age ≥85th percentile). Children (N = 16,271) between the ages of 11‐14 years with a BMI for age ≥5th percentile who attended public school were included. Children living in states with weak competitive food laws for middle schools had over a 20% higher odds of being overweight or obese than children living in states with either no or strong school competitive food laws. State‐level school competitive food and beverage laws merit attention with efforts to address the childhood obesity epidemic. Attention to the specificity and requirements of these laws should also be considered.
JF - The Journal of School Health
AU - Hennessy, Erin
AU - Oh, April
AU - Agurs‐Collins, Tanya
AU - Chriqui, Jamie F
AU - Msse, Louise C
AU - Moser, Richard P
AU - Perna, Frank
AD - Leidos Biomedical Research Inc., Frederick National Laboratory for Cancer Research, Support to Behavioral Research Program, Division of Cancer Control and Population Sciences. National Cancer Institute erin.hennessy@fnlcr.nih.gov; Health Communication and Informatics Research Branch, Behavioral Research Program, Division of Cancer Control and Population Sciences. National Cancer Institute ohay@mail.nih.gov; Health Behaviors Research Branch, Behavioral Research Program, Division of Cancer Control and Population Sciences. National Cancer Institute collinsta@mail.nih.gov pernafm@mail.nih.gov; Institute for Health Research and Policy. University of Illinois at Chicago (MC 275) jchriqui@uic.edu; School of Population and Public Health, University of British Columbia. BC Children's Hospital and BC Women's Hospital & Health Centre lmasse@cfri.ubc.ca; Science of Research and Technology Branch, Behavioral Research Program, Division of Cancer Control and Population Sciences. National Cancer Institute moserr@mail.nih.gov; Leidos Biomedical Research Inc., Frederick National Laboratory for Cancer Research, Support to Behavioral Research Program, Division of Cancer Control and Population Sciences. National Cancer Institute
Y1 - 2014/09//
PY - 2014
DA - Sep 2014
SP - 609
EP - 616
CY - Kent
PB - Wiley Subscription Services, Inc.
VL - 84
IS - 9
SN - 0022-4391
KW - Physical Fitness And Hygiene
KW - Body mass
KW - Attention
KW - Codification
KW - Obesity
KW - School meals
KW - Body Mass Index
KW - Body weight
KW - Childhood
KW - Children
KW - Classification
KW - Demographic aspects
KW - Drinks
KW - Food
KW - Health
KW - Healthy food
KW - Meals
KW - Middle schools
KW - Nutrition
KW - Obese children
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+School+Health&rft.atitle=State%E2%80%90Level+School+Competitive+Food+and+Beverage+Laws+Are+Associated+With+Children%27s+Weight+Status&rft.au=Hennessy%2C+Erin%3BOh%2C+April%3BAgurs%E2%80%90Collins%2C+Tanya%3BChriqui%2C+Jamie+F%3BMsse%2C+Louise+C%3BMoser%2C+Richard+P%3BPerna%2C+Frank&rft.aulast=Hennessy&rft.aufirst=Erin&rft.date=2014-09-01&rft.volume=84&rft.issue=9&rft.spage=609&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+School+Health&rft.issn=00224391&rft_id=info:doi/10.1111%2Fjosh.12181
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Date revised - 2014-10-14
N1 - Last updated - 2016-05-12
DO - http://dx.doi.org/10.1111/josh.12181
ER -
TY - JOUR
T1 - In Vivo Imaging of Tumor Physiological, Metabolic, and Redox Changes in Response to the Anti-Angiogenic Agent Sunitinib: Longitudinal Assessment to Identify Transient Vascular Renormalization
AN - 1746891209; PQ0001373072
AB - Aims: The tumor microenvironment is characterized by a highly reducing redox status, a low pH, and hypoxia. Anti-angiogenic therapies for solid tumors frequently function in two steps: the transient normalization of structurally and functionally aberrant tumor blood vessels with increased blood perfusion, followed by the pruning of tumor blood vessels and the resultant cessation of nutrients and oxygen delivery required for tumor growth. Conventional anatomic or vascular imaging is impractical or insufficient to distinguish between the two steps of tumor response to anti-angiogenic therapies. Here, we investigated whether the noninvasive imaging of the tumor redox state and energy metabolism could be used to characterize anti-angiogenic drug-induced transient vascular normalization. Results: Daily treatment of squamous cell carcinoma (SCCVII) tumor-bearing mice with the multi-tyrosine kinase inhibitor sunitinib resulted in a rapid decrease in tumor microvessel density and the suppression of tumor growth. Tumor pO sub(2) imaging by electron paramagnetic resonance imaging showed a transient increase in tumor oxygenation after 2-4 days of sunitinib treatment, implying improved tumor perfusion. During this window of vascular normalization, magnetic resonance imaging of the redox status using an exogenously administered nitroxide probe and hyperpolarized super(13)C MRI of the metabolic flux of pyruvate/lactate couple revealed an oxidative shift in tumor redox status. Innovation: Redox-sensitive metabolic couples can serve as noninvasive surrogate markers to identify the vascular normalization window in tumors with imaging techniques. Conclusion: A multimodal imaging approach to characterize physiological, metabolic, and redox changes in tumors is useful to distinguish between the different stages of anti-angiogenic treatment.
JF - Antioxidants and Redox Signaling
AU - Matsumoto, Shingo
AU - Saito, Keita
AU - Takakusagi, Yoichi
AU - Matsuo, Masayuki
AU - Munasinghe, Jeeva P
AU - Morris, Herman D
AU - Lizak, Martin J
AU - Merkle, Hellmut
AU - Yasukawa, Keiji
AU - Devasahayam, Nallathamby
AU - Suburamanian, Sankaran
AU - Mitchell, James B
AU - Krishna, Murali C
AD - Radiation Biology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, murali@helix.nih.gov
PY - 2014
SP - 1145
EP - 1155
PB - Mary Ann Liebert, Inc., 2 Madison Ave Larchmont NY 10538-1962 United States
VL - 21
IS - 8
SN - 1523-0864, 1523-0864
KW - Toxicology Abstracts
KW - Redox properties
KW - Antioxidants
KW - Perfusion
KW - Energy metabolism
KW - Solid tumors
KW - Magnetic resonance imaging
KW - Probes
KW - Nutrients
KW - squamous cell carcinoma
KW - Tumors
KW - Oxygen
KW - Pyruvic acid
KW - Blood vessels
KW - Lactic acid
KW - Microenvironments
KW - Pruning
KW - Nitroxide
KW - pH effects
KW - metabolic flux
KW - X 24390:Radioactive Materials
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Antioxidants+and+Redox+Signaling&rft.atitle=In+Vivo+Imaging+of+Tumor+Physiological%2C+Metabolic%2C+and+Redox+Changes+in+Response+to+the+Anti-Angiogenic+Agent+Sunitinib%3A+Longitudinal+Assessment+to+Identify+Transient+Vascular+Renormalization&rft.au=Matsumoto%2C+Shingo%3BSaito%2C+Keita%3BTakakusagi%2C+Yoichi%3BMatsuo%2C+Masayuki%3BMunasinghe%2C+Jeeva+P%3BMorris%2C+Herman+D%3BLizak%2C+Martin+J%3BMerkle%2C+Hellmut%3BYasukawa%2C+Keiji%3BDevasahayam%2C+Nallathamby%3BSuburamanian%2C+Sankaran%3BMitchell%2C+James+B%3BKrishna%2C+Murali+C&rft.aulast=Matsumoto&rft.aufirst=Shingo&rft.date=2014-09-01&rft.volume=21&rft.issue=8&rft.spage=1145&rft.isbn=&rft.btitle=&rft.title=Antioxidants+and+Redox+Signaling&rft.issn=15230864&rft_id=info:doi/10.1089%2Fars.2013.5725
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-12-01
N1 - Last updated - 2016-01-21
N1 - SubjectsTermNotLitGenreText - Redox properties; Perfusion; Antioxidants; Energy metabolism; Solid tumors; Magnetic resonance imaging; Probes; squamous cell carcinoma; Nutrients; Tumors; Oxygen; Pyruvic acid; Blood vessels; Lactic acid; Microenvironments; Pruning; pH effects; Nitroxide; metabolic flux
DO - http://dx.doi.org/10.1089/ars.2013.5725
ER -
TY - JOUR
T1 - Correlates of Current Smoking Among Malaysian Secondary School Children
AN - 1701480360; PQ0001677906
AB - Cigarette smoking in adolescent is a significant public health problem, leading to the risk of addiction, morbidity, and mortality in the long term. This study determined the prevalence and correlates of current smoking among adolescent school children. A nationwide school-based survey among 25 507 students between Forms 1 to 5 (aged 12-17) was conducted using a 2-stage cluster sampling design. The prevalence of current smoking was 11.5%. Multivariable logistic regression analysis revealed that current smoking was significantly associated with males (adjusted odds ratio [aOR] = 3.25; 95% confidence interval [CI] = 1.87, 4.98), current drinking (aOR = 2.34; 95% CI = 1.46, 3.74), drug used (aOR = 2.97; 95% CI = 1.24, 7.11), and being bullied (aOR = 1.41; 95% CI = 1.00, 1.98) at least once in the past 12 months. Smoking is associated with several behaviors that pose risks to adolescents, such as social issues and smoking-related health problems. Thus, early and integrated prevention programs that address multiple risk behaviors simultaneously are required.
JF - Asia-Pacific Journal of Public Health
AU - Tee, Guat Hiong
AU - Kaur, Gurpreet
AD - Institute for Public Health, National Institutes of Health, Ministry of Health, Kuala Lumpur, Malaysia
Y1 - 2014/09//
PY - 2014
DA - Sep 2014
SP - 70S
EP - 80S
PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom
VL - 26
IS - 5
SN - 1010-5395, 1010-5395
KW - Risk Abstracts; Health & Safety Science Abstracts
KW - smoking
KW - drinking alcohol
KW - substance use
KW - bullying
KW - Global School Health Survey (GSHS)
KW - Malaysia
KW - adolescent
KW - Mortality
KW - Health problems
KW - Cigarettes
KW - Risk taking
KW - Children
KW - Morbidity
KW - Public health
KW - Prevention
KW - Behavior
KW - Drugs
KW - Adolescents
KW - Bullying
KW - R2 23060:Medical and environmental health
KW - H 12000:Epidemiology and Public Health
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1701480360?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Asia-Pacific+Journal+of+Public+Health&rft.atitle=Correlates+of+Current+Smoking+Among+Malaysian+Secondary+School+Children&rft.au=Tee%2C+Guat+Hiong%3BKaur%2C+Gurpreet&rft.aulast=Tee&rft.aufirst=Guat&rft.date=2014-09-01&rft.volume=26&rft.issue=5&rft.spage=70S&rft.isbn=&rft.btitle=&rft.title=Asia-Pacific+Journal+of+Public+Health&rft.issn=10105395&rft_id=info:doi/10.1177%2F1010539514540468
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-08-01
N1 - Number of references - 30
N1 - Last updated - 2015-08-05
N1 - SubjectsTermNotLitGenreText - Mortality; Health problems; Prevention; Cigarettes; Behavior; Risk taking; Children; Drugs; Bullying; Morbidity; Adolescents; Public health
DO - http://dx.doi.org/10.1177/1010539514540468
ER -
TY - JOUR
T1 - Time Perspective and Exercise, Obesity, and Smoking: Moderation of Associations by Age
AN - 1665152161
AB - Purpose. Time perspective, a psychological construct denoting subjective orientation to either present or future concerns, has been inconsistently associated with healthy behaviors in adults. We hypothesized that associations would be stronger in young adults, who are first developing independent attitudes, than in older adults. Design. Cross-sectional survey. Setting. The study was conducted in three cities in the Mid-Atlantic region. Subjects. Subjects were 790 patrons of barber and beauty shops. Measures. Measures used were the Zimbardo Time Perspective Inventory future, present-fatalistic, and present-hedonistic subscales and current smoking, days per week of recreational exercise, and height and weight, by self-report. Analysis. We tested if associations between time perspective and exercise, obesity, and current smoking differed by age group (18-24 years, 25-34 years, and 35 years and older) using analysis of variance and logistic regression. Results. Higher future time perspective scores, indicating greater focus on future events, ivas associated with more frequent exercise, whereas higher present-fatalistic time perspective scores, indicating more hopelessness, was associated with less frequent exercise in 18- to 24-year-olds, but not in older individuals. Lower future time perspective scores, and higher present-hedonistic time perspective scores, indicating interest in pleasure-seeking, were also associated with obesity only in 18- to 24-year-olds. Current smoking was not related to time perspective in any age group. Conclusion. Time perspective has age-specific associations with exercise and obesity, suggesting stages when lime perspective may influence health behavior decision making.
JF - American Journal of Health Promotion : AJHP.
AU - Guthrie, Lori C
AU - Butler, Stephen C
AU - Lessl, Kristen
AU - Ochi, Onyinyechukwu
AU - Ward, Michael M
AD - National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland ; National Institutes of Health, Building 10 CRC, Room 4-1339, Bethesda, MD, 20892 ; National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland
Y1 - 2014///Sep/Oct
PY - 2014
DA - Sep/Oct 2014
SP - 9
EP - 16
CY - Birmingham
PB - Mosby-Year Book, Inc.
VL - 29
IS - 1
SN - 0890-1171
KW - Physical Fitness And Hygiene
KW - Age differences
KW - Associations
KW - Selfreport
KW - Shops
KW - Smoking
KW - Young adults
KW - Attitudes
KW - Beauty
KW - Decision making
KW - Elderly people
KW - Exercise
KW - Future events
KW - Health behaviour
KW - Healthy habits
KW - Hopelessness
KW - Moderation
KW - Obesity
KW - Older people
KW - Patrons
KW - Pleasure
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665152161?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Health+Promotion+%3A+AJHP.&rft.atitle=Time+Perspective+and+Exercise%2C+Obesity%2C+and+Smoking%3A+Moderation+of+Associations+by+Age&rft.au=Guthrie%2C+Lori+C%3BButler%2C+Stephen+C%3BLessl%2C+Kristen%3BOchi%2C+Onyinyechukwu%3BWard%2C+Michael+M&rft.aulast=Guthrie&rft.aufirst=Lori&rft.date=2014-09-01&rft.volume=29&rft.issue=1&rft.spage=9&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Health+Promotion+%3A+AJHP.&rft.issn=08901171&rft_id=info:doi/10.4278%2Fajhp.130122-QUAN-39
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Date revised - 2015-01-09
N1 - Last updated - 2016-05-12
DO - http://dx.doi.org/10.4278/ajhp.130122-QUAN-39
ER -
TY - JOUR
T1 - Clear Water Flows from Its Origin: Congratulations on the 30 super(th) Anniversary Celebration of Journal of Environmental and Occupational Medicine
AN - 1654666361; 21198189
AB - Abstract not available.
JF - Huanjing yu Zhiye Yixue
AU - HU, Hui
AD - Environmental Health Perspectives, National Institute of Environmental Health Sciences, NC 27709, USA, hu@niehs.nih.gov
Y1 - 2014/09//
PY - 2014
DA - Sep 2014
SP - 686
PB - Shanghai Shi Jibing Fangkongzhi Zhongxin, 1105 Zhongxing Lu Shanghai 200070 China
VL - 31
IS - 9
SN - 1006-3617, 1006-3617
KW - Health & Safety Science Abstracts; Environment Abstracts
KW - Journal of Environmental and Occupational Medicine
KW - public health
KW - Environmental Health Perspectives(EHP)
KW - Water flow
KW - H 1000:Occupational Safety and Health
KW - ENA 02:Toxicology & Environmental Safety
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Huanjing+yu+Zhiye+Yixue&rft.atitle=Clear+Water+Flows+from+Its+Origin%3A+Congratulations+on+the+30+super%28th%29+Anniversary+Celebration+of+Journal+of+Environmental+and+Occupational+Medicine&rft.au=HU%2C+Hui&rft.aulast=HU&rft.aufirst=Hui&rft.date=2014-09-01&rft.volume=31&rft.issue=9&rft.spage=686&rft.isbn=&rft.btitle=&rft.title=Huanjing+yu+Zhiye+Yixue&rft.issn=10063617&rft_id=info:doi/10.13213%2Fj.cnki.jeom.2014.0166
LA - Chinese
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-02-01
N1 - Last updated - 2015-04-16
N1 - SubjectsTermNotLitGenreText - Water flow
DO - http://dx.doi.org/10.13213/j.cnki.jeom.2014.0166
ER -
TY - JOUR
T1 - Nonmedical Prescription Drug Use Comorbidity: Developing a Cohesive Risk Model
AN - 1627733707
AB - Nonmedical Prescription Drug Use (NMPDU) is a growing issue world-wide. Previously, NMPDU comorbidity has been investigated using bivariate approaches, providing a piecemeal understanding of NMPDU’s relationship to other mental disorders. We investigate how NMPDU fits within the multivariate meta-structure of psychiatric comorbidity and how this might vary as a function of gender. Data were collected as part of the National Epidemiological Survey on Alcohol and Related Conditions (NESARC) in 2001–2002 on 43,093 individuals 18 years or older living in the US. The Alcohol Use Disorder and Associated Disabilities Interview Schedule DSM-IV version IV (AUDADIS-IV) assessed psychiatric diagnoses and sedative, tranquilizer, opioid, and amphetamine NMPDU. Using confirmatory factor analysis, NMPDU was introduced into the internalizing-externalizing model of common mental disorders to determine where it best fits. Models were examined separately for men and women and tested for gender invariance. NMPDU was strongly associated with the externalizing factor, and also showed a very small secondary association with the fear subfactor of internalizing. This structure was gender invariant. Differences between men and women’s prevalence rates originate at the level of the latent factors. Results indicate a shared liability to NMPDU and other forms of externalizing psychopathology such as other substance use disorders, as well as antisocial behaviors. Research on NMPDU can benefit from focusing on the externalizing factor, aiming to understand how risk factors for diverse externalizing disorders may also manifest as NMPDU. Prescribers should be particularly attentive to the presence of the entire spectrum of externalizing disorders, as they may signal risk for NMPDU.
JF - Journal of Psychopathology and Behavioral Assessment
AU - Ofrat, Shani
AU - Krueger, Robert F
AU - Eaton, Nicholas R
AU - Keyes, Katherine M
AU - Skodol, Andrew E
AU - Grant, Bridget F
AU - Hasin, Deborah S
AD - Department of Psychology, University of Minnesota, 75 East River Road, Minneapolis, MN, 55455, USA krueg038@umn.edu krueg038@umn.edu; Stony Brook University, Stony Brook, NY, USA ; Columbia University, New York, NY, USA ; Columbia University, New York, NY, USA, University of Arizona, Phoenix, AZ, USA ; National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD, USA ; Department of Psychology, University of Minnesota, 75 East River Road, Minneapolis, MN, 55455, USA
Y1 - 2014/09//
PY - 2014
DA - Sep 2014
SP - 371
EP - 379
CY - New York
PB - Springer Science & Business Media
VL - 36
IS - 3
SN - 0882-2689
KW - Psychology
KW - Alcohol consumption
KW - Alcohol related disorders
KW - Amphetamines
KW - Antisocial behaviour
KW - Risk factors
KW - Substance abuse disorders
KW - Comorbidity
KW - Confirmatory factor analysis
KW - Drug abuse
KW - Externalizing behaviour
KW - Externalizing problems
KW - Factor analysis
KW - Fear
KW - Gender
KW - Gender differences
KW - Internalization
KW - Liability
KW - Prevalence
KW - Psychiatric disorders
KW - Psychopathology
KW - United States--US
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Psychopathology+and+Behavioral+Assessment&rft.atitle=Nonmedical+Prescription+Drug+Use+Comorbidity%3A+Developing+a+Cohesive+Risk+Model&rft.au=Ofrat%2C+Shani%3BKrueger%2C+Robert+F%3BEaton%2C+Nicholas+R%3BKeyes%2C+Katherine+M%3BSkodol%2C+Andrew+E%3BGrant%2C+Bridget+F%3BHasin%2C+Deborah+S&rft.aulast=Ofrat&rft.aufirst=Shani&rft.date=2014-09-01&rft.volume=36&rft.issue=3&rft.spage=371&rft.isbn=&rft.btitle=&rft.title=Journal+of+Psychopathology+and+Behavioral+Assessment&rft.issn=08822689&rft_id=info:doi/10.1007%2Fs10862-014-9409-2
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Date revised - 2014-10-14
N1 - Last updated - 2016-05-13
N1 - SubjectsTermNotLitGenreText - United States--US
DO - http://dx.doi.org/10.1007/s10862-014-9409-2
ER -
TY - JOUR
T1 - Regulation of Motor Function and Behavior by Atypical Chemokine Receptor 1
AN - 1627730456
AB - Atypical Chemokine Receptor 1 (ACKR1), previously known as Duffy Antigen Receptor for Chemokines, stands out among chemokine receptors for high selective expression on cerebellar Purkinje neurons. Although ACKR1 ligands activate Purkinje cells in vitro, evidence for ACKR1 regulation of brain function in vivo is lacking. Here we demonstrate that Ackr1 −/− mice have markedly impaired balance and ataxia on a rotating rod and increased tremor when injected with harmaline, which induces whole-body tremor by activating Purkinje cells. Ackr1 −/− mice also exhibited impaired exploratory behavior, increased anxiety-like behavior and frequent episodes of marked hypoactivity under low-stress conditions. Surprisingly, Ackr1 + /− had similar behavioral abnormalities, indicating pronounced haploinsufficiency. The behavioral phenotype of Ackr1 − /− mice was the opposite of mouse models of cerebellar degeneration, and the defects persisted when Ackr1 was deficient only on non-hematopoietic cells. Together, the results suggest that normal motor function and behavior may partly depend on negative regulation of Purkinje cell activity by Ackr1.
JF - Behavior Genetics
AU - Schneider, Erich H
AU - Fowler, Stephen C
AU - Lionakis, Michail S
AU - Swamydas, Muthulekha
AU - Holmes, Gibran
AU - Diaz, Vivian
AU - Munasinghe, Jeeva
AU - Peiper, Stephen C
AU - Gao, Ji-Liang
AU - Murphy, Philip M
AD - Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases (NIAID)/NIH, Bethesda, MD, USA, Institute of Pharmacology, Hannover Medical School, Hannover, Germany ; Department of Pharmacology and Toxicology, University of Kansas, Lawrence, KS, USA ; Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases (NIAID)/NIH, Bethesda, MD, USA, Fungal Pathogenesis Unit, Laboratory of Clinical Infectious Diseases, NIAID/NIH, Bethesda, MD, USA ; Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases (NIAID)/NIH, Bethesda, MD, USA ; In Vivo NMR Center, National Institute of Neurological Diseases and Stroke (NINDS)/NIH, Bethesda, MD, USA ; Institute of Pathology, Anatomy and Cell Biology, Jefferson Medical College, Philadelphia, PA, USA ; Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases (NIAID)/NIH, Bethesda, MD, USA, Bldg 10, Room 11N113, NIH, Bethesda, MD, 20892, USA ; Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases (NIAID)/NIH, Bethesda, MD, USA; Institute of Pharmacology, Hannover Medical School, Hannover, Germany
Y1 - 2014/09//
PY - 2014
DA - Sep 2014
SP - 498
EP - 515
CY - New York
PB - Springer Science & Business Media
VL - 44
IS - 5
SN - 0001-8244
KW - Biology
KW - Animals
KW - Behaviour
KW - Anxiety
KW - Ataxia
KW - Brain
KW - Defects
KW - Motor performance
KW - Neurons
KW - Regulation
KW - Stress
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Behavior+Genetics&rft.atitle=Regulation+of+Motor+Function+and+Behavior+by+Atypical+Chemokine+Receptor+1&rft.au=Schneider%2C+Erich+H%3BFowler%2C+Stephen+C%3BLionakis%2C+Michail+S%3BSwamydas%2C+Muthulekha%3BHolmes%2C+Gibran%3BDiaz%2C+Vivian%3BMunasinghe%2C+Jeeva%3BPeiper%2C+Stephen+C%3BGao%2C+Ji-Liang%3BMurphy%2C+Philip+M&rft.aulast=Schneider&rft.aufirst=Erich&rft.date=2014-09-01&rft.volume=44&rft.issue=5&rft.spage=498&rft.isbn=&rft.btitle=&rft.title=Behavior+Genetics&rft.issn=00018244&rft_id=info:doi/10.1007%2Fs10519-014-9665-7
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Date revised - 2014-11-10
N1 - Last updated - 2016-05-24
DO - http://dx.doi.org/10.1007/s10519-014-9665-7
ER -
TY - JOUR
T1 - Dark matter in archaeal genomes: a rich source of novel mobile elements, defense systems and secretory complexes
AN - 1618155698; 20849255
AB - Microbial genomes encompass a sizable fraction of poorly characterized, narrowly spread fast-evolving genes. Using sensitive methods for sequences comparison and protein structure prediction, we performed a detailed comparative analysis of clusters of such genes, which we denote "dark matter islands", in archaeal genomes. The dark matter islands comprise up to 20 % of archaeal genomes and show remarkable heterogeneity and diversity. Nevertheless, three classes of entities are common in these genomic loci: (a) integrated viral genomes and other mobile elements; (b) defense systems, and (c) secretory and other membrane-associated systems. The dark matter islands in the genome of thermophiles and mesophiles show similar general trends of gene content, but thermophiles are substantially enriched in predicted membrane proteins whereas mesophiles have a greater proportion of recognizable mobile elements. Based on this analysis, we predict the existence of several novel groups of viruses and mobile elements, previously unnoticed variants of CRISPR-Cas immune systems, and new secretory systems that might be involved in stress response, intermicrobial conflicts and biogenesis of novel, uncharacterized membrane structures.
JF - Extremophiles
AU - Makarova, Kira S
AU - Wolf, Yuri I
AU - Forterre, Patrick
AU - Prangishvili, David
AU - Krupovic, Mart
AU - Koonin, Eugene V
AD - National Center for Biotechnology Information, National Library of Medicine, Bethesda, MD, 20894, USA, koonin@ncbi.nlm.nih.gov
Y1 - 2014/09//
PY - 2014
DA - September 2014
SP - 877
EP - 893
PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL - 18
IS - 5
SN - 1431-0651, 1431-0651
KW - ASFA 1: Biological Sciences & Living Resources; Microbiology Abstracts B: Bacteriology
KW - Genomes
KW - Membrane structure
KW - Immune system
KW - Viruses
KW - Membrane proteins
KW - Protein structure
KW - Islands
KW - Genes
KW - Biogenesis
KW - genomics
KW - New species
KW - Q1 08205:Genetics and evolution
KW - J 02350:Immunology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Extremophiles&rft.atitle=Dark+matter+in+archaeal+genomes%3A+a+rich+source+of+novel+mobile+elements%2C+defense+systems+and+secretory+complexes&rft.au=Makarova%2C+Kira+S%3BWolf%2C+Yuri+I%3BForterre%2C+Patrick%3BPrangishvili%2C+David%3BKrupovic%2C+Mart%3BKoonin%2C+Eugene+V&rft.aulast=Makarova&rft.aufirst=Kira&rft.date=2014-09-01&rft.volume=18&rft.issue=5&rft.spage=877&rft.isbn=&rft.btitle=&rft.title=Extremophiles&rft.issn=14310651&rft_id=info:doi/10.1007%2Fs00792-014-0672-7
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-10-01
N1 - Number of references - 73
N1 - Last updated - 2016-12-22
N1 - SubjectsTermNotLitGenreText - Genomes; Genes; Viruses; Biogenesis; New species; Protein structure; Islands; Immune system; Membrane structure; Membrane proteins; genomics
DO - http://dx.doi.org/10.1007/s00792-014-0672-7
ER -
TY - JOUR
T1 - Structural enzymology and inhibition of the bi-functional folate pathway enzyme HPPK-DHPS from the biowarfare agent Francisella tularensis
AN - 1618150282; 20761541
AB - Two valid targets for antibiotic development, 6-hydroxymethyl-7,8-dihydropterin pyrophosphokinase (HPPK) and dihydropteroate synthase (DHPS), catalyze consecutive reactions in folate biosynthesis. In Francisella tularensis (Ft), these two activities are contained in a single protein, FtHPPK-DHPS. Although Pemble et al. (PLoS One 5, e14165) determined the structure of FtHPPK-DHPS, they were unable to measure the kinetic parameters of the enzyme. In this study, we elucidated the binding and inhibitory activities of two HPPK inhibitors (HP-18 and HP-26) against FtHPPK-DHPS, determined the structure of FtHPPK-DHPS in complex with HP-26, and measured the kinetic parameters for the dual enzymatic activities of FtHPPK-DHPS. The biochemical analyses showed that HP-18 and HP-26 have significant isozyme selectivity, and that FtHPPK-DHPS is unique in that the catalytic efficiency of its DHPS activity is only 1/260,000 of that of Escherichia coli DHPS. Sequence and structural analyses suggest that HP-26 is an excellent lead for developing therapeutic agents for tularemia, and that the very low DHPS activity is due, at least in part, to the lack of a key residue that interacts with the substrate p-aminobenzoic acid (pABA). A BLAST search of the genomes of ten F. tularensis strains indicated that the bacterium contains a single FtHPPK-DHPS. The marginal DHPS activity and the single copy existence of FtHPPK-DHPS in F. tularensis make this bacterium more vulnerable to DHPS inhibitors. Current sulfa drugs are ineffective against tularemia; new inhibitors targeting the unique pABA-binding pocket may be effective and less subject to resistance because any mutations introducing resistance may make the marginal DHPS activity unable to support the growth of F. tularensis. The coordinates and structure factors have been deposited in the Protein Data Bank under accession code 4PZV. In Francisella tularensis (Ft), 6-hydroxymethyl-7,8-dihydropterin pyrophosphokinase (HPPK) and dihydropteroate synthase (DHPS) form the bifunctional enzyme FtHPPK-DHPS. Here, we report the activities of two HPPK inhibitors (HP-18 and HP-26) against FtHPPK-DHPS, the structure of FtHPPK-DHPS in complex with HP-26, and the kinetic parameters of FtHPPK-DHPS. The catalytic efficiency of FtDHPS is unique, which is only 1/2.6 105 that of Escherichia coli DHPS.
JF - FEBS Journal
AU - Shaw, Gary X
AU - Li, Yue
AU - Shi, Genbin
AU - Wu, Yan
AU - Cherry, Scott
AU - Needle, Danielle
AU - Zhang, Di
AU - Tropea, Joseph E
AU - Waugh, David S
AU - Yan, Honggao
AU - Ji, Xinhua
AD - Macromolecular Crystallography Laboratory. National Cancer Institute
Y1 - 2014/09//
PY - 2014
DA - September 2014
SP - 4123
EP - 4137
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 281
IS - 18
SN - 1742-464X, 1742-464X
KW - Microbiology Abstracts B: Bacteriology
KW - Genomes
KW - Bifunctional enzymes
KW - Biochemical analysis
KW - Francisella tularensis
KW - Antibiotics
KW - Dihydropteroate synthase
KW - p-Aminobenzoic acid
KW - Data banks
KW - Tularemia
KW - Kinetics
KW - Escherichia coli
KW - Isoenzymes
KW - Enzymatic activity
KW - Folic acid
KW - Mutation
KW - J 02310:Genetics & Taxonomy
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=FEBS+Journal&rft.atitle=Structural+enzymology+and+inhibition+of+the+bi-functional+folate+pathway+enzyme+HPPK-DHPS+from+the+biowarfare+agent+Francisella+tularensis&rft.au=Shaw%2C+Gary+X%3BLi%2C+Yue%3BShi%2C+Genbin%3BWu%2C+Yan%3BCherry%2C+Scott%3BNeedle%2C+Danielle%3BZhang%2C+Di%3BTropea%2C+Joseph+E%3BWaugh%2C+David+S%3BYan%2C+Honggao%3BJi%2C+Xinhua&rft.aulast=Shaw&rft.aufirst=Gary&rft.date=2014-09-01&rft.volume=281&rft.issue=18&rft.spage=4123&rft.isbn=&rft.btitle=&rft.title=FEBS+Journal&rft.issn=1742464X&rft_id=info:doi/10.1111%2Ffebs.12896
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-10-01
N1 - Last updated - 2016-08-17
N1 - SubjectsTermNotLitGenreText - Genomes; Biochemical analysis; Bifunctional enzymes; Antibiotics; Dihydropteroate synthase; p-Aminobenzoic acid; Data banks; Tularemia; Kinetics; Isoenzymes; Enzymatic activity; Folic acid; Mutation; Escherichia coli; Francisella tularensis
DO - http://dx.doi.org/10.1111/febs.12896
ER -
TY - JOUR
T1 - Mn complex-mediated enhancement of antitumor response through modulating myeloid-derived suppressor cells in drug-resistant tumor.
AN - 1614684093; 25189907
AB - The tumor microenvironment (TME) renders tumor cells more resistant to chemotherapy. However, effective immunomodulators for cancer therapy are still elusive. We hypothesized that Mn-N-(2-hydroxyacetophenone) glycinate (MnNG), reported to be an antitumor agent, can modulate the TME.
Immunomodulatory effects of MnNG were performed through assessing Myeloid Derived Suppressor Cells (MDSCs), Interferon-γ (Ifnγ)- and Interleukin-4 (Il4)-secreting Cluster of Differentiation 4 (Cd4)(+) T-cells by annexin V-binding assay in drug-resistant TME and T-cell proliferation following in vitro co-culture assay by flow cytometry. MnNG induced infiltration of Ifnγ-secreting Cd4(+) T-cells and reduces MDSC numbers in vivo. Furthermore, it modulated differentiation of MDSCs towards dendritic cells with up-regulation of co-stimulatory molecules and reversed the suppressive function of MDSC's that enhances T-helper cell 1 (Th1) response. MnNG treatment resulted in reduced expression of IL4, but enhanced expression of Ifnγ when Cd4(+) T-cells were co-cultured with MDSCs.
MnNG modulates MDSCs differentiaton towards dendritic cells and enhances Th1 response in drug-resistant TME, leading to immunomodulatory efficacy. Copyright © 2014 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved.
JF - In vivo (Athens, Greece)
AU - Das, Satyajit
AU - Banerjee, Kaushik
AU - Roy, Susmita
AU - Majumder, Saikat
AU - Chatterjee, Mitali
AU - Majumdar, Subrata
AU - Choudhuri, Soumitra Kumar
AD - Department of In Vitro Carcinogenesis and Cellular Chemotherapy, Chittaranjan National Cancer Institute, Kolkata, India. ; Department of Pharmacology, Institute of Postgraduate Medical Education and Research, Kolkata, India. ; Division of Molecular Medicine, Bose Institute, Kolkata, India. ; Department of In Vitro Carcinogenesis and Cellular Chemotherapy, Chittaranjan National Cancer Institute, Kolkata, India soumitra01@yahoo.com.
PY - 2014
SP - 909
EP - 918
VL - 28
IS - 5
KW - Cytokines
KW - 0
KW - Immunologic Factors
KW - Manganese
KW - 42Z2K6ZL8P
KW - Index Medicus
KW - myeloid derived suppressor cells
KW - MDR
KW - Mn complex
KW - Th1 response
KW - immunomodulation
KW - T-Lymphocyte Subsets -- metabolism
KW - Animals
KW - Lymphocytes, Tumor-Infiltrating -- immunology
KW - CD4-Positive T-Lymphocytes -- metabolism
KW - T-Lymphocyte Subsets -- drug effects
KW - T-Lymphocyte Subsets -- immunology
KW - Disease Models, Animal
KW - CD4-Positive T-Lymphocytes -- immunology
KW - Mice
KW - Cytokines -- metabolism
KW - CD4-Positive T-Lymphocytes -- drug effects
KW - Immunophenotyping
KW - Male
KW - Lymphocytes, Tumor-Infiltrating -- metabolism
KW - Female
KW - Manganese -- pharmacology
KW - Neoplasms -- pathology
KW - Manganese -- chemistry
KW - Immunologic Factors -- pharmacology
KW - Myeloid Cells -- immunology
KW - Immunologic Factors -- chemistry
KW - Drug Resistance, Neoplasm
KW - Neoplasms -- therapy
KW - Myeloid Cells -- drug effects
KW - Immunomodulation -- drug effects
KW - Neoplasms -- metabolism
KW - Neoplasms -- immunology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=In+vivo+%28Athens%2C+Greece%29&rft.atitle=Mn+complex-mediated+enhancement+of+antitumor+response+through+modulating+myeloid-derived+suppressor+cells+in+drug-resistant+tumor.&rft.au=Das%2C+Satyajit%3BBanerjee%2C+Kaushik%3BRoy%2C+Susmita%3BMajumder%2C+Saikat%3BChatterjee%2C+Mitali%3BMajumdar%2C+Subrata%3BChoudhuri%2C+Soumitra+Kumar&rft.aulast=Das&rft.aufirst=Satyajit&rft.date=2014-09-01&rft.volume=28&rft.issue=5&rft.spage=909&rft.isbn=&rft.btitle=&rft.title=In+vivo+%28Athens%2C+Greece%29&rft.issn=1791-7549&rft_id=info:doi/
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-05-22
N1 - Date created - 2014-09-05
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
ER -
TY - JOUR
T1 - The role of health systems and policy in producing behavior and social change to enhance child survival and development in low- and middle-income countries: an examination of the evidence
AN - 1613947810; 4608959
AB - Evidence-based behavior change interventions addressing health systems must be identified and disseminated to improve child health outcomes. Studies of the efficacy of such interventions were identified from systematic searches of the published literature. Two hundred twenty-nine of the initially identified references were judged to be relevant and were further reviewed for the quality and strength of the evidence. Studies were eligible if an intervention addressed policy or health systems interventions, measured relevant behavioral or health outcomes (e.g., nutrition, childhood immunization, malaria prevention and treatment), used at least a moderate quality research design, and were implemented in low- or middle-income countries. Policy or systems interventions able to produce behavior change reviewed included media (e.g., mass media, social media), community mobilization, educational programs (for caregivers, communities, or providers), social marketing, opinion leadership, economic incentives (for both caregiver and provider), health systems strengthening/policy/legislation, and others. Recommendations for policy, practice, and research are given based on fairly strong data across the areas of health service delivery, health workforce, health financing, governance and leadership, and research. Reprinted by permission of Taylor & Francis Ltd.
JF - Journal of health communication
AU - Vélez, Luis F
AU - Sanitato, Mary
AU - Barry, Donna
AU - Alilio, Martin
AU - Apfel, Franklin
AU - Coe, Gloria
AU - Garcia, Amparo
AU - Kaufman, Michelle
AU - Klein, Jonathan
AU - Kutlesic, Vesna
AU - Meadowcroft, Lisa
AU - Nilsen, Wendy
AU - O'Sullivan, Gael
AU - Peterson, Stefan
AU - Raiten, Daniel
AU - Vorkoper, Susan
AD - DePelchin Children's Center ; US Agency for International Development ; Center for American Progress ; World Health Communication Associates ; US Forest Service ; Johns Hopkins Bloomberg School of Public Health ; American Academy of Pediatrics ; National Institutes of Health ; African Medical and Research Foundation ; ABT Associates ; Karolinska Institute
Y1 - 2014/09//
PY - 2014
DA - Sep 2014
SP - 89
EP - 121
VL - 19
IS - Supp.1
SN - 1081-0730, 1081-0730
KW - Sociology
KW - Political Science
KW - Child mortality
KW - Social change
KW - Health
KW - U.S.A.
KW - Public policy
KW - Child development
KW - Low income
KW - Community care
KW - Policy consultation
KW - Health policy
KW - Evidence
KW - Infants
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1613947810?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+health+communication&rft.atitle=The+role+of+health+systems+and+policy+in+producing+behavior+and+social+change+to+enhance+child+survival+and+development+in+low-+and+middle-income+countries%3A+an+examination+of+the+evidence&rft.au=V%C3%A9lez%2C+Luis+F%3BSanitato%2C+Mary%3BBarry%2C+Donna%3BAlilio%2C+Martin%3BApfel%2C+Franklin%3BCoe%2C+Gloria%3BGarcia%2C+Amparo%3BKaufman%2C+Michelle%3BKlein%2C+Jonathan%3BKutlesic%2C+Vesna%3BMeadowcroft%2C+Lisa%3BNilsen%2C+Wendy%3BO%27Sullivan%2C+Gael%3BPeterson%2C+Stefan%3BRaiten%2C+Daniel%3BVorkoper%2C+Susan&rft.aulast=V%C3%A9lez&rft.aufirst=Luis&rft.date=2014-09-01&rft.volume=19&rft.issue=Supp.1&rft.spage=89&rft.isbn=&rft.btitle=&rft.title=Journal+of+health+communication&rft.issn=10810730&rft_id=info:doi/10.1080%2F10810730.2014.939313
LA - English
DB - International Bibliography of the Social Sciences (IBSS)
N1 - Date revised - 2014-10-20
N1 - Last updated - 2014-10-20
N1 - SubjectsTermNotLitGenreText - 7553 6271; 5788 11888 10472; 2604 11949 13521; 2203 2212 8291 3409 6306; 4560; 2197 2212 6075 3483; 11783; 6495 2212; 5772; 10472; 9619 9628 9625; 433 293 14
DO - http://dx.doi.org/10.1080/10810730.2014.939313
ER -
TY - JOUR
T1 - Caregiver behavior change for child survival and development in low- and middle-income countries: an examination of the evidence
AN - 1613947546; 4608960
AB - In June of 2012, representatives from more than 80 countries promulgated a Child Survival Call to Action, which called for reducing child mortality to 20 or fewer child deaths per 1,000 live births in every country by 2035. To address the problem of ending preventable child deaths, the U.S. Agency for International Development and the United Nations Children's Fund convened, on June 3-4, 2013, an Evidence Summit on Enhancing Child Survival and Development in Lower- and Middle-Income Countries by Achieving Population-Level Behavior Change. Six evidence review teams were established on different topics related to child survival and healthy development to identify the relevant evidence-based interventions and to prepare reports. This article was developed by the evidence review team responsible for identifying the research literature on caregiver change for child survival and development. This article is organized into childhood developmental periods and cross-cutting issues that affect child survival and healthy early development across all these periods. On the basis of this review, the authors present evidence-based recommendations for programs focused on caregivers to increase child survival and promote healthy development. Last, promising directions for future research to change caregivers' behaviors are given. Reprinted by permission of Taylor & Francis Ltd.
JF - Journal of health communication
AU - Elder, John P
AU - Pequegnat, Willo
AU - Ahmed, Saifuddin
AU - Bachman, Gretchen
AU - Bullock, Merry
AU - Carlo, Waldemar A
AU - Chandra-Mouli, Venkatraman
AU - Fox, Nathan A
AU - Harkness, Sara
AU - Huebner, Gillian
AU - Lombardi, Joan
AU - Murry, Velma McBride
AU - Moran, Allisyn
AU - Norton, Maureen
AU - Mulik, Jennifer
AU - Parks, Will
AU - Raikes, Helen H
AU - Smyser, Joseph
AU - Sugg, Caroline
AU - Sweat, Michael
AD - Diego State University ; National Institute of Mental Health ; Johns Hopkins Bloomberg School of Public Health ; US Agency for International Development ; American Psychological Association ; University of Alabama, Birmingham ; World Health Organization ; University of Maryland ; University of Connecticut ; Bernard van Leer Foundation ; Vanderbilt University ; United States Agency for International Development ; UNICEF ; University of Nebraska ; British Broadcasting Company ; Medical University of South Carolina
Y1 - 2014/09//
PY - 2014
DA - Sep 2014
SP - 25
EP - 66
VL - 19
IS - Supp.1
SN - 1081-0730, 1081-0730
KW - Sociology
KW - Political Science
KW - Child mortality
KW - Policy consultation
KW - Social change
KW - Health
KW - U.S.A.
KW - Evidence
KW - Public policy
KW - Child development
KW - Low income
KW - Infants
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1613947546?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+health+communication&rft.atitle=Caregiver+behavior+change+for+child+survival+and+development+in+low-+and+middle-income+countries%3A+an+examination+of+the+evidence&rft.au=Elder%2C+John+P%3BPequegnat%2C+Willo%3BAhmed%2C+Saifuddin%3BBachman%2C+Gretchen%3BBullock%2C+Merry%3BCarlo%2C+Waldemar+A%3BChandra-Mouli%2C+Venkatraman%3BFox%2C+Nathan+A%3BHarkness%2C+Sara%3BHuebner%2C+Gillian%3BLombardi%2C+Joan%3BMurry%2C+Velma+McBride%3BMoran%2C+Allisyn%3BNorton%2C+Maureen%3BMulik%2C+Jennifer%3BParks%2C+Will%3BRaikes%2C+Helen+H%3BSmyser%2C+Joseph%3BSugg%2C+Caroline%3BSweat%2C+Michael&rft.aulast=Elder&rft.aufirst=John&rft.date=2014-09-01&rft.volume=19&rft.issue=Supp.1&rft.spage=25&rft.isbn=&rft.btitle=&rft.title=Journal+of+health+communication&rft.issn=10810730&rft_id=info:doi/10.1080%2F10810730.2014.940477
LA - English
DB - International Bibliography of the Social Sciences (IBSS)
N1 - Date revised - 2014-10-20
N1 - Last updated - 2014-10-20
N1 - SubjectsTermNotLitGenreText - 7553 6271; 2203 2212 8291 3409 6306; 4560; 2197 2212 6075 3483; 11783; 6495 2212; 5772; 10472; 9619 9628 9625; 433 293 14
DO - http://dx.doi.org/10.1080/10810730.2014.940477
ER -
TY - JOUR
T1 - US lung cancer trends by histologic type
AN - 1611613985; 20690441
AB - BACKGROUND Lung cancer incidence rates overall are declining in the United States. This study investigated the trends by histologic type and demographic characteristics. METHODS Surveillance, Epidemiology, and End Results (SEER) program rates of microscopically confirmed lung cancer overall and squamous cell, small cell, adenocarcinoma, large cell, other, and unspecified carcinomas among US whites and blacks diagnosed from 1977 to 2010 and white non-Hispanics, Asian/Pacific Islanders, and white Hispanics diagnosed from 1992 to 2010 were analyzed by sex and age. RESULTS Squamous and small cell carcinoma rates declined since the 1990s, although less rapidly among females than males. Adenocarcinoma rates decreased among males and only through 2005, after which they then rose during 2006 to 2010 among every racial/ethnic/sex group; rates for unspecified type declined. Male/female rate ratios declined among whites and blacks more than among other groups. Recent rates among young females were higher than among males for adenocarcinoma among all racial/ethnic groups and for other specified carcinomas among whites. CONCLUSIONS US lung cancer trends vary by sex, histologic type, racial/ethnic group, and age, reflecting historical cigarette smoking rates, duration, cessation, cigarette composition, and exposure to other carcinogens. Substantial excesses among males have diminished and higher rates of adenocarcinoma among young females have emerged as rates among males declined more rapidly. The recognition of EGFR mutation and ALK rearrangements that occur primarily in adenocarcinomas are the primary basis for the molecular revolution that has transformed lung cancer diagnosis and treatment over the past decade, and these changes have affected recent type-specific trends. Cancer 2014; 120:2883-2892. copyright 2014 American Cancer Society. This analysis of lung cancer trends by histologic type represents a fresh classification of lung cancer histology and reveals several new incidence trends by sex and race/ethnicity. This new analysis by histologic type is important in the context of molecular-based diagnosis and should inform additional research that will direct therapy appropriate to the specific lung cancer type.
JF - Cancer
AU - Lewis, Denise Riedel
AU - Check, David P
AU - Caporaso, Neil E
AU - Travis, William D
AU - Devesa, Susan S
AD - Surveillance Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, Bethesda, Maryland.
Y1 - 2014/09//
PY - 2014
DA - Sep 2014
SP - 2883
EP - 2892
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 120
IS - 18
SN - 0008-543X, 0008-543X
KW - Health & Safety Science Abstracts
KW - Demography
KW - Historical account
KW - USA
KW - Age
KW - Cigarettes
KW - Classification
KW - Histology
KW - I, Pacific
KW - Carcinogens
KW - Mutation
KW - Ethnic groups
KW - H 11000:Diseases/Injuries/Trauma
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer&rft.atitle=US+lung+cancer+trends+by+histologic+type&rft.au=Lewis%2C+Denise+Riedel%3BCheck%2C+David+P%3BCaporaso%2C+Neil+E%3BTravis%2C+William+D%3BDevesa%2C+Susan+S&rft.aulast=Lewis&rft.aufirst=Denise&rft.date=2014-09-01&rft.volume=120&rft.issue=18&rft.spage=2883&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/10.1002%2Fcncr.28749
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-10-01
N1 - Last updated - 2014-10-30
N1 - SubjectsTermNotLitGenreText - Demography; Historical account; Age; Histology; Classification; Cigarettes; Carcinogens; Mutation; Ethnic groups; USA; I, Pacific
DO - http://dx.doi.org/10.1002/cncr.28749
ER -
TY - JOUR
T1 - Antiretroviral therapy: current drugs.
AN - 1609306097; 25151562
AB - The rapid advances in drug discovery and the development of antiretroviral therapy is unprecedented in the history of modern medicine. The administration of chronic combination antiretroviral therapy targeting different stages of the human immunodeficiency virus' replicative life cycle allows for durable and maximal suppression of plasma viremia. This suppression has resulted in dramatic improvement of patient survival. This article reviews the history of antiretroviral drug development and discusses the clinical pharmacology, efficacy, and toxicities of the antiretroviral agents most commonly used in clinical practice to date.
Published by Elsevier Inc.
JF - Infectious disease clinics of North America
AU - Pau, Alice K
AU - George, Jomy M
AD - Division of Clinical Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 10, Room 11C103 (MSC 1880), Bethesda, MD 20892, USA. Electronic address: apau@niaid.nih.gov. ; Department of Pharmacy Practice and Administration, Philadelphia College of Pharmacy, University of the Sciences in Philadelphia, 600 South 43rd Street, GH-108K, Philadelphia, PA 19104, USA.
Y1 - 2014/09//
PY - 2014
DA - September 2014
SP - 371
EP - 402
VL - 28
IS - 3
KW - Anti-Retroviral Agents
KW - 0
KW - Index Medicus
KW - Non-nucleoside reverse transcriptase inhibitors
KW - Fusion inhibitor
KW - CCR5 antagonist
KW - Protease inhibitors
KW - Nucleoside/nucleotide reverse transcriptase inhibitors
KW - Integrase strand transfer inhibitors
KW - Antiretroviral therapy
KW - HIV
KW - History, 21st Century
KW - History, 20th Century
KW - Humans
KW - Drug Discovery -- trends
KW - Antiretroviral Therapy, Highly Active -- adverse effects
KW - Anti-Retroviral Agents -- pharmacokinetics
KW - HIV Infections -- drug therapy
KW - Anti-Retroviral Agents -- adverse effects
KW - Antiretroviral Therapy, Highly Active -- history
KW - Antiretroviral Therapy, Highly Active -- methods
KW - Anti-Retroviral Agents -- pharmacology
KW - Anti-Retroviral Agents -- therapeutic use
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-04-23
N1 - Date created - 2014-08-25
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.idc.2014.06.001
ER -
TY - JOUR
T1 - Jonathan Silvertown The Long and the Short of It: The Science of Life Span and Aging
AN - 1566851757; 20739526
JF - Population And Development Review
AU - Haaga, John G
AD - National Institute on Aging.
Y1 - 2014/09//
PY - 2014
DA - Sep 2014
SP - 565
EP - 566
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 40
IS - 3
SN - 0098-7921, 0098-7921
KW - Sustainability Science Abstracts
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1566851757?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Assamodule&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Population+And+Development+Review&rft.atitle=Jonathan+Silvertown+The+Long+and+the+Short+of+It%3A+The+Science+of+Life+Span+and+Aging&rft.au=Haaga%2C+John+G&rft.aulast=Haaga&rft.aufirst=John&rft.date=2014-09-01&rft.volume=40&rft.issue=3&rft.spage=565&rft.isbn=&rft.btitle=&rft.title=Population+And+Development+Review&rft.issn=00987921&rft_id=info:doi/10.1111%2Fj.1728-4457.2014.00701.x
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-09-01
N1 - Last updated - 2014-10-02
DO - http://dx.doi.org/10.1111/j.1728-4457.2014.00701.x
ER -
TY - JOUR
T1 - Ebola Virus Modulates Transforming Growth Factor beta Signaling and Cellular Markers of Mesenchyme-Like Transition in Hepatocytes
AN - 1566850801; 20698556
AB - Ebola virus (EBOV) causes a severe hemorrhagic disease in humans and nonhuman primates, with a median case fatality rate of 78.4%. Although EBOV is considered a public health concern, there is a relative paucity of information regarding the modulation of the functional host response during infection. We employed temporal kinome analysis to investigate the relative early, intermediate, and late host kinome responses to EBOV infection in human hepatocytes. Pathway overrepresentation analysis and functional network analysis of kinome data revealed that transforming growth factor (TGF- beta )-mediated signaling responses were temporally modulated in response to EBOV infection. Upregulation of TGF- beta signaling in the kinome data sets correlated with the upregulation of TGF- beta secretion from EBOV-infected cells. Kinase inhibitors targeting TGF- beta signaling, or additional cell receptors and downstream signaling pathway intermediates identified from our kinome analysis, also inhibited EBOV replication. Further, the inhibition of select cell signaling intermediates identified from our kinome analysis provided partial protection in a lethal model of EBOV infection. To gain perspective on the cellular consequence of TGF- beta signaling modulation during EBOV infection, we assessed cellular markers associated with upregulation of TGF- beta signaling. We observed upregulation of matrix metalloproteinase 9, N-cadherin, and fibronectin expression with concomitant reductions in the expression of E-cadherin and claudin-1, responses that are standard characteristics of an epithelium-to-mesenchyme-like transition. Additionally, we identified phosphorylation events downstream of TGF- beta that may contribute to this process. From these observations, we propose a model for a broader role of TGF- beta -mediated signaling responses in the pathogenesis of Ebola virus disease. IMPORTANCE Ebola virus (EBOV), formerly Zaire ebolavirus, causes a severe hemorrhagic disease in humans and nonhuman primates and is the most lethal Ebola virus species, with case fatality rates of up to 90%. Although EBOV is considered a worldwide concern, many questions remain regarding EBOV molecular pathogenesis. As it is appreciated that many cellular processes are regulated through kinase-mediated phosphorylation events, we employed temporal kinome analysis to investigate the functional responses of human hepatocytes to EBOV infection. Administration of kinase inhibitors targeting signaling pathway intermediates identified in our kinome analysis inhibited viral replication in vitro and reduced EBOV pathogenesis in vivo. Further analysis of our data also demonstrated that EBOV infection modulated TGF- beta -mediated signaling responses and promoted "mesenchyme-like" phenotypic changes. Taken together, these results demonstrated that EBOV infection specifically modulates TGF- beta -mediated signaling responses in epithelial cells and may have broader implications in EBOV pathogenesis.
JF - Journal of Virology
AU - Kindrachuk, Jason
AU - Wahl-Jensen, Victoria
AU - Safronetz, David
AU - Trost, Brett
AU - Hoenen, Thomas
AU - Arsenault, Ryan
AU - Feldmann, Friederike
AU - Traynor, Dawn
AU - Postnikova, Elena
AU - Kusalik, Anthony
AD - Emerging Viral Pathogens Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA, kindrachuk.kenneth@nih.gov.
Y1 - 2014/09//
PY - 2014
DA - Sep 2014
SP - 9877
EP - 9892
PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL - 88
IS - 17
SN - 0022-538X, 0022-538X
KW - Health & Safety Science Abstracts; Virology & AIDS Abstracts
KW - Transforming growth factor
KW - Epithelial cells
KW - Hepatocytes
KW - Fibronectin
KW - Secretion
KW - Animal models
KW - Matrix metalloproteinase
KW - Ebola virus
KW - Infection
KW - Angola, Zaire
KW - Public health
KW - Phosphorylation
KW - Downstream
KW - Growth factors
KW - Mortality
KW - Data processing
KW - Replication
KW - Primates
KW - E-Cadherin
KW - N-Cadherin
KW - Transforming growth factor- beta
KW - Hemorrhagic disease
KW - Signal transduction
KW - H 6000:Natural Disasters/Civil Defense/Emergency Management
KW - V 22320:Replication
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-09-01
N1 - Number of references - 68
N1 - Last updated - 2015-11-25
N1 - SubjectsTermNotLitGenreText - Epithelial cells; Transforming growth factor; Data processing; Hepatocytes; Replication; Secretion; Fibronectin; Animal models; Matrix metalloproteinase; Infection; E-Cadherin; Public health; Phosphorylation; N-Cadherin; Transforming growth factor- beta; Hemorrhagic disease; Signal transduction; Mortality; Downstream; Growth factors; Primates; Ebola virus; Angola, Zaire
DO - http://dx.doi.org/10.1128/JVI.01410-14
ER -
TY - JOUR
T1 - Introductions and Evolution of Human-Origin Seasonal Influenza A Viruses in Multinational Swine Populations
AN - 1566846982; 20698539
AB - The capacity of influenza A viruses to cross species barriers presents a continual threat to human and animal health. Knowledge of the human-swine interface is particularly important for understanding how viruses with pandemic potential evolve in swine hosts. We sequenced the genomes of 141 influenza viruses collected from North American swine during 2002 to 2011 and identified a swine virus that possessed all eight genome segments of human seasonal A/H3N2 virus origin. A molecular clock analysis indicates that this virus-A/sw/Saskatchewan/02903/2009(H3N2)-has likely circulated undetected in swine for at least 7 years. For historical context, we performed a comprehensive phylogenetic analysis of an additional 1,404 whole-genome sequences from swine influenza A viruses collected globally during 1931 to 2013. Human-to-swine transmission occurred frequently over this time period, with 20 discrete introductions of human seasonal influenza A viruses showing sustained onward transmission in swine for at least 1 year since 1965. Notably, human-origin hemagglutinin (H1 and H3) and neuraminidase (particularly N2) segments were detected in swine at a much higher rate than the six internal gene segments, suggesting an association between the acquisition of swine-origin internal genes via reassortment and the adaptation of human influenza viruses to new swine hosts. Further understanding of the fitness constraints on the adaptation of human viruses to swine, and vice versa, at a genomic level is central to understanding the complex multihost ecology of influenza and the disease threats that swine and humans pose to each other. IMPORTANCE The swine origin of the 2009 A/H1N1 pandemic virus underscored the importance of understanding how influenza A virus evolves in these animals hosts. While the importance of reassortment in generating genetically diverse influenza viruses in swine is well documented, the role of human-to-swine transmission has not been as intensively studied. Through a large-scale sequencing effort, we identified a novel influenza virus of wholly human origin that has been circulating undetected in swine for at least 7 years. In addition, we demonstrate that human-to-swine transmission has occurred frequently on a global scale over the past decades but that there is little persistence of human virus internal gene segments in swine.
JF - Journal of Virology
AU - Nelson, Martha I
AU - Wentworth, David E
AU - Culhane, Marie R
AU - Vincent, Amy L
AU - Viboud, Cecile
AU - LaPointe, Matthew P
AU - Lin, Xudong
AU - Holmes, Edward C
AU - Detmer, Susan E
AD - Fogarty International Center, National Institutes of Health, Bethesda, Maryland, USA, nelsonma@mail.nih.gov.
Y1 - 2014/09//
PY - 2014
DA - Sep 2014
SP - 10110
EP - 10119
PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL - 88
IS - 17
SN - 0022-538X, 0022-538X
KW - Health & Safety Science Abstracts; Virology & AIDS Abstracts
KW - Genomes
KW - Fitness
KW - Phylogeny
KW - Historical account
KW - Adaptations
KW - Canada, Saskatchewan
KW - Influenza A
KW - Hemagglutinins
KW - Viruses
KW - Swine influenza
KW - Influenza
KW - Ecology
KW - Adaptability
KW - pandemics
KW - Sulfur dioxide
KW - Influenza A virus
KW - genomics
KW - Exo- alpha -sialidase
KW - Seasonal variations
KW - Evolution
KW - H 6000:Natural Disasters/Civil Defense/Emergency Management
KW - V 22310:Genetics, Taxonomy & Structure
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-09-01
N1 - Number of references - 46
N1 - Last updated - 2015-04-02
N1 - SubjectsTermNotLitGenreText - Phylogeny; Fitness; Genomes; pandemics; Adaptations; Hemagglutinins; Influenza A; Swine influenza; Exo- alpha -sialidase; genomics; Evolution; Ecology; Influenza; Historical account; Adaptability; Sulfur dioxide; Viruses; Seasonal variations; Influenza A virus; Canada, Saskatchewan
DO - http://dx.doi.org/10.1128/JVI.01080-14
ER -
TY - CONF
T1 - Cancer treatment-related cardiotoxicity: current state of knowledge and future research priorities.
AN - 1561972361; 25210198
AB - Cardiotoxicity resulting from direct myocyte damage has been a known complication of cancer treatment for decades. More recently, the emergence of hypertension as a clinically significant side effect of several new agents has been recognized as adversely affecting cancer treatment outcomes. With cancer patients living longer, in part because of treatment advances, these adverse events have become increasingly important to address. However, little is known about the cardiovascular pathogenic mechanisms associated with cancer treatment and even less about how to optimally prevent and manage short- and long-term cardiovascular complications, leading to improved patient safety and clinical outcomes. To identify research priorities, allocate resources, and establish infrastructure required to address cardiotoxicity associated with cancer treatment, the National Cancer Institute (NCI) and National Heart, Lung and Blood Institute (NHLBI) sponsored a two-day workshop, "Cancer treatment-related cardiotoxicity: Understanding the current state of knowledge and future research priorities," in March 2013 in Bethesda, MD. Participants included leading oncology and cardiology researchers and health professionals, patient advocates and industry representatives, with expertise ranging from basic to clinical science. Attendees were charged with identifying research opportunities to advance the understanding of cancer treatment-related cardiotoxicity across basic and clinical science. This commentary highlights the key discussion points and overarching recommendations from that workshop.
Published by Oxford University Press 2014.
JF - Journal of the National Cancer Institute
AU - Shelburne, Nonniekaye
AU - Adhikari, Bishow
AU - Brell, Joanna
AU - Davis, Myrtle
AU - Desvigne-Nickens, Patrice
AU - Freedman, Andrew
AU - Minasian, Lori
AU - Force, Thomas
AU - Remick, Scot C
Y1 - 2014/09//
PY - 2014
DA - September 2014
VL - 106
IS - 9
KW - Antineoplastic Agents
KW - 0
KW - Index Medicus
KW - United States
KW - Health Personnel -- education
KW - National Cancer Institute (U.S.)
KW - Humans
KW - Muscle Cells -- drug effects
KW - National Heart, Lung, and Blood Institute (U.S.)
KW - Neoplasms -- drug therapy
KW - Antineoplastic Agents -- administration & dosage
KW - Heart Diseases -- chemically induced
KW - Heart -- drug effects
KW - Heart Diseases -- prevention & control
KW - Antineoplastic Agents -- adverse effects
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=Cancer+treatment-related+cardiotoxicity%3A+current+state+of+knowledge+and+future+research+priorities.&rft.au=Shelburne%2C+Nonniekaye%3BAdhikari%2C+Bishow%3BBrell%2C+Joanna%3BDavis%2C+Myrtle%3BDesvigne-Nickens%2C+Patrice%3BFreedman%2C+Andrew%3BMinasian%2C+Lori%3BForce%2C+Thomas%3BRemick%2C+Scot+C&rft.aulast=Shelburne&rft.aufirst=Nonniekaye&rft.date=2014-09-01&rft.volume=106&rft.issue=9&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=1460-2105&rft_id=info:doi/10.1093%2Fjnci%2Fdju232
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-11-14
N1 - Date created - 2014-09-11
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Circ Res. 2013 Aug 30;113(6):754-64 [23989717]
Circulation. 2013 Jul 9;128(2):152-61 [23757312]
Int J Cardiovasc Imaging. 2013 Oct;29(7):1459-76 [23744127]
Circulation. 2013 Oct 22;128(17):1927-95 [24081971]
J Cardiovasc Transl Res. 2014 Mar;7(2):250-61 [24309956]
J Am Coll Cardiol. 2014 Mar 4;63(8):809-16 [24291281]
Toxicol Sci. 2014 Aug 1;140(2):445-61 [24812011]
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J Clin Oncol. 2001 Jul 1;19(13):3163-72 [11432882]
Ann Oncol. 2002 Jun;13(6):819-29 [12123328]
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Cancer. 2003 Jun 1;97(11):2869-79 [12767102]
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Mol Pharmacol. 2005 Aug;68(2):261-71 [15883202]
J Clin Oncol. 2006 Jul 20;24(21):3509-10; author reply 3510-1 [16849773]
J Clin Oncol. 2009 May 10;27(14):2339-55 [19364955]
J Am Coll Cardiol. 2009 Jun 16;53(24):2231-47 [19520246]
Cancer Epidemiol Biomarkers Prev. 2010 Jan;19(1):170-81 [20056636]
J Natl Cancer Inst. 2010 May 5;102(9):596-604 [20351338]
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Prog Cardiovasc Dis. 2010 Sep-Oct;53(2):94-104 [20728696]
Prog Cardiovasc Dis. 2010 Sep-Oct;53(2):173-9 [20728705]
Eur J Heart Fail. 2011 Jan;13(1):1-10 [21169385]
Am J Cardiol. 2011 May 1;107(9):1375-80 [21371685]
Am Heart J. 2012 Feb;163(2):156-63 [22305831]
J Natl Cancer Inst. 2012 Mar 7;104(5):357-70 [22312134]
J Nucl Cardiol. 2012 Apr;19(2):377-88 [22351492]
Cancer. 2012 Apr 15;118(8 Suppl):2270-6 [22488701]
Cochrane Database Syst Rev. 2012;4:CD006243 [22513938]
BMC Physiol. 2012;12:3 [22449203]
Curr Cardiol Rev. 2011 Nov;7(4):234-44 [22758624]
CA Cancer J Clin. 2012 Jul-Aug;62(4):220-41 [22700443]
Eur Heart J. 2012 Jul;33(14):1787-847 [22611136]
Circ Cardiovasc Imaging. 2012 Sep 1;5(5):596-603 [22744937]
J Transl Med. 2012;10:140 [22768802]
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Circulation. 2013 Jul 9;128(2):98-100 [23757311]
J Nucl Med Technol. 2013 Sep;41(3):170-81 [23929800]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/jnci/dju232
ER -
TY - JOUR
T1 - Effects of methylprednisolone and 4-chloro-3-hydroxyanthranilic acid in experimental spinal cord injury in the guinea pig appear to be mediated by different and potentially complementary mechanisms.
AN - 1560585260; 25047053
AB - Blinded, placebo-controlled, parallel treatment group studies of the effects of methylprednisolone (MP) or 4-chloro-3-hydroxyanthranilate (4-Cl-3-HAA) on behavioral outcome and quinolinic acid tissue levels from experimental thoracic spinal cord injury in adult guinea pigs.
To compare the effects of treatment with high-dose MP, a corticosteroid, and 4-Cl-3-HAA, a compound that inhibits synthesis of the neurotoxin quinolinic acid (QUIN) by activated macrophages. To explore the effect of different times of treatment using these two approaches to ameliorating secondary tissue damage. Laboratory animal studies at the University of North Carolina, Chapel Hill, NC, USA.
Standardized spinal cord injuries were produced in anesthetized guinea pigs, using lateral compression of the spinal cord. Behavioral impairment and recovery were measured by placing and toe-spread responses (motor function), cutaneus trunci muscle reflex receptive field areas and somatosensory-evoked potentials (sensory function). Tissue quinolinic acid levels were measured by gas chromatograph/mass spectrometry. The current experiments showed a reduction in delayed loss of motor and sensory function in the guinea pig with MP (150 mg kg(-1), intraperitoneally in split doses between 0.5 and 6 h), but no significant reduction in tissue QUIN. Improved sensory function was seen with a single dose of 60 mg kg(-1) MP intraperitoneally at 5 h after injury, but not at 10 h after injury. A single dose of 4-Cl-3-HAA at 5 h in the guinea pig did not produce the sensory and motor improvements seen in previous studies with 12 days of dosing, beginning at 5 h.
These studies, together with earlier findings, indicate that both drugs can attenuate secondary pathologic damage after SCI, but through separate mechanisms. These are most likely an acute reduction by MP of oxidative processes and reduction by 4-Cl-3-HAA of QUIN synthesis.
JF - Spinal cord
AU - Yates, J R
AU - Gay, E A
AU - Heyes, M P
AU - Blight, A R
AD - 1] Curriculum in Neurobiology and Division of Neurosurgery, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA [2] Acorda Therapeutics Inc., Ardsley, NY, USA [3] Department of Psychology, Ohio Wesleyan University, Delaware, OH, USA. ; Curriculum in Neurobiology and Division of Neurosurgery, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. ; Laboratory of Neurotoxicology, National Institute of Mental Health, Chapel Hill, NC, USA. ; 1] Curriculum in Neurobiology and Division of Neurosurgery, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA [2] Acorda Therapeutics Inc., Ardsley, NY, USA.
Y1 - 2014/09//
PY - 2014
DA - September 2014
SP - 662
EP - 666
VL - 52
IS - 9
KW - 3-Hydroxyanthranilic Acid
KW - 1UQB1BT4OT
KW - 4-chloro-3-hydroxyanthranilic acid
KW - 23219-33-2
KW - Quinolinic Acid
KW - F6F0HK1URN
KW - Methylprednisolone
KW - X4W7ZR7023
KW - Index Medicus
KW - Animals
KW - Quinolinic Acid -- metabolism
KW - Guinea Pigs
KW - Disease Models, Animal
KW - Evoked Potentials, Somatosensory
KW - Female
KW - Spinal Cord Injuries -- metabolism
KW - 3-Hydroxyanthranilic Acid -- pharmacology
KW - Methylprednisolone -- pharmacology
KW - Spinal Cord Injuries -- drug therapy
KW - Behavior, Animal -- physiology
KW - Spinal Cord Injuries -- physiopathology
KW - 3-Hydroxyanthranilic Acid -- analogs & derivatives
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Spinal+cord&rft.atitle=Effects+of+methylprednisolone+and+4-chloro-3-hydroxyanthranilic+acid+in+experimental+spinal+cord+injury+in+the+guinea+pig+appear+to+be+mediated+by+different+and+potentially+complementary+mechanisms.&rft.au=Yates%2C+J+R%3BGay%2C+E+A%3BHeyes%2C+M+P%3BBlight%2C+A+R&rft.aulast=Yates&rft.aufirst=J&rft.date=2014-09-01&rft.volume=52&rft.issue=9&rft.spage=662&rft.isbn=&rft.btitle=&rft.title=Spinal+cord&rft.issn=1476-5624&rft_id=info:doi/10.1038%2Fsc.2014.118
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-10-12
N1 - Date created - 2014-09-05
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1038/sc.2014.118
ER -
TY - JOUR
T1 - Reliability of triclosan measures in repeated urine samples from Norwegian pregnant women
AN - 1560138677; 20621177
AB - Triclosan (TCS) is a synthetic antibacterial chemical that is used in personal care products and is measurable in urine. Urinary TCS has been associated with allergy in children in Norway and the United States. A reasonable degree of temporal reliability of TCS urinary concentrations has been reported among US children as well as for Puerto Rican pregnant women. We examined the reliability of TCS measures in urine among Norwegian pregnant women. TCS was measured in spot urine samples collected in gestational weeks 17, 23, and 29 from 45 women in The Norwegian Mother and Child Cohort Study (MoBa) enrolled in 2007 and 2008. Spearman's rank correlation coefficient (r sub(s)) and intraclass correlation coefficient (ICC) statistics were calculated. Fifty-six percent of the 45 women had a least one sample with a value above the method limit of detection (2.3 mu g/l). The correlation coefficients were 0.61 for TCS concentrations at 17 and 23 weeks and 0.49 for concentrations at 17 and 29 weeks. For the three time points, the ICC was 0.49. The reliability of TCS concentrations in repeated urine samples from pregnant Norwegian women was reasonably good, suggesting a single urine sample can adequately represent TCS exposure during pregnancy.
JF - Journal of Exposure Science and Environmental Epidemiology
AU - Bertelsen, Randi J
AU - Engel, Stephanie M
AU - Jusko, Todd A
AU - Calafat, Antonia M
AU - Hoppin, Jane A
AU - London, Stephanie J
AU - Eggesboe, Merete
AU - Aase, Heidi
AU - Zeiner, Pal
AU - Reichborn-Kjennerud, Ted
AU - Knudsen, Gun P
AU - Guidry, Virginia T
AU - Longnecker, Matthew P
AD - 1] Epidemiology Branch, National Institute of Environmental Health Sciences (NIEHS/NIH), Research Triangle Park, North Cardina, USA [2] Department of food, water and cosmetics, Norwegian Institute of Public Health, Oslo, Norway
Y1 - 2014/09//
PY - 2014
DA - Sep 2014
SP - 517
EP - 521
PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL - 24
IS - 5
SN - 1559-0631, 1559-0631
KW - Toxicology Abstracts; Health & Safety Science Abstracts
KW - Statistics
KW - Consumer products
KW - Children
KW - Allergies
KW - Pregnancy
KW - USA
KW - Hypersensitivity
KW - Urine
KW - Females
KW - Norway
KW - Triclosan
KW - H 12000:Epidemiology and Public Health
KW - X 24300:Methods
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Exposure+Science+and+Environmental+Epidemiology&rft.atitle=Reliability+of+triclosan+measures+in+repeated+urine+samples+from+Norwegian+pregnant+women&rft.au=Bertelsen%2C+Randi+J%3BEngel%2C+Stephanie+M%3BJusko%2C+Todd+A%3BCalafat%2C+Antonia+M%3BHoppin%2C+Jane+A%3BLondon%2C+Stephanie+J%3BEggesboe%2C+Merete%3BAase%2C+Heidi%3BZeiner%2C+Pal%3BReichborn-Kjennerud%2C+Ted%3BKnudsen%2C+Gun+P%3BGuidry%2C+Virginia+T%3BLongnecker%2C+Matthew+P&rft.aulast=Bertelsen&rft.aufirst=Randi&rft.date=2014-09-01&rft.volume=24&rft.issue=5&rft.spage=517&rft.isbn=&rft.btitle=&rft.title=Journal+of+Exposure+Science+and+Environmental+Epidemiology&rft.issn=15590631&rft_id=info:doi/10.1038%2Fjes.2013.95
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-09-01
N1 - Last updated - 2014-10-30
N1 - SubjectsTermNotLitGenreText - Hypersensitivity; Statistics; Urine; Children; Triclosan; Pregnancy; Consumer products; Females; Allergies; USA; Norway
DO - http://dx.doi.org/10.1038/jes.2013.95
ER -
TY - JOUR
T1 - Isolation of rare recombinants without using selectable markers for one-step seamless BAC mutagenesis.
AN - 1558529894; 25028895
AB - Current methods to isolate rare (1:10,000-1:100,000) bacterial artificial chromosome (BAC) recombinants require selectable markers. For seamless BAC mutagenesis, selectable markers need to be removed after isolation of recombinants through counterselection. Here we illustrate founder principle-driven enrichment (FPE), a simple method to rapidly isolate rare recombinants without using selectable markers, allowing one-step seamless BAC mutagenesis. As proof of principle, we isolated 1:100,000 seamless fluorescent protein-modified Nodal BACs and confirmed BAC functionality by generating fluorescent reporter mice. We also isolated small indel P1 phage-derived artificial chromosome (PAC) and BAC recombinants. Statistical analysis revealed that 1:100,000 recombinants can be isolated with <40 PCRs, and we developed a web-based calculator to optimize FPE.
JF - Nature methods
AU - Lyozin, George T
AU - Bressloff, Paul C
AU - Kumar, Amit
AU - Kosaka, Yasuhiro
AU - Demarest, Bradley L
AU - Yost, H Joseph
AU - Kuehn, Michael R
AU - Brunelli, Luca
AD - Department of Pediatrics, University of Utah School of Medicine, Salt Lake City, Utah, USA. ; 1] Department of Mathematics, University of Utah, Salt Lake City, Utah, USA. [2]. ; 1] Laboratory of Protein Dynamics and Signaling, National Cancer Institute, Frederick, Maryland, USA. [2]. ; Department of Neurobiology and Anatomy, University of Utah School of Medicine, Salt Lake City, Utah, USA. ; 1] Department of Pediatrics, University of Utah School of Medicine, Salt Lake City, Utah, USA. [2] Department of Neurobiology and Anatomy, University of Utah School of Medicine, Salt Lake City, Utah, USA. ; Laboratory of Protein Dynamics and Signaling, National Cancer Institute, Frederick, Maryland, USA.
Y1 - 2014/09//
PY - 2014
DA - September 2014
SP - 966
EP - 970
VL - 11
IS - 9
KW - Genetic Markers
KW - 0
KW - Recombinant Proteins
KW - Index Medicus
KW - Animals
KW - Genetic Markers -- genetics
KW - Mice
KW - Recombinant Proteins -- isolation & purification
KW - Mutagenesis, Site-Directed -- methods
KW - Protein Engineering -- methods
KW - Chromosomes, Artificial, Bacterial -- genetics
KW - Recombinant Proteins -- genetics
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-12-04
N1 - Date created - 2014-08-29
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1038/nmeth.3030
ER -
TY - JOUR
T1 - Transforming growth factor alpha is a critical mediator of radiation lung injury.
AN - 1558524652; 25117621
AB - Radiation fibrosis of the lung is a late toxicity of thoracic irradiation. Epidermal growth factor (EGF) signaling has previously been implicated in radiation lung injury. We hypothesized that TGF-α, an EGF receptor ligand, plays a key role in radiation-induced fibrosis in lung. Mice deficient in transforming growth factor (TGF-α(-/-)) and control C57Bl/6J (C57-WT) mice were exposed to thoracic irradiation in 5 daily fractions of 6 Gy. Cohorts of mice were followed for survival (n ≥ 5 per group) and tissue collection (n = 3 per strain and time point). Collagen accumulation in irradiated lungs was assessed by Masson's trichrome staining and analysis of hydroxyproline content. Cytokine levels in lung tissue were assessed with ELISA. The effects of TGF-α on pneumocyte and fibroblast proliferation and collagen production were analyzed in vitro. Lysyl oxidase (LOX) expression and activity were measured in vitro and in vivo. Irradiated C57-WT mice had a median survival of 24.4 weeks compared to 48.2 weeks for irradiated TGF-α(-/-) mice (P = 0.001). At 20 weeks after irradiation, hydroxyproline content was markedly increased in C57-WT mice exposed to radiation compared to TGF-α(-/-) mice exposed to radiation or unirradiated C57-WT mice (63.0, 30.5 and 37.6 μg/lung, respectively, P = 0.01). C57-WT mice exposed to radiation had dense foci of subpleural fibrosis at 20 weeks after exposure, whereas the lungs of irradiated TGF-α (-/-) mice were largely devoid of fibrotic foci. Lung tissue concentrations of IL-1β, IL-4, TNF-α, TGF-β and EGF at multiple time points after irradiation were similar in C57-WT and TGF-α(-/-) mice. TGF-α in lung tissue of C57-WT mice rose rapidly after irradiation and remained elevated through 20 weeks. TGF-α(-/-) mice had lower basal LOX expression than C57-WT mice. Both LOX expression and LOX activity were increased after irradiation in all mice but to a lesser degree in TGF-α(-/-) mice. Treatment of NIH-3T3 fibroblasts with TGF-α resulted in increases in proliferation, collagen production and LOX activity. These studies identify TGF-α as a critical mediator of radiation-induced lung injury and a novel therapeutic target in this setting. Further, these data implicate TGF-α as a mediator of collagen maturation through a TGF-β independent activation of lysyl oxidase.
JF - Radiation research
AU - Chung, Eun Joo
AU - Hudak, Kathryn
AU - Horton, Jason A
AU - White, Ayla
AU - Scroggins, Bradley T
AU - Vaswani, Shiva
AU - Citrin, Deborah
AD - Radiation Oncology Branch, Center for Cancer Research, National Institutes of Health, Bethesda, Maryland.
Y1 - 2014/09//
PY - 2014
DA - September 2014
SP - 350
EP - 362
VL - 182
IS - 3
KW - Cytokines
KW - 0
KW - Transforming Growth Factor alpha
KW - Collagen
KW - 9007-34-5
KW - Protein-Lysine 6-Oxidase
KW - EC 1.4.3.13
KW - Index Medicus
KW - Space life sciences
KW - Animals
KW - Pulmonary Fibrosis -- etiology
KW - Collagen -- metabolism
KW - Cytokines -- biosynthesis
KW - Mice, Inbred C57BL
KW - Mice
KW - Protein-Lysine 6-Oxidase -- metabolism
KW - NIH 3T3 Cells
KW - Female
KW - Transforming Growth Factor alpha -- physiology
KW - Radiation Injuries -- metabolism
KW - Radiation Injuries -- pathology
KW - Radiation Injuries -- etiology
KW - Lung -- radiation effects
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Radiation+research&rft.atitle=Transforming+growth+factor+alpha+is+a+critical+mediator+of+radiation+lung+injury.&rft.au=Chung%2C+Eun+Joo%3BHudak%2C+Kathryn%3BHorton%2C+Jason+A%3BWhite%2C+Ayla%3BScroggins%2C+Bradley+T%3BVaswani%2C+Shiva%3BCitrin%2C+Deborah&rft.aulast=Chung&rft.aufirst=Eun&rft.date=2014-09-01&rft.volume=182&rft.issue=3&rft.spage=350&rft.isbn=&rft.btitle=&rft.title=Radiation+research&rft.issn=1938-5404&rft_id=info:doi/10.1667%2FRR13625.1
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-10-24
N1 - Date created - 2014-08-28
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1667/RR13625.1
ER -
TY - JOUR
T1 - Transarterial embolization (TAE) is equally effective and slightly safer than transarterial chemoembolization (TACE) to manage liver metastases in neuroendocrine tumors.
AN - 1558521613; 24385266
AB - Liver metastases from neuroendocrine tumor (NET) can be treated by transarterial embolization (TAE) or transarterial chemoembolization (TACE). The goal of TAE and TACE is to reduce blood flow to the tumor resulting in tumor ischemia and necrosis. In this retrospective study, the effectiveness and safety of TAE-TACE in the treatment of liver metastases in patients with NET was compared. Thirty patients with a histologically confirmed gastro-entero-pancreatic NET with liver metastases were retrospectively investigated. Seventeen patients underwent TAE, while 13 patients underwent TACE. Tumor response, degree of devascularization in treated lesions, and progression free survival (PFS) were evaluated in the whole population and then separately in TAE and TACE subgroups. In all patients treated with TAE and TACE, there was a significant size reduction of lesions as compared to baseline. Per lesion reduction was 2.2 ± 1.4 versus 3.3 ± 1.5 cm for TAE (p < 0.001) and 2.2 ± 1.5 versus 3.4 ± 1.7 cm for TACE (p < 0.001). In the whole population, the median PFS for all patients was 36 months (16.2-55.7 CI), without significant difference between TAE and TACE. In no patient did adverse events grade 3 and 4 as well as TAE/TACE-related death occurred, while the post-embolization syndrome occurred in 41 % of patients treated with TAE and 61 % of those treated with TACE. TAE and TACE are both effective in NET patients with liver metastases. TAE should be preferred to TACE in light of its similar anti-tumor effects and slightly better toxicity profile.
JF - Endocrine
AU - Fiore, Francesco
AU - Del Prete, Michela
AU - Franco, Renato
AU - Marotta, Vincenzo
AU - Ramundo, Valeria
AU - Marciello, Francesca
AU - Di Sarno, Antonella
AU - Carratù, Anna Chiara
AU - de Luca di Roseto, Chiara
AU - Colao, Annamaria
AU - Faggiano, Antongiulio
AD - Interventional Radiology, National Cancer Institute, Fondazione "G. Pascale", Naples, Italy, doc.fiore@virgilio.it.
Y1 - 2014/09//
PY - 2014
DA - September 2014
SP - 177
EP - 182
VL - 47
IS - 1
KW - Index Medicus
KW - Young Adult
KW - Disease-Free Survival
KW - Humans
KW - Aged
KW - Gastrointestinal Neoplasms -- therapy
KW - Chemoembolization, Therapeutic -- adverse effects
KW - Pancreatic Neoplasms -- pathology
KW - Pancreatic Neoplasms -- therapy
KW - Aged, 80 and over
KW - Chemoembolization, Therapeutic -- methods
KW - Adult
KW - Treatment Outcome
KW - Middle Aged
KW - Gastrointestinal Neoplasms -- pathology
KW - Female
KW - Male
KW - Neuroendocrine Tumors -- therapy
KW - Neuroendocrine Tumors -- pathology
KW - Embolization, Therapeutic -- methods
KW - Liver Neoplasms -- therapy
KW - Liver Neoplasms -- secondary
KW - Embolization, Therapeutic -- adverse effects
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Endocrine&rft.atitle=Transarterial+embolization+%28TAE%29+is+equally+effective+and+slightly+safer+than+transarterial+chemoembolization+%28TACE%29+to+manage+liver+metastases+in+neuroendocrine+tumors.&rft.au=Fiore%2C+Francesco%3BDel+Prete%2C+Michela%3BFranco%2C+Renato%3BMarotta%2C+Vincenzo%3BRamundo%2C+Valeria%3BMarciello%2C+Francesca%3BDi+Sarno%2C+Antonella%3BCarrat%C3%B9%2C+Anna+Chiara%3Bde+Luca+di+Roseto%2C+Chiara%3BColao%2C+Annamaria%3BFaggiano%2C+Antongiulio&rft.aulast=Fiore&rft.aufirst=Francesco&rft.date=2014-09-01&rft.volume=47&rft.issue=1&rft.spage=177&rft.isbn=&rft.btitle=&rft.title=Endocrine&rft.issn=1559-0100&rft_id=info:doi/10.1007%2Fs12020-013-0130-9
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-06-08
N1 - Date created - 2014-08-27
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1007/s12020-013-0130-9
ER -
TY - JOUR
T1 - Joint analysis of three genome-wide association studies of esophageal squamous cell carcinoma in Chinese populations.
AN - 1558519653; 25129146
AB - We conducted a joint (pooled) analysis of three genome-wide association studies (GWAS) of esophageal squamous cell carcinoma (ESCC) in individuals of Chinese ancestry (5,337 ESCC cases and 5,787 controls) with 9,654 ESCC cases and 10,058 controls for follow-up. In a logistic regression model adjusted for age, sex, study and two eigenvectors, two new loci achieved genome-wide significance, marked by rs7447927 at 5q31.2 (per-allele odds ratio (OR) = 0.85, 95% confidence interval (CI) = 0.82-0.88; P = 7.72 × 10(-20)) and rs1642764 at 17p13.1 (per-allele OR = 0.88, 95% CI = 0.85-0.91; P = 3.10 × 10(-13)). rs7447927 is a synonymous SNP in TMEM173, and rs1642764 is an intronic SNP in ATP1B2, near TP53. Furthermore, a locus in the HLA class II region at 6p21.32 (rs35597309) achieved genome-wide significance in the two populations at highest risk for ESSC (OR = 1.33, 95% CI = 1.22-1.46; P = 1.99 × 10(-10)). Our joint analysis identifies new ESCC susceptibility loci overall as well as a new locus unique to the population in the Taihang Mountain region at high risk of ESCC.
JF - Nature genetics
AU - Wu, Chen
AU - Wang, Zhaoming
AU - Song, Xin
AU - Feng, Xiao-Shan
AU - Abnet, Christian C
AU - He, Jie
AU - Hu, Nan
AU - Zuo, Xian-Bo
AU - Tan, Wen
AU - Zhan, Qimin
AU - Hu, Zhibin
AU - He, Zhonghu
AU - Jia, Weihua
AU - Zhou, Yifeng
AU - Yu, Kai
AU - Shu, Xiao-Ou
AU - Yuan, Jian-Min
AU - Zheng, Wei
AU - Zhao, Xue-Ke
AU - Gao, She-Gan
AU - Yuan, Zhi-Qing
AU - Zhou, Fu-You
AU - Fan, Zong-Min
AU - Cui, Ji-Li
AU - Lin, Hong-Li
AU - Han, Xue-Na
AU - Li, Bei
AU - Chen, Xi
AU - Dawsey, Sanford M
AU - Liao, Linda
AU - Lee, Maxwell P
AU - Ding, Ti
AU - Qiao, You-Lin
AU - Liu, Zhihua
AU - Liu, Yu
AU - Yu, Dianke
AU - Chang, Jiang
AU - Wei, Lixuan
AU - Gao, Yu-Tang
AU - Koh, Woon-Puay
AU - Xiang, Yong-Bing
AU - Tang, Ze-Zhong
AU - Fan, Jin-Hu
AU - Han, Jing-Jing
AU - Zhou, Sheng-Li
AU - Zhang, Peng
AU - Zhang, Dong-Yun
AU - Yuan, Yuan
AU - Huang, Ying
AU - Liu, Chunling
AU - Zhai, Kan
AU - Qiao, Yan
AU - Jin, Guangfu
AU - Guo, Chuanhai
AU - Fu, Jianhua
AU - Miao, Xiaoping
AU - Lu, Changdong
AU - Yang, Haijun
AU - Wang, Chaoyu
AU - Wheeler, William A
AU - Gail, Mitchell
AU - Yeager, Meredith
AU - Yuenger, Jeff
AU - Guo, Er-Tao
AU - Li, Ai-Li
AU - Zhang, Wei
AU - Li, Xue-Min
AU - Sun, Liang-Dan
AU - Ma, Bao-Gen
AU - Li, Yan
AU - Tang, Sa
AU - Peng, Xiu-Qing
AU - Liu, Jing
AU - Hutchinson, Amy
AU - Jacobs, Kevin
AU - Giffen, Carol
AU - Burdette, Laurie
AU - Fraumeni, Joseph F
AU - Shen, Hongbing
AU - Ke, Yang
AU - Zeng, Yixin
AU - Wu, Tangchun
AU - Kraft, Peter
AU - Chung, Charles C
AU - Tucker, Margaret A
AU - Hou, Zhi-Chao
AU - Liu, Ya-Li
AU - Hu, Yan-Long
AU - Wang, Li
AU - Yuan, Guo
AU - Chen, Li-Sha
AU - Liu, Xiao
AU - Ma, Teng
AU - Meng, Hui
AU - Sun, Li
AU - Li, Xin-Min
AU - Li, Xiu-Min
AU - Ku, Jian-Wei
AU - Zhou, Ying-Fa
AU - Yang, Liu-Qin
AU - Wang, Zhou
AU - Li, Yin
AU - Qige, Qirenwang
AU - Yang, Wen-Jun
AU - Lei, Guang-Yan
AU - Chen, Long-Qi
AU - Li, En-Min
AU - Yuan, Ling
AU - Yue, Wen-Bin
AU - Wang, Ran
AU - Wang, Lu-Wen
AU - Fan, Xue-Ping
AU - Zhu, Fang-Heng
AU - Zhao, Wei-Xing
AU - Mao, Yi-Min
AU - Zhang, Mei
AU - Xing, Guo-Lan
AU - Li, Ji-Lin
AU - Han, Min
AU - Ren, Jing-Li
AU - Liu, Bin
AU - Ren, Shu-Wei
AU - Kong, Qing-Peng
AU - Li, Feng
AU - Sheyhidin, Ilyar
AU - Wei, Wu
AU - Zhang, Yan-Rui
AU - Feng, Chang-Wei
AU - Wang, Jin
AU - Yang, Yu-Hua
AU - Hao, Hong-Zhang
AU - Bao, Qi-De
AU - Liu, Bao-Chi
AU - Wu, Ai-Qun
AU - Xie, Dong
AU - Yang, Wan-Cai
AU - Wang, Liang
AU - Zhao, Xiao-Hang
AU - Chen, Shu-Qing
AU - Hong, Jun-Yan
AU - Zhang, Xue-Jun
AU - Freedman, Neal D
AU - Goldstein, Alisa M
AU - Lin, Dongxin
AU - Taylor, Philip R
AU - Wang, Li-Dong
AU - Chanock, Stephen J
AD - 1] State Key Laboratory of Molecular Oncology, Cancer Institute and Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. [2]. ; 1] Division of Cancer Epidemiology and Genetics, National Cancer Institute, US National Institutes of Health, Bethesda, Maryland, USA. [2] Cancer Genome Research Laboratory, Division of Cancer Epidemiology and Genetics, Advanced Technology Program, SAIC-Frederick, Inc., NCI-Frederick, Frederick, Maryland, USA. [3]. ; 1] Department of Pathology, Cancer Research Center, Basic Medical College, Xinxiang Medical University, Xinxiang, China. [2] Henan Key Laboratory for Esophageal Cancer Research of The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China. [3]. ; 1] Department of Oncology, Pathology, Clinical Laboratory and Respiratory Medicine, The First Affiliated Hospital, Henan University of Science and Technology, Luoyang, China. [2]. ; 1] Division of Cancer Epidemiology and Genetics, National Cancer Institute, US National Institutes of Health, Bethesda, Maryland, USA. [2]. ; 1] Department of Thoracic Surgery, Cancer Institute and Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. [2]. ; 1] Key Laboratory of Dermatology, Anhui Medical University, Anhui, China. [2]. ; State Key Laboratory of Molecular Oncology, Cancer Institute and Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. ; Department of Epidemiology and Biostatistics, Cancer Center, Nanjing Medical University, Nanjing, China. ; Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University School of Oncology, Beijing Cancer Hospital and Institute, Beijing, China. ; 1] State Key Laboratory of Oncology in Southern China, Sun Yat-Sen University Cancer Center, Guangzhou, China. [2] Department of Experimental Research, Sun Yat-Sen University Cancer Center, Guangzhou, China. ; Laboratory of Cancer Molecular Genetics, Medical College of Soochow University, Suzhou, China. ; Division of Cancer Epidemiology and Genetics, National Cancer Institute, US National Institutes of Health, Bethesda, Maryland, USA. ; 1] Department of Medicine, Vanderbilt University, Nashville, Tennessee, USA. [2] Vanderbilt-Ingram Cancer Center, Vanderbilt University, Nashville, Tennessee, USA. ; University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania, USA. ; Henan Key Laboratory for Esophageal Cancer Research of The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China. ; Department of Oncology, Pathology, Clinical Laboratory and Respiratory Medicine, The First Affiliated Hospital, Henan University of Science and Technology, Luoyang, China. ; Department of Pathology, Cancer Research Center, Basic Medical College, Xinxiang Medical University, Xinxiang, China. ; Anyang Tumor Hospital, Anyang, China. ; 1] Department of Pathology, Cancer Research Center, Basic Medical College, Xinxiang Medical University, Xinxiang, China. [2] Henan Key Laboratory for Esophageal Cancer Research of The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China. ; 1] Henan Key Laboratory for Esophageal Cancer Research of The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China. [2] Department of Basic Oncology and Pathology at the College of Medicine, Zhengzhou University, Zhengzhou, China. ; Center for Cancer Research, National Cancer Institute, US National Institutes of Health, Bethesda, Maryland, USA. ; Shanxi Cancer Hospital, Taiyuan, China. ; Department of Epidemiology, Cancer Institute and Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. ; Shanghai Cancer Institute, Shanghai, China. ; Duke-National University of Singapore Graduate Medical School, Singapore. ; Key Laboratory for Environment and Health (Ministry of Education), School of Public Health, Huazhong University of Sciences and Technology, Wuhan, China. ; Information Management Services, Inc., Silver Spring, Maryland, USA. ; 1] Division of Cancer Epidemiology and Genetics, National Cancer Institute, US National Institutes of Health, Bethesda, Maryland, USA. [2] Cancer Genome Research Laboratory, Division of Cancer Epidemiology and Genetics, Advanced Technology Program, SAIC-Frederick, Inc., NCI-Frederick, Frederick, Maryland, USA. ; 1] Henan Key Laboratory for Esophageal Cancer Research of The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China. [2] Department of Medical Oncology, Tumor Hospital of Linzhou, Linzhou, China. ; Department of Pathology and Thoracic Surgery, Centre for Health Screening and Endoscopy, Cixian Hospital, Cixian, China. ; Key Laboratory of Dermatology, Anhui Medical University, Anhui, China. ; 1] Department of Gastroenterology, Henan Provincial People's Hospital, Zhengzhou, China. [2] Department of Hematology, Henan Provincial People's Hospital, Zhengzhou, China. [3] Central Laboratory, Henan Provincial People's Hospital, Zhengzhou, China. ; 1] Henan Key Laboratory for Esophageal Cancer Research of The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China. [2] Department of Oncology, Pathology, Clinical Laboratory and Respiratory Medicine, The First Affiliated Hospital, Henan University of Science and Technology, Luoyang, China. ; Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA. ; 1] Department of Pathology, Cancer Research Center, Basic Medical College, Xinxiang Medical University, Xinxiang, China. [2] Department of Basic Oncology, Pathology and Gastroenterology, The Second Affiliated Hospital, Zhengzhou University, Zhengzhou, China. ; 1] Henan Key Laboratory for Esophageal Cancer Research of The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China. [2] Department of Oncology, The Second Affiliated Hospital of Nanyang Medical College, Nanyang, China. ; 1] Henan Key Laboratory for Esophageal Cancer Research of The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China. [2] Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA. ; Department of Radiotherapy, Pathology and Pediatrics, Central Hospital of Xinxiang, Xinxiang, China. ; Department of Thoracic Surgery, Provincial Hospital affiliated to Shandong University, Jinan, China. ; Department of Thoracic Surgery and Radiotherapy, Cancer Hospital of Henan Province, Zhengzhou, China. ; Department of Internal Mongolia Medicine, The Affiliated Hospital, Inner Mongolia Medical College, Hohhot, China. ; Department of Biotechnology, Ningxia Medical University, Yinchuan, China. ; Department of Thoracic Surgery, Tumor Hospital of Shaanxi Province, Xi'an, China. ; Department of Thoracic and Cardiovascular Surgery, West China Hospital, Sichuan University, Chengdu, China. ; 1] Department of Oncologic Pathology, Medical College of Shantou University, Shantou, China. [2] Department of Biochemistry and Molecular Biology, Medical College of Shantou University, Shantou, China. ; 1] Henan Key Laboratory for Esophageal Cancer Research of The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China. [2] Department of Oncology, Puyang City Oil Field General Hospital, Puyang, China. ; Department of Pathology and Thoracic Surgery, Linzhou Esophageal Cancer Hospital, Linzhou, China. ; Department of Gastroenterology and Thoracic Surgery, The First People's Hospital of Shangqiu, Shangqiu, China. ; Department of Basic Oncology, Pathology and Gastroenterology, The Second Affiliated Hospital, Zhengzhou University, Zhengzhou, China. ; Department of Gastroenterology, Beijing Tongren Hospital affiliated to Capital Medical University, Beijing, China. ; Department of Oncology, Xinyang Central Hospital, Xinyang, China. ; State Key Laboratory of Genetic Resource and Evolution, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, China. ; Department of Pathology, Shihezi University School of Medicine, Shihezi, China. ; 1] Department of Thoracic Surgery, The First Affiliated Hospital, Xinjiang Medical University, Urumqi, China. [2] Medical Research Center, The First Affiliated Hospital, Xinjiang Medical University, Urumqi, China. ; 1] Institute of Hematologic Disease, Changzhi Medical University, Changzhi, China. [2] Department of Pathology, Changzhi Medical University, Changzhi, China. ; Department of Surgery, Hebi Dahejian Hospital, Hebi, China. ; Anyang District Hospital, Anyang, China. ; Surgical Department of the Shanghai Public Health Clinical Center, Fudan University, Shanghai, China. ; Department of Anatomy, the Second Military Medical University of the Chinese People's Liberation Army, Shanghai, China. ; Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China. ; 1] Department of Pathology, Cancer Research Center, Basic Medical College, Xinxiang Medical University, Xinxiang, China. [2] Medical College of Wisconsin, Cancer Research Center, Milwaukee, Wisconsin, USA. ; National Laboratory of Molecular Oncology, Cancer Institute and Hospital, Chinese Academy of Medical Sciences, Beijing, China. ; College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China. ; 1] College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China. [2] Department of Environmental and Occupational Health, University of Medicine and Dentistry of New Jersey, Newark, New Jersey, USA.
Y1 - 2014/09//
PY - 2014
DA - September 2014
SP - 1001
EP - 1006
VL - 46
IS - 9
KW - Index Medicus
KW - Genotype
KW - Risk
KW - Polymorphism, Single Nucleotide
KW - Alleles
KW - Genetic Loci
KW - Humans
KW - Case-Control Studies
KW - Middle Aged
KW - Genetic Predisposition to Disease
KW - Genome-Wide Association Study -- methods
KW - Male
KW - Female
KW - Esophageal Neoplasms -- genetics
KW - Carcinoma, Squamous Cell -- genetics
KW - Asian Continental Ancestry Group -- genetics
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-01-15
N1 - Date created - 2014-08-28
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1038/ng.3064
ER -
TY - JOUR
T1 - Cross-cancer pleiotropic analysis of endometrial cancer: PAGE and E2C2 consortia.
AN - 1558519031; 24832084
AB - Genome-wide association studies (GWAS) have identified a large number of cancer-associated single nucleotide polymorphisms (SNPs), several of which have been associated with multiple cancer sites suggesting pleiotropic effects and shared biological mechanisms across some cancers. We hypothesized that SNPs associated with other cancers may be additionally associated with endometrial cancer. We examined 213 SNPs previously associated with 14 other cancers for their associations with endometrial cancer in 3758 endometrial cancer cases and 5966 controls of European ancestry from two consortia: Population Architecture Using Genomics and Epidemiology and the Epidemiology of Endometrial Cancer Consortium. Study-specific logistic regression estimates adjusted for age, body mass index and the most significant principal components of genetic ancestry were combined using fixed-effect meta-analysis to evaluate the association between each SNP and endometrial cancer risk. A Bonferroni-corrected P value of 2.35×10(-4) was used to determine statistical significance of the associations. SNP rs7679673, ~6.3kb upstream of TET2 and previously reported to be associated with prostate cancer risk, was associated with endometrial cancer risk in the direction opposite to that for prostate cancer [meta-analysis odds ratio = 0.87 (per copy of the C allele), 95% confidence interval = 0.81, 0.93; P = 7.37×10(-5)] with no evidence of heterogeneity across studies (P heterogeneity = 0.66). This pleiotropic analysis is the first to suggest TET2 as a susceptibility locus for endometrial cancer. © The Author 2014. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.
JF - Carcinogenesis
AU - Setiawan, Veronica Wendy
AU - Schumacher, Fredrick
AU - Prescott, Jennifer
AU - Haessler, Jeffrey
AU - Malinowski, Jennifer
AU - Wentzensen, Nicolas
AU - Yang, Hannah
AU - Chanock, Stephen
AU - Brinton, Louise
AU - Hartge, Patricia
AU - Lissowska, Jolanta
AU - Park, S Lani
AU - Cheng, Iona
AU - Bush, William S
AU - Crawford, Dana C
AU - Ursin, Giske
AU - Horn-Ross, Pamela
AU - Bernstein, Leslie
AU - Lu, Lingeng
AU - Risch, Harvey
AU - Yu, Herbert
AU - Sakoda, Lori C
AU - Doherty, Jennifer
AU - Chen, Chu
AU - Jackson, Rebecca
AU - Yasmeen, Shagufta
AU - Cote, Michele
AU - Kocarnik, Jonathan M
AU - Peters, Ulrike
AU - Kraft, Peter
AU - De Vivo, Immaculata
AU - Haiman, Christopher A
AU - Kooperberg, Charles
AU - Le Marchand, Loic
AD - Department of Preventive Medicine, Keck School of Medicine, and Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA 90089, USA, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA, Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA, Center for Human Genetics Research, Vanderbilt University, Nashville, TN 37235, USA, National Cancer Institute, Bethesda, MD 20892, USA, M.Sklodowska-Curie Memorial Cancer Center and Institute of Oncology, 02-781 Warsaw, Poland, Cancer Prevention Institute of California, Fremont, CA 94538, USA, Institute of Population Based Cancer Research, Cancer Registry of Norway, N-0304 Oslo, Norway, Division of Cancer Etiology, Beckman Research Institute of City of Hope, Duarte, CA 91010, USA, Department of Epidemiology, Yale School of Public Health, New Haven CT 06520, USA, Cancer Epidemiology Program, University of Hawaii Cancer Center, Honolulu, HI 96813, USA, Division of Research, Kaiser Permanente Northern California, Oakland, CA 94611, USA, Section of Biostatistics and Epidemiology, Department of Community and Family Medicine, Geisel School of Medicine, Dartmouth College, Lebanon, NH 03756, USA, Division of Endocrinology, Diabetes and Metabolism, Ohio State University, Columbus, OH 43210, USA, Department of Obstetrics and Gynecology, University of California, Davis, CA 95616, USA, Department of Oncology, Wayne State University School of Medicine and Population Studies and Disparities Research, Karmanos Cancer Institute, Detroit, MI 48202, USA and Department of Epidemiology, Harvard School of Public Health, Boston, MA 02115, USA vsetiawa@usc.edu. ; Department of Preventive Medicine, Keck School of Medicine, and Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA 90089, USA, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA, Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA, Center for Human Genetics Research, Vanderbilt University, Nashville, TN 37235, USA, National Cancer Institute, Bethesda, MD 20892, USA, M.Sklodowska-Curie Memorial Cancer Center and Institute of Oncology, 02-781 Warsaw, Poland, Cancer Prevention Institute of California, Fremont, CA 94538, USA, Institute of Population Based Cancer Research, Cancer Registry of Norway, N-0304 Oslo, Norway, Division of Cancer Etiology, Beckman Research Institute of City of Hope, Duarte, CA 91010, USA, Department of Epidemiology, Yale School of Public Health, New Haven CT 06520, USA, Cancer Epidemiology Program, University of Hawaii Cancer Center, Honolulu, HI 96813, USA, Division of Research, Kaiser Permanente Northern California, Oakland, CA 94611, USA, Section of Biostatistics and Epidemiology, Department of Community and Family Medicine, Geisel School of Medicine, Dartmouth College, Lebanon, NH 03756, USA, Division of Endocrinology, Diabetes and Metabolism, Ohio State University, Columbus, OH 43210, USA, Department of Obstetrics and Gynecology, University of California, Davis, CA 95616, USA, Department of Oncology, Wayne State University School of Medicine and Population Studies and Disparities Research, Karmanos Cancer Institute, Detroit, MI 48202, USA and Department of Epidemiology, Harvard School of Public Health, Boston, MA 02115, USA. ; Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA. ; Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA. ; Center for Human Genetics Research, Vanderbilt University, Nashville, TN 37235, USA. ; National Cancer Institute, Bethesda, MD 20892, USA. ; M.Sklodowska-Curie Memorial Cancer Center and Institute of Oncology, 02-781 Warsaw, Poland. ; Cancer Prevention Institute of California, Fremont, CA 94538, USA. ; Institute of Population Based Cancer Research, Cancer Registry of Norway, N-0304 Oslo, Norway. ; Division of Cancer Etiology, Beckman Research Institute of City of Hope, Duarte, CA 91010, USA. ; Department of Epidemiology, Yale School of Public Health, New Haven CT 06520, USA. ; Cancer Epidemiology Program, University of Hawaii Cancer Center, Honolulu, HI 96813, USA. ; Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA, Division of Research, Kaiser Permanente Northern California, Oakland, CA 94611, USA. ; Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA, Section of Biostatistics and Epidemiology, Department of Community and Family Medicine, Geisel School of Medicine, Dartmouth College, Lebanon, NH 03756, USA. ; Division of Endocrinology, Diabetes and Metabolism, Ohio State University, Columbus, OH 43210, USA. ; Department of Obstetrics and Gynecology, University of California, Davis, CA 95616, USA. ; Department of Oncology, Wayne State University School of Medicine and Population Studies and Disparities Research, Karmanos Cancer Institute, Detroit, MI 48202, USA and. ; Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA, Department of Epidemiology, Harvard School of Public Health, Boston, MA 02115, USA.
Y1 - 2014/09//
PY - 2014
DA - September 2014
SP - 2068
EP - 2073
VL - 35
IS - 9
KW - DNA-Binding Proteins
KW - 0
KW - Proto-Oncogene Proteins
KW - TET2 protein, human
KW - Index Medicus
KW - Genetic Pleiotropy
KW - Risk Factors
KW - Humans
KW - Case-Control Studies
KW - Genetic Predisposition to Disease
KW - Female
KW - Genome-Wide Association Study
KW - Polymorphism, Single Nucleotide
KW - DNA-Binding Proteins -- genetics
KW - Endometrial Neoplasms -- genetics
KW - Proto-Oncogene Proteins -- genetics
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1558519031?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Cross-cancer+pleiotropic+analysis+of+endometrial+cancer%3A+PAGE+and+E2C2+consortia.&rft.au=Setiawan%2C+Veronica+Wendy%3BSchumacher%2C+Fredrick%3BPrescott%2C+Jennifer%3BHaessler%2C+Jeffrey%3BMalinowski%2C+Jennifer%3BWentzensen%2C+Nicolas%3BYang%2C+Hannah%3BChanock%2C+Stephen%3BBrinton%2C+Louise%3BHartge%2C+Patricia%3BLissowska%2C+Jolanta%3BPark%2C+S+Lani%3BCheng%2C+Iona%3BBush%2C+William+S%3BCrawford%2C+Dana+C%3BUrsin%2C+Giske%3BHorn-Ross%2C+Pamela%3BBernstein%2C+Leslie%3BLu%2C+Lingeng%3BRisch%2C+Harvey%3BYu%2C+Herbert%3BSakoda%2C+Lori+C%3BDoherty%2C+Jennifer%3BChen%2C+Chu%3BJackson%2C+Rebecca%3BYasmeen%2C+Shagufta%3BCote%2C+Michele%3BKocarnik%2C+Jonathan+M%3BPeters%2C+Ulrike%3BKraft%2C+Peter%3BDe+Vivo%2C+Immaculata%3BHaiman%2C+Christopher+A%3BKooperberg%2C+Charles%3BLe+Marchand%2C+Loic&rft.aulast=Setiawan&rft.aufirst=Veronica&rft.date=2014-09-01&rft.volume=35&rft.issue=9&rft.spage=2068&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgu107
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-10-21
N1 - Date created - 2014-08-28
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/carcin/bgu107
ER -
TY - JOUR
T1 - Fecal metabolomics: assay performance and association with colorectal cancer.
AN - 1558518851; 25037050
AB - Metabolomic analysis of feces may provide insights on colorectal cancer (CRC) if assay performance is satisfactory. In lyophilized feces from 48 CRC cases, 102 matched controls, and 48 masked quality control specimens, 1043 small molecules were detected with a commercial platform. Assay reproducibility was good for 527 metabolites [technical intraclass correlation coefficient (ICC) >0.7 in quality control specimens], but reproducibility in 6-month paired specimens was lower for the majority of metabolites (within-subject ICC ≤0.5). In the CRC cases and controls, significant differences (false discovery rate ≤0.10) were found for 41 of 1043 fecal metabolites. Direct cancer association was found with three fecal heme-related molecules [covariate-adjusted 90th versus 10th percentile odds ratio (OR) = 17-345], 18 peptides/amino acids (OR = 3-14), palmitoyl-sphingomyelin (OR = 14), mandelate (OR = 3) and p-hydroxy-benzaldehyde (OR = 4). Conversely, cancer association was inverse with acetaminophen metabolites (OR <0.1), tocopherols (OR = 0.3), sitostanol (OR = 0.2), 3-dehydrocarnitine (OR = 0.4), pterin (OR = 0.3), conjugated-linoleate-18-2N7 (OR = 0.2), N-2-furoyl-glycine (OR = 0.3) and p-aminobenzoate (PABA, OR = 0.2). Correlations suggested an independent role for palmitoyl-sphingomyelin and a central role for PABA (which was stable over 6 months, within-subject ICC 0.67) modulated by p-hydroxy-benzaldehyde. Power calculations based on ICCs indicate that only 45% of metabolites with a true relative risk 5.0 would be found in prospectively collected, prediagnostic specimens from 500 cases and 500 controls. Thus, because fecal metabolites vary over time, very large studies will be needed to reliably detect associations of many metabolites that potentially contribute to CRC.
Published by Oxford University Press 2014.
JF - Carcinogenesis
AU - Goedert, James J
AU - Sampson, Joshua N
AU - Moore, Steven C
AU - Xiao, Qian
AU - Xiong, Xiaoqin
AU - Hayes, Richard B
AU - Ahn, Jiyoung
AU - Shi, Jianxin
AU - Sinha, Rashmi
AD - Epidemiology and Biostatistics Program, Division of Cancer Epidemiology and Genetics, National Cancer Institute, 9609 Medical Center Drive, Bethesda, MD 20892-9704, USA, Information Management Services, 6110 Executive Boulevard, Rockville, MD 20852, USA and Division of Epidemiology, Department of Population Health, New York University School of Medicine, 650 First Avenue, #518, New York, NY 10016, USA goedertj@mail.nih.gov. ; Epidemiology and Biostatistics Program, Division of Cancer Epidemiology and Genetics, National Cancer Institute, 9609 Medical Center Drive, Bethesda, MD 20892-9704, USA, Information Management Services, 6110 Executive Boulevard, Rockville, MD 20852, USA and Division of Epidemiology, Department of Population Health, New York University School of Medicine, 650 First Avenue, #518, New York, NY 10016, USA. ; Information Management Services, 6110 Executive Boulevard, Rockville, MD 20852, USA and. ; Division of Epidemiology, Department of Population Health, New York University School of Medicine, 650 First Avenue, #518, New York, NY 10016, USA.
Y1 - 2014/09//
PY - 2014
DA - September 2014
SP - 2089
EP - 2096
VL - 35
IS - 9
KW - Biomarkers, Tumor
KW - 0
KW - Hippurates
KW - Peptides
KW - Heme
KW - 42VZT0U6YR
KW - salicylurate
KW - 487-54-7
KW - Index Medicus
KW - Humans
KW - Reference Standards
KW - Case-Control Studies
KW - Peptides -- metabolism
KW - Hippurates -- metabolism
KW - Middle Aged
KW - Heme -- metabolism
KW - Metabolomics -- standards
KW - Male
KW - Female
KW - Biomarkers, Tumor -- metabolism
KW - Metabolome
KW - Colorectal Neoplasms -- metabolism
KW - Feces -- chemistry
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1558518851?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Fecal+metabolomics%3A+assay+performance+and+association+with+colorectal+cancer.&rft.au=Goedert%2C+James+J%3BSampson%2C+Joshua+N%3BMoore%2C+Steven+C%3BXiao%2C+Qian%3BXiong%2C+Xiaoqin%3BHayes%2C+Richard+B%3BAhn%2C+Jiyoung%3BShi%2C+Jianxin%3BSinha%2C+Rashmi&rft.aulast=Goedert&rft.aufirst=James&rft.date=2014-09-01&rft.volume=35&rft.issue=9&rft.spage=2089&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgu131
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-10-21
N1 - Date created - 2014-08-28
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/carcin/bgu131
ER -
TY - JOUR
T1 - Elevated HERV-K mRNA expression in PBMC is associated with a prostate cancer diagnosis particularly in older men and smokers.
AN - 1558518181; 24858205
AB - Aberrant expression of subgroup k human endogenous retroviruses (HERV-K) has been observed in prostate cancer. This subgroup is unique because it encodes sequences in the human genome containing open reading frames for near intact retroviruses. We hypothesized that HERV-K reactivation could serve as a non-invasive early disease detection marker for prostate cancer. We evaluated HERV-K gag messenger RNA (mRNA) expression in blood samples of African-American and European-American men using a case-control design via quantitative real-time PCR. Additionally, we examined HERV-K envelope protein expression in prostate tumors by immunohistochemistry. HERV-K envelope protein was commonly upregulated in prostate tumors, but more so in tumors of African-American than European-American patients (61% versus 40%, P 12-fold increased odds {odds ratio = 12.87 [95% confidence interval 6.3-26.25]} of being diagnosed with prostate cancer than those in the lowest quartile. Moreover, our results showed that HERV-K expression may perform better as a disease biomarker in older than younger men (whereas the sensitivity of prostate-specific antigen (PSA) testing decreases with age) and in men with a smoking history compared with never smokers. Combining non-invasive HERV-K testing with PSA testing may improve the efficacy of prostate cancer detection specifically among older men and smokers who tend to develop a more aggressive disease. Published by Oxford University Press 2014.
JF - Carcinogenesis
AU - Wallace, Tiffany A
AU - Downey, Ronan F
AU - Seufert, Caleb J
AU - Schetter, Aaron
AU - Dorsey, Tiffany H
AU - Johnson, Carol A
AU - Goldman, Radoslav
AU - Loffredo, Christopher A
AU - Yan, Peisha
AU - Sullivan, Francis J
AU - Giles, Francis J
AU - Wang-Johanning, Feng
AU - Ambs, Stefan
AU - Glynn, Sharon A
AD - Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA, Prostate Cancer Institute, Biosciences Research Building, National University of Ireland Galway, Dangan, Corrib Village, Galway, Ireland, Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC 20057-1465, USA, Department of Pathology and Laboratory Medicine, The University of Texas Health Science Center at Houston, Houston, TX 77030, USA, Department of Radiation Oncology, Galway University Hospital, Galway, Ireland and Viral Oncology, Center for Cancer and Metabolism, Stanford Research Institute International, Menlo Park, CA 94025, USA. ; Prostate Cancer Institute, Biosciences Research Building, National University of Ireland Galway, Dangan, Corrib Village, Galway, Ireland. ; Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC 20057-1465, USA. ; Department of Pathology and Laboratory Medicine, The University of Texas Health Science Center at Houston, Houston, TX 77030, USA. ; Prostate Cancer Institute, Biosciences Research Building, National University of Ireland Galway, Dangan, Corrib Village, Galway, Ireland, Department of Radiation Oncology, Galway University Hospital, Galway, Ireland and. ; Viral Oncology, Center for Cancer and Metabolism, Stanford Research Institute International, Menlo Park, CA 94025, USA. ; Prostate Cancer Institute, Biosciences Research Building, National University of Ireland Galway, Dangan, Corrib Village, Galway, Ireland, sharon.glynn@nuigalway.ie.
Y1 - 2014/09//
PY - 2014
DA - September 2014
SP - 2074
EP - 2083
VL - 35
IS - 9
KW - CXCL10 protein, human
KW - 0
KW - Chemokine CXCL10
KW - Gene Products, gag
KW - RNA, Messenger
KW - Interferon-gamma
KW - 82115-62-6
KW - Index Medicus
KW - RNA, Messenger -- blood
KW - Chemokine CXCL10 -- blood
KW - Risk Factors
KW - Humans
KW - Endogenous Retroviruses -- enzymology
KW - Gene Expression
KW - Interferon-gamma -- blood
KW - RNA, Messenger -- genetics
KW - Male
KW - Adenocarcinoma -- diagnosis
KW - Adenocarcinoma -- blood
KW - Smoking -- blood
KW - Prostatic Neoplasms -- diagnosis
KW - Leukocytes, Mononuclear -- virology
KW - Gene Products, gag -- blood
KW - Prostatic Neoplasms -- virology
KW - Prostatic Neoplasms -- blood
KW - Leukocytes, Mononuclear -- metabolism
KW - Adenocarcinoma -- virology
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1558518181?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Elevated+HERV-K+mRNA+expression+in+PBMC+is+associated+with+a+prostate+cancer+diagnosis+particularly+in+older+men+and+smokers.&rft.au=Wallace%2C+Tiffany+A%3BDowney%2C+Ronan+F%3BSeufert%2C+Caleb+J%3BSchetter%2C+Aaron%3BDorsey%2C+Tiffany+H%3BJohnson%2C+Carol+A%3BGoldman%2C+Radoslav%3BLoffredo%2C+Christopher+A%3BYan%2C+Peisha%3BSullivan%2C+Francis+J%3BGiles%2C+Francis+J%3BWang-Johanning%2C+Feng%3BAmbs%2C+Stefan%3BGlynn%2C+Sharon+A&rft.aulast=Wallace&rft.aufirst=Tiffany&rft.date=2014-09-01&rft.volume=35&rft.issue=9&rft.spage=2074&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgu114
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-10-21
N1 - Date created - 2014-08-28
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
JAMA. 2011 Jun 22;305(24):2548-55 [21693743]
Cancer Epidemiol Biomarkers Prev. 2011 May;20(5):740-50 [21546365]
Carcinogenesis. 2011 Oct;32(10):1484-92 [21828060]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/carcin/bgu114
ER -
TY - JOUR
T1 - Identification of a melanoma susceptibility locus and somatic mutation in TET2.
AN - 1558518161; 24980573
AB - Although genetic studies have reported a number of loci associated with melanoma risk, the complex genetic architecture of the disease is not yet fully understood. We sought to identify common genetic variants associated with melanoma risk in a genome-wide association study (GWAS) of 2298 cases and 6654 controls. Thirteen of 15 known loci were replicated with nominal significance. A total of 69 single-nucleotide polymorphisms (SNPs) were selected for in silico replication in two independent melanoma GWAS datasets (a total of 5149 cases and 12 795 controls). Seven novel loci were nominally significantly associated with melanoma risk. These seven SNPs were further genotyped in 234 melanoma cases and 238 controls. The SNP rs4698934 was nominally significantly associated with melanoma risk. The combined odds ratio per T allele = 1.18; 95% confidence interval (1.10-1.25); combined P = 7.70 × 10(-) (7). This SNP is located in the intron of the TET2 gene on chromosome 4q24. In addition, a novel somatic mutation of TET2 was identified by next-generation sequencing in 1 of 22 sporadic melanoma cases. TET2 encodes a member of TET family enzymes that oxidizes 5-methylcytosine to 5-hydroxymethylcytosine (5hmC). It is a putative epigenetic biomarker of melanoma as we previously reported, with observation of reduced TET2 transcriptional expression. This study is the first to implicate TET2 genetic variation and mutation in melanoma.
© The Author 2014. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.
JF - Carcinogenesis
AU - Song, Fengju
AU - Amos, Christopher I
AU - Lee, Jeffrey E
AU - Lian, Christine G
AU - Fang, Shenying
AU - Liu, Hongliang
AU - MacGregor, Stuart
AU - Iles, Mark M
AU - Law, Matthew H
AU - Lindeman, Neal I
AU - Montgomery, Grant W
AU - Duffy, David L
AU - Cust, Anne E
AU - Jenkins, Mark A
AU - Whiteman, David C
AU - Kefford, Richard F
AU - Giles, Graham G
AU - Armstrong, Bruce K
AU - Aitken, Joanne F
AU - Hopper, John L
AU - Brown, Kevin M
AU - Martin, Nicholas G
AU - Mann, Graham J
AU - Bishop, D Timothy
AU - Bishop, Julia A Newton
AU - GenoMEL consortium
AU - Kraft, Peter
AU - Qureshi, Abrar A
AU - Kanetsky, Peter A
AU - Hayward, Nicholas K
AU - Hunter, David J
AU - Wei, Qingyi
AU - Han, Jiali
AD - Department of Epidemiology and Biostatistics, Key Laboratory of Cancer Prevention and Therapy, National Clinical Research Center of Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, P.R. China. ; Department of Community and Family Medicine, Center for Genomic Medicine, Geisel School of Medicine, Dartmouth College, Lebanon, NH 03755, USA. ; Department of Surgical Oncology, MD Anderson Cancer Center, Houston, TX 77030, USA. ; Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. ; Duke Cancer Institute, Duke University Medical Center, Durham, NC 27710, USA. ; Queensland Institute of Medical Research, Brisbane, Queensland 4029, Australia. ; Leeds Institute of Cancer and Pathology, University of Leeds, Leeds LS9 7TF, UK. ; Centre for Molecular, Environmental, Genetic and Analytic Epidemiology, School of Population Health, University of Melbourne, Melbourne, Victoria 3052, Australia, Cancer Epidemiology and Services Research, Sydney School of Public Health, University of Sydney, Sydney, New South Wales 2006, Australia. ; Centre for Molecular, Environmental, Genetic and Analytic Epidemiology, School of Population Health, University of Melbourne, Melbourne, Victoria 3052, Australia. ; Westmead Institute of Cancer Research, University of Sydney at Westmead Millennium Institute and Melanoma Institute Australia, Westmead, New South Wales 2145, Australia. ; Cancer Epidemiology Centre, The Cancer Council Victoria, Carlton, Victoria 3053, Australia. ; Cancer Epidemiology and Services Research, Sydney School of Public Health, University of Sydney, Sydney, New South Wales 2006, Australia. ; Viertel Centre for Research in Cancer Control, Cancer Council Queensland, Brisbane, Queensland 4004, Australia. ; Laboratory of Translational Genomics, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD 20852, USA. ; GenoMEL consortium ; Department of Epidemiology, Harvard School of Public Health, Boston, MA 02115, USA. ; Channing Division of Network Medicine and Department of Dermatology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA. ; Department of Biostatistics and Epidemiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. ; Oncogenomics Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, Queensland 4029, Australia. ; Duke Cancer Institute, Duke University Medical Center, Durham, NC 27710, USA, jialhan@iu.edu qingyi.wei@duke.edu. ; Department of Epidemiology and Biostatistics, Key Laboratory of Cancer Prevention and Therapy, National Clinical Research Center of Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, P.R. China, Department of Epidemiology, Harvard School of Public Health, Boston, MA 02115, USA, Channing Division of Network Medicine and Department of Dermatology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA, Department of Epidemiology, Fairbanks School of Public Health, Indiana University, Indianapolis, IN 46202, USA, Simon Cancer Center, Indiana University, Indianapolis, IN 46202, USA and Department of Dermatology, School of Medicine, Indiana University, Indianapolis, IN 46202, USA jialhan@iu.edu.
Y1 - 2014/09//
PY - 2014
DA - September 2014
SP - 2097
EP - 2101
VL - 35
IS - 9
KW - DNA-Binding Proteins
KW - 0
KW - Proto-Oncogene Proteins
KW - TET2 protein, human
KW - Index Medicus
KW - Polymorphism, Single Nucleotide
KW - Risk Factors
KW - Humans
KW - Case-Control Studies
KW - Genetic Predisposition to Disease
KW - Mutation
KW - Genome-Wide Association Study
KW - Skin Neoplasms -- genetics
KW - Melanoma -- genetics
KW - DNA-Binding Proteins -- genetics
KW - Proto-Oncogene Proteins -- genetics
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1558518161?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Identification+of+a+melanoma+susceptibility+locus+and+somatic+mutation+in+TET2.&rft.au=Song%2C+Fengju%3BAmos%2C+Christopher+I%3BLee%2C+Jeffrey+E%3BLian%2C+Christine+G%3BFang%2C+Shenying%3BLiu%2C+Hongliang%3BMacGregor%2C+Stuart%3BIles%2C+Mark+M%3BLaw%2C+Matthew+H%3BLindeman%2C+Neal+I%3BMontgomery%2C+Grant+W%3BDuffy%2C+David+L%3BCust%2C+Anne+E%3BJenkins%2C+Mark+A%3BWhiteman%2C+David+C%3BKefford%2C+Richard+F%3BGiles%2C+Graham+G%3BArmstrong%2C+Bruce+K%3BAitken%2C+Joanne+F%3BHopper%2C+John+L%3BBrown%2C+Kevin+M%3BMartin%2C+Nicholas+G%3BMann%2C+Graham+J%3BBishop%2C+D+Timothy%3BBishop%2C+Julia+A+Newton%3BGenoMEL+consortium%3BKraft%2C+Peter%3BQureshi%2C+Abrar+A%3BKanetsky%2C+Peter+A%3BHayward%2C+Nicholas+K%3BHunter%2C+David+J%3BWei%2C+Qingyi%3BHan%2C+Jiali&rft.aulast=Song&rft.aufirst=Fengju&rft.date=2014-09-01&rft.volume=35&rft.issue=9&rft.spage=2097&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgu140
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-10-21
N1 - Date created - 2014-08-28
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
J Dermatol Sci. 2014 Feb;73(2):161-3 [24169492]
Mod Pathol. 2014 Jul;27(7):936-44 [24390216]
Hum Genet. 2011 Mar;129(3):247-53 [21116649]
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Hum Mol Genet. 2011 Jul 1;20(13):2673-9 [21478494]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/carcin/bgu140
ER -
TY - JOUR
T1 - Modulation of miR-29 expression by α-fetoprotein is linked to the hepatocellular carcinoma epigenome.
AN - 1557082548; 24798303
AB - Globally, hepatocellular carcinoma (HCC) accounts for 70%-85% of primary liver cancers and ranks as the second leading cause of male cancer death. Serum alpha-fetoprotein (AFP), normally highly expressed in the liver only during fetal development, is reactivated in 60% of HCC tumors and associated with poor patient outcome. We hypothesize that AFP+ and AFP- tumors differ biologically. Multivariable analysis in 237 HCC cases demonstrates that AFP level predicts poor survival independent of tumor stage (P<0.043). Using microarray-based global microRNA (miRNA) profiling, we found that miRNA-29 (miR-29) family members were the most significantly (P<0.001) down-regulated miRNAs in AFP+ tumors. Consistent with miR-29's role in targeting DNA methyltransferase 3A (DNMT3A), a key enzyme regulating DNA methylation, we found a significant inverse correlation (P<0.001) between miR-29 and DNMT3A gene expression, suggesting that they might be functionally antagonistic. Moreover, global DNA methylation profiling reveals that AFP+ and AFP- HCC tumors have distinct global DNA methylation patterns and that increased DNA methylation is associated with AFP+ HCC. Experimentally, we found that AFP expression in AFP- HCC cells induces cell proliferation, migration, and invasion. Overexpression of AFP, or conditioned media from AFP+ cells, inhibits miR-29a expression and induces DNMT3A expression in AFP- HCC cells. AFP also inhibited transcription of the miR-29a/b-1 locus, and this effect is mediated through c-MYC binding to the transcript of miR-29a/b-1. Furthermore, AFP expression promotes tumor growth of AFP- HCC cells in nude mice.
Tumor biology differs considerably between AFP+ HCC and AFP- HCC; AFP is a functional antagonist of miR-29, which may contribute to global epigenetic alterations and poor prognosis in HCC. © 2014 by the American Association for the Study of Liver Diseases. This article has been contributed to by U.S. Government employees and their work is in the public domain in the USA.
JF - Hepatology (Baltimore, Md.)
AU - Parpart, Sonya
AU - Roessler, Stephanie
AU - Dong, Fei
AU - Rao, Vinay
AU - Takai, Atsushi
AU - Ji, Junfang
AU - Qin, Lun-Xiu
AU - Ye, Qing-Hai
AU - Jia, Hu-Liang
AU - Tang, Zhao-You
AU - Wang, Xin Wei
AD - Laboratory of Human Carcinogenesis, National Cancer Institute, Bethesda, MD; Tumor Biology Department, Georgetown University, Washington, DC.
Y1 - 2014/09//
PY - 2014
DA - September 2014
SP - 872
EP - 883
VL - 60
IS - 3
KW - MIRN29 microRNA, human
KW - 0
KW - MicroRNAs
KW - alpha-Fetoproteins
KW - Index Medicus
KW - Animals
KW - Liver Neoplasms, Experimental -- genetics
KW - Humans
KW - Liver Neoplasms, Experimental -- enzymology
KW - Mice, Nude
KW - Mice
KW - Cell Line, Tumor
KW - DNA Methylation -- genetics
KW - Down-Regulation -- genetics
KW - Liver Neoplasms, Experimental -- mortality
KW - Adult
KW - Cohort Studies
KW - Middle Aged
KW - Female
KW - Male
KW - MicroRNAs -- genetics
KW - alpha-Fetoproteins -- biosynthesis
KW - Liver Neoplasms -- enzymology
KW - Liver Neoplasms -- mortality
KW - MicroRNAs -- biosynthesis
KW - MicroRNAs -- antagonists & inhibitors
KW - Gene Expression Regulation, Neoplastic
KW - Carcinoma, Hepatocellular -- genetics
KW - Carcinoma, Hepatocellular -- enzymology
KW - alpha-Fetoproteins -- genetics
KW - Carcinoma, Hepatocellular -- mortality
KW - Epigenomics
KW - Liver Neoplasms -- genetics
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Hepatology+%28Baltimore%2C+Md.%29&rft.atitle=Modulation+of+miR-29+expression+by+%CE%B1-fetoprotein+is+linked+to+the+hepatocellular+carcinoma+epigenome.&rft.au=Parpart%2C+Sonya%3BRoessler%2C+Stephanie%3BDong%2C+Fei%3BRao%2C+Vinay%3BTakai%2C+Atsushi%3BJi%2C+Junfang%3BQin%2C+Lun-Xiu%3BYe%2C+Qing-Hai%3BJia%2C+Hu-Liang%3BTang%2C+Zhao-You%3BWang%2C+Xin+Wei&rft.aulast=Parpart&rft.aufirst=Sonya&rft.date=2014-09-01&rft.volume=60&rft.issue=3&rft.spage=872&rft.isbn=&rft.btitle=&rft.title=Hepatology+%28Baltimore%2C+Md.%29&rft.issn=1527-3350&rft_id=info:doi/10.1002%2Fhep.27200
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-10-30
N1 - Date created - 2014-08-26
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Hepatology. 2009 Aug;50(2):472-80 [19585654]
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Cancer Biol Ther. 2009 Sep;8(18):1686-93 [19901517]
Hepatology. 2010 Mar;51(3):836-45 [20041405]
J Cell Biochem. 2010 Aug 1;110(5):1155-64 [20564213]
BMC Cancer. 2010;10:399 [20678188]
Adv Genet. 2010;70:27-56 [20920744]
Adv Genet. 2010;70:87-99 [20920746]
J Hematol Oncol. 2010;3:37 [20925959]
Clin Liver Dis. 2001 Feb;5(1):145-59 [11218912]
Cell. 2004 Jan 23;116(2):281-97 [14744438]
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Cancer Res. 1983 Aug;43(8):3739-41 [6190555]
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J Formos Med Assoc. 1993 Oct;92(10):866-70 [7511953]
Oncogene. 1997 Jan 30;14(4):395-404 [9053836]
Mol Endocrinol. 1998 Oct;12(10):1551-7 [9773978]
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CA Cancer J Clin. 2011 Mar-Apr;61(2):69-90 [21296855]
Gastroenterology. 2012 Apr;142(4):957-966.e12 [22202459] Gastroenterology. 2012 Jun;142(7):1431-43 [22504185]
Ann Surg Oncol. 2013 Dec;20 Suppl 3:S625-35 [23864307]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1002/hep.27200
ER -
TY - JOUR
T1 - Carboplatin-Paclitaxel versus Cisplatin-Ifosfamide in the treatment of uterine carcinosarcoma: a retrospective cohort study.
AN - 1557081203; 25078338
AB - Uterine carcinosarcoma (CS) is a rare neoplasm whose adjuvant treatment has not been yet defined. We report on the activity and toxicity of cisplatin-ifosfamide and carboplatin-paclitaxel as adjuvant treatments for patients with uterine CS.
Data of International Federation of Gynecology and Obstetrics (FIGO) stage I to IV uterine CS patients treated between 2006 and 2012 with adjuvant chemotherapy (cisplatin 20 mg/mq and ifosfamide 1500 mg/mq day 1 to 4 every 3 weeks plus prophylactic Granulocyte colony-stimulating factor (G-CSF) support [group A] or carboplatin area under the curve -5 (AUC-5) and paclitaxel 175 mg/mq d1q21 [group B]) were retrospectively reviewed. Progression-free survival, overall survival, and chemotherapy-related toxicities were compared between the 2 groups. A subanalysis of oncologic outcomes according to the sarcomatous component (homologous vs heterologous) was performed. Forty-six women were evaluated-21 in group A and 25 in group B. At a median follow-up of 30 months, the median progression-free survival was 11.6 months (95% confidence interval [CI], 6.3-16.9) and 16.6 months (95% CI, 14.7-18.5) for group A and B, respectively (P = 0.20). The median overall survival was 17.1 months (95% CI, 12.6-21.5) and 35.1 months (95% CI, 26.3-43.7) for group A and B, respectively (P = 0.14). No differences were identified among heterologous or homologous components according to chemotherapy treatment. Toxicity profiles widely differ between treatment arms. Because of the super imposable activity and the better toxicity profile, carboplatin-paclitaxel may be a suitable alternative to cisplatin-ifosfamide in the treatment of uterine CS.
JF - International journal of gynecological cancer : official journal of the International Gynecological Cancer Society
AU - Lorusso, Domenica
AU - Martinelli, Fabio
AU - Mancini, Maria
AU - Sarno, Italo
AU - Ditto, Antonino
AU - Raspagliesi, Francesco
AD - Department of Gynecologic Oncology, IRCCS Foundation National Cancer Institute, Milan, Italy.
Y1 - 2014/09//
PY - 2014
DA - September 2014
SP - 1256
EP - 1261
VL - 24
IS - 7
KW - Carboplatin
KW - BG3F62OND5
KW - Paclitaxel
KW - P88XT4IS4D
KW - Cisplatin
KW - Q20Q21Q62J
KW - Ifosfamide
KW - UM20QQM95Y
KW - Index Medicus
KW - Paclitaxel -- administration & dosage
KW - Aged, 80 and over
KW - Humans
KW - Adult
KW - Retrospective Studies
KW - Aged
KW - Middle Aged
KW - Carboplatin -- administration & dosage
KW - Female
KW - Survival Analysis
KW - Ifosfamide -- administration & dosage
KW - Cisplatin -- administration & dosage
KW - Carcinosarcoma -- pathology
KW - Uterine Neoplasms -- drug therapy
KW - Carcinosarcoma -- drug therapy
KW - Carcinosarcoma -- mortality
KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use
KW - Uterine Neoplasms -- mortality
KW - Uterine Neoplasms -- pathology
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-07-02
N1 - Date created - 2014-08-26
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1097/IGC.0000000000000215
ER -
TY - JOUR
T1 - Relationship between characteristics of medications and drug-induced liver disease phenotype and outcome.
AN - 1555619978; 24362054
AB - It is not known whether specific characteristics of medication are associated with type of drug-induced liver injury (DILI) or outcome. We examined the relationships among select characteristics of medications and DILI phenotype and outcome.
We analyzed 383 cases of DILI caused by a single orally administered prescription agent from the DILI Network Prospective Study with causalities of definite, highly likely, or probable. Relationship of daily dosage (≥50 mg vs ≤49 mg), preponderance of hepatic metabolism (≥50% vs <50%), or Biopharmaceutics Drug Disposition Classification System (BDDCS) class (1-4, based on solubility and metabolism of the drug) were compared with clinical characteristics and outcomes.
Compared with cases of DILI in the ≤49 mg/day group, those associated with daily dosages ≥50 mg had shorter latency (median, 38 days vs 56 days; P = .03) and a different biochemical pattern of liver injury (P = .04); no differences in recovery, severity, or outcome were observed. Patients with DILI caused by medications with or without preponderant hepatic metabolism did not differ in clinical characteristics or outcomes. Compared with other classes of BDDCS, DILI caused by BDDCS class 1 medications had significantly longer latency (P < .001) and greater proportion of hepatocellular injury (P = .001). However, peak liver biochemical values and patients' time to recovery, disease severity, and outcomes did not differ among the 4 BDDCS classes.
Characteristics of medications (dosage, hepatic metabolism, and solubility) are associated with features of DILI such as latency and pattern of liver injury, but not with recovery, severity, or outcome. Copyright © 2014 AGA Institute. Published by Elsevier Inc. All rights reserved.
JF - Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association
AU - Vuppalanchi, Raj
AU - Gotur, Raghavender
AU - Reddy, K Rajender
AU - Fontana, Robert J
AU - Ghabril, Marwan
AU - Kosinski, Andrzej S
AU - Gu, Jiezhun
AU - Serrano, Jose
AU - Chalasani, Naga
AD - Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana. ; Department of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania. ; Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan. ; Duke Clinical Research Institute, Durham, North Carolina. ; Liver Disease Research Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland. ; Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana. Electronic address: nchalasa@iu.edu.
Y1 - 2014/09//
PY - 2014
DA - September 2014
SP - 1550
EP - 1555
VL - 12
IS - 9
KW - Index Medicus
KW - Overdose
KW - ALT
KW - Liver Toxicity
KW - Side Effect
KW - DILIN
KW - Prospective Studies
KW - Humans
KW - Adult
KW - Treatment Outcome
KW - Aged
KW - Middle Aged
KW - Male
KW - Female
KW - Chemical and Drug Induced Liver Injury -- etiology
KW - Chemical and Drug Induced Liver Injury -- mortality
KW - Chemical and Drug Induced Liver Injury -- pathology
KW - Drug Therapy -- methods
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+gastroenterology+and+hepatology+%3A+the+official+clinical+practice+journal+of+the+American+Gastroenterological+Association&rft.atitle=Relationship+between+characteristics+of+medications+and+drug-induced+liver+disease+phenotype+and+outcome.&rft.au=Vuppalanchi%2C+Raj%3BGotur%2C+Raghavender%3BReddy%2C+K+Rajender%3BFontana%2C+Robert+J%3BGhabril%2C+Marwan%3BKosinski%2C+Andrzej+S%3BGu%2C+Jiezhun%3BSerrano%2C+Jose%3BChalasani%2C+Naga&rft.aulast=Vuppalanchi&rft.aufirst=Raj&rft.date=2014-09-01&rft.volume=12&rft.issue=9&rft.spage=1550&rft.isbn=&rft.btitle=&rft.title=Clinical+gastroenterology+and+hepatology+%3A+the+official+clinical+practice+journal+of+the+American+Gastroenterological+Association&rft.issn=1542-7714&rft_id=info:doi/10.1016%2Fj.cgh.2013.12.016
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-05-27
N1 - Date created - 2014-08-22
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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AAPS J. 2011 Dec;13(4):519-47 [21818695]
Clin Pharmacol Ther. 2012 Sep;92(3):376-80 [22850601]
Pharmacogenet Genomics. 2012 Nov;22(11):784-95 [22968431]
J Pharm Sci. 2013 Jan;102(1):34-42 [23147500]
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Comment In:
Clin Gastroenterol Hepatol. 2014 Sep;12(9):1556-61 [24530601]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.cgh.2013.12.016
ER -
TY - JOUR
T1 - A new antiviral: chimeric 3TC-AZT phosphonate efficiently inhibits HIV-1 in human tissues ex vivo.
AN - 1554469325; 25010891
AB - Although more-recently developed antivirals target different molecules in the HIV-1 replication cycle, nucleoside reverse transcriptase inhibitors (NRTIs) remain central for HIV-1 therapy. Here, we test the anti-HIV activity of a phosphonate chimera of two well-known NRTIs, namely AZT and 3TC. We show that this newly synthesized compound suppressed HIV-1 infection in lymphoid tissue ex vivo more efficiently than did other phosphonates of NRTIs. Moreover, the new compound was not toxic for tissue cells, thus making the chimeric phosphonate strategy a valid approach for the development of anti HIV-1 compound heterodimers.
Published by Elsevier B.V.
JF - Antiviral research
AU - Vanpouille, Christophe
AU - Khandazhinskaya, Anastasia
AU - Karpenko, Inna
AU - Zicari, Sonia
AU - Barreto-de-Souza, Victor
AU - Frolova, Svetlana
AU - Margolis, Leonid
AU - Kochetkov, Sergey
AD - Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, United States. ; Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, Russian Federation. ; Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, United States. Electronic address: margolis@helix.nih.gov. ; Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, Russian Federation. Electronic address: kochet@eimb.ru.
Y1 - 2014/09//
PY - 2014
DA - September 2014
SP - 125
EP - 131
VL - 109
KW - Anti-HIV Agents
KW - 0
KW - Dideoxynucleotides
KW - Thymine Nucleotides
KW - Lamivudine
KW - 2T8Q726O95
KW - Zidovudine
KW - 4B9XT59T7S
KW - 3'-azido-3'-deoxythymidine 5'-triphosphate
KW - 6RGF96R053
KW - Index Medicus
KW - Depot form
KW - NRTI
KW - HIV-1
KW - Virus Replication -- drug effects
KW - Humans
KW - In Vitro Techniques
KW - Drug Evaluation, Preclinical
KW - Zidovudine -- analogs & derivatives
KW - Anti-HIV Agents -- chemistry
KW - Dideoxynucleotides -- chemistry
KW - HIV Infections -- virology
KW - Zidovudine -- pharmacology
KW - Lamivudine -- chemistry
KW - Lamivudine -- pharmacology
KW - HIV-1 -- physiology
KW - Thymine Nucleotides -- chemistry
KW - Anti-HIV Agents -- chemical synthesis
KW - Palatine Tonsil -- drug effects
KW - Dideoxynucleotides -- pharmacology
KW - Anti-HIV Agents -- pharmacology
KW - Thymine Nucleotides -- pharmacology
KW - HIV Infections -- drug therapy
KW - Zidovudine -- chemistry
KW - HIV-1 -- drug effects
KW - Palatine Tonsil -- virology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Antiviral+research&rft.atitle=A+new+antiviral%3A+chimeric+3TC-AZT+phosphonate+efficiently+inhibits+HIV-1+in+human+tissues+ex+vivo.&rft.au=Vanpouille%2C+Christophe%3BKhandazhinskaya%2C+Anastasia%3BKarpenko%2C+Inna%3BZicari%2C+Sonia%3BBarreto-de-Souza%2C+Victor%3BFrolova%2C+Svetlana%3BMargolis%2C+Leonid%3BKochetkov%2C+Sergey&rft.aulast=Vanpouille&rft.aufirst=Christophe&rft.date=2014-09-01&rft.volume=109&rft.issue=&rft.spage=125&rft.isbn=&rft.btitle=&rft.title=Antiviral+research&rft.issn=1872-9096&rft_id=info:doi/10.1016%2Fj.antiviral.2014.06.019
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-04-06
N1 - Date created - 2014-08-18
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Nature. 2002 May 2;417(6884):95-8 [11986671]
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Curr Top Med Chem. 2003;3(13):1467-95 [14529522]
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Antiviral Res. 1990 Jul;14(1):11-23 [1964371]
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J Med Chem. 1995 May 12;38(10):1641-9 [7538589]
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J Hepatol. 1999 Jan;30(1):156-60 [9927163]
Pharmacol Rep. 2006 Sep-Oct;58(5):599-613 [17085852]
Cell Host Microbe. 2008 Sep 11;4(3):260-70 [18779052]
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Chem Biol Drug Des. 2011 Jul;78(1):50-6 [21518262]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.antiviral.2014.06.019
ER -
TY - JOUR
T1 - Comparative toxicity and efficacy of engineered anthrax lethal toxin variants with broad anti-tumor activities.
AN - 1554459061; 24971906
AB - We have previously designed and characterized versions of anthrax lethal toxin that are selectively cytotoxic in the tumor microenvironment and which display broad and potent anti-tumor activities in vivo. Here, we have performed the first direct comparison of the safety and efficacy of three engineered anthrax lethal toxin variants requiring activation by either matrix-metalloproteinases (MMPs), urokinase plasminogen activator (uPA) or co-localized MMP/uPA activities. C57BL/6J mice were challenged with six doses of engineered toxins via intraperitoneal (I.P.) or intravenous (I.V.) dose routes to determine the maximum tolerated dose for six administrations (MTD6) and dose-limiting toxicities. Efficacy was evaluated using the B16-BL6 syngraft model of melanoma; mice bearing established tumors were treated with six I.P. doses of toxin and tumor measurements and immunohistochemistry, paired with terminal blood work, were used to elaborate upon the anti-tumor mechanism and relative efficacy of each variant. We found that MMP-, uPA- and dual MMP/uPA-activated anthrax lethal toxins exhibited the same dose-limiting toxicity; dose-dependent GI toxicity. In terms of efficacy, all three toxins significantly reduced primary B16-BL6 tumor burden, ranging from 32% to 87% reduction, and they also delayed disease progression as evidenced by dose-dependent normalization of blood work values. While target organ toxicity and effective doses were similar amongst the variants, the dual MMP/uPA-activated anthrax lethal toxin exhibited the highest I.P. MTD6 and was 1.5-3-fold better tolerated than the single MMP- and uPA-activated toxins. Overall, we demonstrate that this dual MMP/uPA-activated anthrax lethal toxin can be administered safely and is highly effective in a preclinical model of melanoma. This modified bacterial cytotoxin is thus a promising candidate for further clinical development and evaluation for use in treating human cancers.
Published by Elsevier Inc.
JF - Toxicology and applied pharmacology
AU - Peters, Diane E
AU - Hoover, Benjamin
AU - Cloud, Loretta Grey
AU - Liu, Shihui
AU - Molinolo, Alfredo A
AU - Leppla, Stephen H
AU - Bugge, Thomas H
AD - Proteases and Tissue Remodeling Section, Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA; Program of Pharmacology and Experimental Therapeutics, Tufts University School of Medicine, Boston, MA, USA. ; Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA. ; Proteases and Tissue Remodeling Section, Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA. ; Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA. ; Proteases and Tissue Remodeling Section, Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA. Electronic address: thomas.bugge@nih.go.
Y1 - 2014/09/01/
PY - 2014
DA - 2014 Sep 01
SP - 220
EP - 229
VL - 279
IS - 2
KW - Antigens, Bacterial
KW - 0
KW - Antineoplastic Agents
KW - Bacterial Toxins
KW - Biomarkers, Tumor
KW - Prodrugs
KW - anthrax toxin
KW - Urokinase-Type Plasminogen Activator
KW - EC 3.4.21.73
KW - Matrix Metalloproteinases
KW - EC 3.4.24.-
KW - Index Medicus
KW - Bacterial cytotoxin
KW - Protease
KW - Prodrug
KW - Cancer
KW - Melanoma
KW - Injections, Intraperitoneal
KW - Animals
KW - Injections, Intravenous
KW - Dose-Response Relationship, Drug
KW - Mice
KW - Urokinase-Type Plasminogen Activator -- metabolism
KW - Tumor Burden -- drug effects
KW - Mice, Inbred C57BL
KW - Matrix Metalloproteinases -- metabolism
KW - Maximum Tolerated Dose
KW - Biomarkers, Tumor -- blood
KW - Time Factors
KW - Female
KW - Prodrugs -- toxicity
KW - Antigens, Bacterial -- pharmacology
KW - Antigens, Bacterial -- genetics
KW - Skin Neoplasms -- blood
KW - Skin Neoplasms -- drug therapy
KW - Bacterial Toxins -- genetics
KW - Skin Neoplasms -- enzymology
KW - Protein Engineering
KW - Prodrugs -- pharmacology
KW - Antigens, Bacterial -- toxicity
KW - Antigens, Bacterial -- metabolism
KW - Antineoplastic Agents -- administration & dosage
KW - Antineoplastic Agents -- metabolism
KW - Skin Neoplasms -- pathology
KW - Bacterial Toxins -- pharmacology
KW - Bacterial Toxins -- administration & dosage
KW - Melanoma, Experimental -- pathology
KW - Prodrugs -- administration & dosage
KW - Melanoma, Experimental -- blood
KW - Bacterial Toxins -- metabolism
KW - Melanoma, Experimental -- enzymology
KW - Antineoplastic Agents -- toxicity
KW - Melanoma, Experimental -- drug therapy
KW - Antigens, Bacterial -- administration & dosage
KW - Bacterial Toxins -- toxicity
KW - Antineoplastic Agents -- pharmacology
KW - Prodrugs -- metabolism
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+and+applied+pharmacology&rft.atitle=Comparative+toxicity+and+efficacy+of+engineered+anthrax+lethal+toxin+variants+with+broad+anti-tumor+activities.&rft.au=Peters%2C+Diane+E%3BHoover%2C+Benjamin%3BCloud%2C+Loretta+Grey%3BLiu%2C+Shihui%3BMolinolo%2C+Alfredo+A%3BLeppla%2C+Stephen+H%3BBugge%2C+Thomas+H&rft.aulast=Peters&rft.aufirst=Diane&rft.date=2014-09-01&rft.volume=279&rft.issue=2&rft.spage=220&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+applied+pharmacology&rft.issn=1096-0333&rft_id=info:doi/10.1016%2Fj.taap.2014.06.010
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-10-12
N1 - Date created - 2014-08-18
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Science. 1998 May 1;280(5364):734-7 [9563949]
Biochem Biophys Res Commun. 1998 Jul 30;248(3):706-11 [9703991]
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Mol Cancer Ther. 2006 Jan;5(1):89-96 [16432166]
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Cancer Res. 2007 Apr 1;67(7):3329-36 [17409442]
J Biol Chem. 2008 Jan 4;283(1):529-40 [17974567]
Cell Cycle. 2008 Mar 15;7(6):745-9 [18245947]
Curr Protoc Immunol. 2001 May;Chapter 20:Unit 20.1 [18432774]
Front Biosci (Landmark Ed). 2009;14:2335-57 [19273204]
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J Clin Oncol. 2009 Nov 1;27(31):5287-97 [19738110]
Mol Cancer Ther. 2010 Jan;9(1):190-201 [20053778]
J Immunol. 2010 Nov 1;185(9):5463-7 [20921524]
Infect Immun. 2011 Jan;79(1):118-24 [20974827]
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Nature. 2013 Sep 5;501(7465):63-8 [23995686]
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Clin Chem Lab Med. 2012 Nov;50(11):1877-91 [23093268]
Protein Expr Purif. 2000 Apr;18(3):293-302 [10733882]
Cancer Res. 2000 Nov 1;60(21):6061-7 [11085528]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.taap.2014.06.010
ER -
TY - JOUR
T1 - Class II human leucocyte antigen DRB1*11 in hairy cell leukaemia patients with and without haemolytic uraemic syndrome.
AN - 1553711783; 24931452
AB - Frequencies of human leucocyte antigens (HLA) were determined in 287 classic hairy cell leukaemia (HCL) patients. With respect to both population (n = 287) and allele (2n = 574) frequency respectively, the most common HLA class I and II antigens expressed were HLA-A*02 (49·1% and 28·6%), HLA-B*07 (21·3% and 11·1%), HLA-C*07 (46·7 and 28·2%), HLA-DQB1*03 (62·7% and 37·3%), HLA-DRB1*11 (30·0% and 16·0%) and HLA-DRB4*01 (45·3% and 29·6%). In comparing 6-14 databases of control Caucasians to 267 Caucasian HCL patients, only HLA-DRB1*11 was consistently over-represented in HCL, 31·1% of patients vs. 17-19·9% of controls (P = 0·0055 to <0·0001) and 16·5% of alleles vs. 6·5-12·3% of control alleles (P = 0·022 to <0·0001). HLA-DRB1*11 is a known risk factor for acquired thrombotic microangiopathy. Anti-CD22 recombinant immunotoxin BL22 in HCL was associated with a 12% incidence of completely reversible grade 3-4 haemolytic uraemic syndrome (HUS), mainly during the second or third retreatment cycle. Of 49 HCL patients receiving ≥2 cycles of BL22, 7 (14%) had HUS and HLA-DRB1*11 was expressed in 71% of 7 with HUS compared with only 21% of 42 without (P = 0·015). These data suggest that DBR1*11 may be a marker for increased susceptibility to HCL and, among HCL patients, could be a risk factor for BL22-induced HUS.
Published 2014. This article is a U.S. Government work and is in the public domain in the USA.
JF - British journal of haematology
AU - Arons, Evgeny
AU - Adams, Sharon
AU - Venzon, David J
AU - Pastan, Ira
AU - Kreitman, Robert J
AD - Laboratory of Molecular Biology, National Cancer Institute, Bethesda, MD, USA.
Y1 - 2014/09//
PY - 2014
DA - September 2014
SP - 729
EP - 738
VL - 166
IS - 5
KW - Bacterial Toxins
KW - 0
KW - Exotoxins
KW - HLA-DRB1 Chains
KW - HLA-DRB1*11 antigen
KW - immunotoxin HA22
KW - Index Medicus
KW - ADAMTS13
KW - HLA-DQB1*03
KW - thrombotic microangiopathy
KW - recombinant immunotoxin
KW - moxetumomab pasudotox
KW - Young Adult
KW - Gene Frequency
KW - Humans
KW - Aged
KW - Tissue Donors
KW - Thrombotic Microangiopathies
KW - Alleles
KW - Aged, 80 and over
KW - Risk Factors
KW - Adult
KW - Bacterial Toxins -- therapeutic use
KW - Middle Aged
KW - Genetic Predisposition to Disease
KW - Exotoxins -- therapeutic use
KW - Female
KW - Male
KW - HLA-DRB1 Chains -- biosynthesis
KW - Hemolytic-Uremic Syndrome -- immunology
KW - Leukemia, Hairy Cell -- metabolism
KW - Hemolytic-Uremic Syndrome -- metabolism
KW - Hemolytic-Uremic Syndrome -- genetics
KW - HLA-DRB1 Chains -- genetics
KW - Leukemia, Hairy Cell -- therapy
KW - Leukemia, Hairy Cell -- immunology
KW - Leukemia, Hairy Cell -- genetics
KW - Hemolytic-Uremic Syndrome -- therapy
KW - HLA-DRB1 Chains -- immunology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+journal+of+haematology&rft.atitle=Class+II+human+leucocyte+antigen+DRB1*11+in+hairy+cell+leukaemia+patients+with+and+without+haemolytic+uraemic+syndrome.&rft.au=Arons%2C+Evgeny%3BAdams%2C+Sharon%3BVenzon%2C+David+J%3BPastan%2C+Ira%3BKreitman%2C+Robert+J&rft.aulast=Arons&rft.aufirst=Evgeny&rft.date=2014-09-01&rft.volume=166&rft.issue=5&rft.spage=729&rft.isbn=&rft.btitle=&rft.title=British+journal+of+haematology&rft.issn=1365-2141&rft_id=info:doi/10.1111%2Fbjh.12956
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-12-08
N1 - Date created - 2014-08-15
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Blood. 2004 Jun 15;103(12):4514-9 [14976043]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1111/bjh.12956
ER -
TY - JOUR
T1 - Indices of methylation in sperm DNA from fertile men differ between distinct geographical regions.
AN - 1553707290; 25035434
AB - Which are the main determinants, if any, of sperm DNA methylation levels?
Geographical region resulted associated with the sperm methylation status assessed on genome-wide repetitive sequences. DNA methylation level, assessed on repetitive sequences from peripheral blood lymphocyte, can vary with age, gender, alcohol consumption and white blood cell counts.
A cross-sectional study. Individual data were collected from 269 young healthy men of proven fertility living in three geographical regions: Inuits from Greenland, Caucasians from Warsaw (Poland) and Kharkiv (Ukraine). Semen samples were collected between May 2002 and February 2004 and aliquots were immediately frozen. We estimated sperm DNA global methylation level (DGML) in two ways. First DNA methylation in repetitive DNA sequences (LINE-1, Satα and Alu) was quantified by PCR pyrosequencing after bisulfite conversion and second by flow cytometry (FCM) using fluorescently labeled monoclonal antibodies anti-5-methylcytosine. We analyzed whether personal characteristics and habits, body mass index, semen quality parameters, sperm chromatin integrity, biomarkers of accessory gland function and the plasma concentration of reproductive hormones were associated with sperm DNA methylation levels in men. Associations were evaluated by analysis of variance and linear regression analyses. The geographical location emerged as the main determinant when using the methylation level in repetitive sequences. FCM DGML results were not associated with those from repetitive sequence analysis. No other consistent associations between methylation markers and the assessed variables were identified across countries.
The methods used are only surrogates of the actual sperm methylome and the methylation levels at individual specific loci were not explored. Sperm DGML is relatively independent from semen quality parameters and is a new candidate biomarker for epidemiological studies of the impact of environmental contaminants on male fertility.
The study is part of the project CLEAR (Climate change, Environmental contaminants and Reproductive health) supported by the European Commission 7th framework program, contract no: FP7-ENV-2008-1-226217. No competing interest is declared. © The Author 2014. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oup.com.
JF - Human reproduction (Oxford, England)
AU - Consales, C
AU - Leter, G
AU - Bonde, J P E
AU - Toft, G
AU - Eleuteri, P
AU - Moccia, T
AU - Budillon, A
AU - Jönsson, B A G
AU - Giwercman, A
AU - Pedersen, H S
AU - Ludwicki, J K
AU - Zviezdai, V
AU - Heederik, D
AU - Spanò, M
AD - Laboratory of Toxicology, Unit of Radiation Biology and Human Health, ENEA Casaccia Research Center, Via Anguillarese 301, 00123 Rome, Italy. ; Department of Occupational and Environmental Medicine, Bispebjerg University Hospital, DK-2400 Copenhagen NV, Denmark. ; Department of Occupational Medicine, Aarhus University Hospital, DK-8000 Aarhus C, Denmark. ; Experimental Pharmacology Unit, Department of Experimental Oncology, National Cancer Institute - G. Pascale, 80131 Naples, Italy. ; Division of Occupational and Environmental Medicine, Department of Laboratory Medicine, Lund University, SE-22185 Lund, Sweden. ; Reproductive Medicine Centre, Skåne University Hospital Malmö, Lund University, Malmö SE-20502, Sweden. ; Centre for Arctic Environmental Medicine, Greenland Institute of Natural Resources, 3900 Nuuk, Greenland. ; Department of Toxicology and Risk Assessment, National Institute of Public Health - National Institute of Hygiene, 00971 Warsaw, Poland. ; Department of Social Medicine and Organization of Public Health, Kharkiv National Medical University, 61022 Kharkiv, Ukraine. ; Institute for Risk Assessment Sciences, Utrecht University, Utrecht, The Netherlands. ; Laboratory of Toxicology, Unit of Radiation Biology and Human Health, ENEA Casaccia Research Center, Via Anguillarese 301, 00123 Rome, Italy marcello.spano@enea.it.
Y1 - 2014/09//
PY - 2014
DA - September 2014
SP - 2065
EP - 2072
VL - 29
IS - 9
KW - DNA
KW - 9007-49-2
KW - Index Medicus
KW - human spermatozoa
KW - pyrosequencing
KW - sperm DNA methylation
KW - epidemiology
KW - flow cytometry
KW - Greenland
KW - Cross-Sectional Studies
KW - Fertility
KW - Genome, Human
KW - Semen Analysis
KW - Poland
KW - Humans
KW - Ukraine
KW - Geography
KW - Male
KW - DNA Methylation
KW - DNA -- metabolism
KW - Spermatozoa -- metabolism
KW - Repetitive Sequences, Nucleic Acid -- genetics
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1553707290?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Human+reproduction+%28Oxford%2C+England%29&rft.atitle=Indices+of+methylation+in+sperm+DNA+from+fertile+men+differ+between+distinct+geographical+regions.&rft.au=Consales%2C+C%3BLeter%2C+G%3BBonde%2C+J+P+E%3BToft%2C+G%3BEleuteri%2C+P%3BMoccia%2C+T%3BBudillon%2C+A%3BJ%C3%B6nsson%2C+B+A+G%3BGiwercman%2C+A%3BPedersen%2C+H+S%3BLudwicki%2C+J+K%3BZviezdai%2C+V%3BHeederik%2C+D%3BSpan%C3%B2%2C+M&rft.aulast=Consales&rft.aufirst=C&rft.date=2014-09-01&rft.volume=29&rft.issue=9&rft.spage=2065&rft.isbn=&rft.btitle=&rft.title=Human+reproduction+%28Oxford%2C+England%29&rft.issn=1460-2350&rft_id=info:doi/10.1093%2Fhumrep%2Fdeu176
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-04-23
N1 - Date created - 2014-08-15
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/humrep/deu176
ER -
TY - JOUR
T1 - Acute and chronic effects of IL-22 on acetaminophen-induced liver injury.
AN - 1553705789; 25063867
AB - Acetaminophen (APAP)-induced liver injury (AILI) accounts for half of the acute liver failure cases in the United States. A better understanding of the underlying mechanisms of AILI is necessary for the development of novel antidotes. We found that pretreatment with IL-22 protected mice from APAP-mediated hepatotoxicity. The protection was dependent on STAT3, as IL-22 failed to reduce APAP hepatotoxicity in liver-specific STAT3 knockout mice. In contrast to the acute exposure to IL-22, the endogenous chronic overexpression of IL-22 in IL-22 transgenic (TG) mice or IL-22 adenovirus treatment for 6 wk resulted in a markedly increased susceptibility to AILI. Furthermore, the hepatic expression levels of cytochrome 2E1 (Cyp2E1) and Cyp1A2 were much higher in IL-22TG mice. Ablation of Cyp2E1 but not hepatic STAT3 abolished AILI and protein-adduct formation in IL-22TG mice. Finally, hepatic expression of HNF-1α, a transcriptional factor that is known to control Cyp2E1 expression, was elevated in IL-22TG mice compared with wild-type mice. Upregulation of hepatic Cyp2E1 was only observed in mice with constitutive overexpression of IL-22 but not with short-term treatment with one dose of IL-22 or multiple doses of IL-22 for 2 wk. In conclusion, short-term acute IL-22 exposure protects mice against AILI through STAT3 activation; however, chronic constitutive overexpression of IL-22 exacerbates AILI by increasing Cyp2E1 and toxic reactive APAP metabolite production. These findings may not only enhance our understanding of the effects of chronic inflammation on AILI in patients with liver disease, but are also helpful to identify novel therapeutic targets for the treatment of AILI.
JF - Journal of immunology (Baltimore, Md. : 1950)
AU - Feng, Dechun
AU - Wang, Yan
AU - Wang, Hua
AU - Weng, Honglei
AU - Kong, Xiaoni
AU - Martin-Murphy, Brittany V
AU - Li, Yongmei
AU - Park, Ogyi
AU - Dooley, Steven
AU - Ju, Cynthia
AU - Gao, Bin
AD - Laboratory of Liver Diseases, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD 20892; ; Medical Clinic, Faculty of Medicine at Mannheim, University of Heidelberg, Mannheim 68167, Germany; ; School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai 200030, China; Med-X Research Institute, Shanghai Jiao Tong University, Shanghai 200030, China; and. ; Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Aurora, CO 80045. ; Laboratory of Liver Diseases, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD 20892; bgao@mail.nih.gov.
Y1 - 2014/09/01/
PY - 2014
DA - 2014 Sep 01
SP - 2512
EP - 2518
VL - 193
IS - 5
KW - Analgesics, Non-Narcotic
KW - 0
KW - Hepatocyte Nuclear Factor 1-alpha
KW - Hnf1a protein, mouse
KW - Interleukins
KW - STAT3 Transcription Factor
KW - Stat3 protein, mouse
KW - interleukin-22
KW - Acetaminophen
KW - 362O9ITL9D
KW - Cytochrome P-450 CYP2E1
KW - EC 1.14.13.-
KW - Abridged Index Medicus
KW - Index Medicus
KW - Acute Disease
KW - Animals
KW - Chemical and Drug Induced Liver Injury -- pathology
KW - Hepatocyte Nuclear Factor 1-alpha -- genetics
KW - Humans
KW - Chemical and Drug Induced Liver Injury -- genetics
KW - Mice
KW - Gene Expression Regulation, Enzymologic -- immunology
KW - Chemical and Drug Induced Liver Injury -- drug therapy
KW - Cytochrome P-450 CYP2E1 -- genetics
KW - Mice, Knockout
KW - Cytochrome P-450 CYP2E1 -- immunology
KW - Gene Expression Regulation, Enzymologic -- drug effects
KW - STAT3 Transcription Factor -- immunology
KW - STAT3 Transcription Factor -- genetics
KW - Chronic Disease
KW - Hepatocyte Nuclear Factor 1-alpha -- immunology
KW - Analgesics, Non-Narcotic -- adverse effects
KW - Interleukins -- pharmacology
KW - Analgesics, Non-Narcotic -- pharmacology
KW - Acetaminophen -- adverse effects
KW - Interleukins -- immunology
KW - Interleukins -- genetics
KW - Acetaminophen -- pharmacology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.atitle=Acute+and+chronic+effects+of+IL-22+on+acetaminophen-induced+liver+injury.&rft.au=Feng%2C+Dechun%3BWang%2C+Yan%3BWang%2C+Hua%3BWeng%2C+Honglei%3BKong%2C+Xiaoni%3BMartin-Murphy%2C+Brittany+V%3BLi%2C+Yongmei%3BPark%2C+Ogyi%3BDooley%2C+Steven%3BJu%2C+Cynthia%3BGao%2C+Bin&rft.aulast=Feng&rft.aufirst=Dechun&rft.date=2014-09-01&rft.volume=193&rft.issue=5&rft.spage=2512&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.issn=1550-6606&rft_id=info:doi/10.4049%2Fjimmunol.1400588
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-12-09
N1 - Date created - 2014-08-16
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Hepatology. 2008 Jul;48(1):240-51 [18537186]
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Curr Drug Metab. 2009 Feb;10(2):164-78 [19275551]
J Immunol. 2009 Apr 15;182(8):4521-8 [19342625]
Exp Cell Res. 2009 Jul 1;315(11):1975-89 [19331832]
Semin Immunopathol. 2010 Mar;32(1):17-31 [20127093]
Biochem Pharmacol. 2010 Nov 15;80(10):1592-600 [20723539]
Hepatology. 2010 Oct;52(4):1291-300 [20842630]
Cytokine Growth Factor Rev. 2010 Oct;21(5):365-79 [20870448]
Hepatology. 2011 Jun;53(6):2042-52 [21433044]
Hepatology. 2011 Jul;54(1):252-61 [21465510]
J Cell Biol. 2011 Oct 17;195(2):263-76 [21987637]
Gastroenterology. 2011 Nov;141(5):1897-906 [21708106]
Sci Signal. 2012 Jan 17;5(207):ra5 [22253262]
J Exp Med. 2012 Feb 13;209(2):307-18 [22291093]
Transplantation. 2012 Mar 15;93(5):485-92 [22262131]
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Gastroenterology. 2012 Jul;143(1):188-98.e7 [22484119]
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Cytokine. 2011 Nov;56(2):174-9 [21843953]
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Toxicology. 1983;28(3):193-206 [6636205]
Toxicol Appl Pharmacol. 1984 Jan;72(1):40-5 [6710483]
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DNA Cell Biol. 1995 Apr;14(4):285-93 [7710685]
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J Pharmacol Exp Ther. 1998 Oct;287(1):352-8 [9765356]
Toxicol Appl Pharmacol. 1998 Sep;152(1):193-9 [9772215]
J Pharmacol Exp Ther. 1999 Mar;288(3):945-50 [10027830]
J Hepatol. 2005 Jan;42(1):110-6 [15629515]
J Clin Invest. 2005 Apr;115(4):860-9 [15761498]
Hepatology. 2005 Dec;42(6):1364-72 [16317692]
Annu Rev Pharmacol Toxicol. 2006;46:123-49 [16402901]
Toxicol Appl Pharmacol. 2006 Oct 1;216(1):1-10 [16712892]
J Immunol. 2007 Mar 15;178(6):3777-85 [17339476]
Hepatology. 2007 Feb;45(2):412-21 [17366662]
Am J Physiol Gastrointest Liver Physiol. 2007 Apr;292(4):G1019-28 [17204547]
Gut. 2007 Jul;56(7):982-90 [17185352]
Immunity. 2007 Oct;27(4):647-59 [17919941]
Cytokine. 2008 Mar;41(3):209-16 [18191408]
Hepatology. 2008 Oct;48(4):1336-41 [18821593]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.4049/jimmunol.1400588
ER -
TY - JOUR
T1 - Self-renewal and cell lineage differentiation strategies in human embryonic stem cells and induced pluripotent stem cells.
AN - 1552374219; 24881868
AB - Since the initial discoveries of human embryonic and induced pluripotent stem cells, many strategies have been developed to utilize the potential of these cells for translational research and disease modeling. The success of these aims and the development of future applications in this area will depend on the ability to generate high-quality and large numbers of differentiated cell types that genetically, epigenetically, and functionally mimic the cells found in the body.
In this review, we highlight the current strategies used to maintain stem cell pluripotency (a measure of stem cell quality), as well as provide an overview of the various differentiation strategies being used to generate cells from all three germ lineages. We also discuss the particular considerations that must be addressed when utilizing these cells for translational therapy, and provide an example of a cell type currently used in clinical trials. The major challenge in regenerative medicine and disease modeling will be in generating functional cells of sufficient quality that are physiologically and epigenetically similar to the diverse cells that they are modeled after. By meeting these criteria, these differentiated products can be successfully used in disease modeling, drug/toxicology screens, and cellular replacement therapy.
JF - Expert opinion on biological therapy
AU - Efthymiou, Anastasia G
AU - Chen, Guibin
AU - Rao, Mahendra
AU - Chen, Guokai
AU - Boehm, Manfred
AD - National Institutes of Health, Center for Regenerative Medicine , Bethesda, MD , USA.
Y1 - 2014/09//
PY - 2014
DA - September 2014
SP - 1333
EP - 1344
VL - 14
IS - 9
KW - Index Medicus
KW - hiPSC
KW - hESC
KW - stem cells
KW - differentiation
KW - self-renewal
KW - Animals
KW - Humans
KW - Cell Culture Techniques
KW - Stem Cells -- physiology
KW - Regenerative Medicine -- methods
KW - Cell- and Tissue-Based Therapy -- methods
KW - Cell Lineage -- physiology
KW - Embryonic Stem Cells -- cytology
KW - Cell Differentiation -- physiology
KW - Induced Pluripotent Stem Cells -- physiology
KW - Embryonic Stem Cells -- physiology
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-07-30
N1 - Date created - 2014-08-08
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1517/14712598.2014.922533
ER -
TY - JOUR
T1 - Prolonged low intensity EPOCH-rituximab has improved toxicity in Burkitt lymphoma compared with standard short, high intensity therapy.
AN - 1552373078; 24919059
AB - Burkitt lymphoma is an aggressive form of non-Hodgkin lymphoma that has a short doubling time, thus intense short-cycle chemotherapy has been thought to be essential. A recent NCI-sponsored clinical trial investigated DA-EPOCH-R given to 19 HIV-negative patients and a short course regimen (SC-EPOCH-RR) given to 11 HIV-positive patients in hopes of maintaining the efficacy of the regimen while decreasing the typical side effects from the intensive short-cycle chemotherapy. Low intensity EPOCH-R based therapy achieved excellent rates of efficacy despite a significant difference in the median cumulative dose between the DA-EPOCH-R and SC-EPOCH-RR cohorts. Furthermore, both cohorts experienced mainly grade 1 and grade 2 toxicities, with SC-EPOCH-RR cohort patients experiencing less adverse events than DA-EPOCH-R cohort patients. This recent clinical investigation suggests the most important therapeutic principle is not the intensity but rather the length of exposure time above an effective threshold concentration. Since short, intense bolus doses are the standard therapy for Burkitt lymphoma, these findings are clinically relevant and significant.
JF - Cancer biology & therapy
AU - Shahbazi, Shandiz
AU - Peer, Cody J
AU - Figg, William D
AD - Clinical Pharmacology Program; Medical Oncology Branch; National Cancer Institute; Bethesda, MD USA.
Y1 - 2014/09//
PY - 2014
DA - September 2014
SP - 1117
EP - 1119
VL - 15
IS - 9
KW - Index Medicus
KW - EPOCH regimen
KW - low-intensity therapy
KW - Burkitt lymphoma
KW - Humans
KW - Male
KW - Female
KW - Antineoplastic Combined Chemotherapy Protocols -- administration & dosage
KW - Burkitt Lymphoma -- drug therapy
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+biology+%26+therapy&rft.atitle=Prolonged+low+intensity+EPOCH-rituximab+has+improved+toxicity+in+Burkitt+lymphoma+compared+with+standard+short%2C+high+intensity+therapy.&rft.au=Shahbazi%2C+Shandiz%3BPeer%2C+Cody+J%3BFigg%2C+William+D&rft.aulast=Shahbazi&rft.aufirst=Shandiz&rft.date=2014-09-01&rft.volume=15&rft.issue=9&rft.spage=1117&rft.isbn=&rft.btitle=&rft.title=Cancer+biology+%26+therapy&rft.issn=1555-8576&rft_id=info:doi/10.4161%2Fcbt.29504
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-07-13
N1 - Date created - 2014-08-09
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Oncologist. 2006 Apr;11(4):375-83 [16614233]
Curr Opin Oncol. 2004 Sep;16(5):429-35 [15314510]
J Clin Oncol. 1996 Mar;14(3):925-34 [8622041]
N Engl J Med. 2013 Nov 14;369(20):1915-25 [24224624]
J Clin Oncol. 2008 Jun 1;26(16):2717-24 [18378569]
Cancer. 2013 May 1;119(9):1660-8 [23361927]
Comment On:
N Engl J Med. 2013 Nov 14;369(20):1915-25 [24224624]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.4161/cbt.29504
ER -
TY - JOUR
T1 - Hepatotoxicity in a 52-week randomized trial of short-term versus long-term treatment with buprenorphine/naloxone in HIV-negative injection opioid users in China and Thailand.
AN - 1552371581; 24999060
AB - Buprenorphine/naloxone (BUP/NX), an effective treatment for opioid dependence, has been implicated in hepatic toxicity. However, as persons taking BUP/NX have multiple hepatic risk factors, comparative data are needed to quantify the risk of hepatoxicity with BUP/NX.
We compared rates of alanine aminotransferase (ALT) elevation≥grade 3 (ALT≥5.1 times the upper limit of normal) and graded bilirubin elevations in HIV-negative opioid injectors randomized to long-term (52 weeks) or short-term (18 days) medication assisted treatment (LT-MAT and ST-MAT, respectively) with BUP/NX in a multisite trial conducted in China and Thailand. ALT and bilirubin were measured at baseline, 12, 26, 40 and 52 weeks, times temporally remote from BUP/NX exposure in the ST-MAT participants. Among1036 subjects with at least one laboratory follow-up measurement, 76 (7%) participants experienced ALT elevation≥grade 3. In an intent-to-treat analysis, the risk of ALT events was similar in participants randomized to LT-MAT compared with ST-MAT (adjusted hazard ratio 1.25, 95% confidence interval 0.79 to 1.98). This finding was supported by an as-treated analysis, in which actual exposure to BUP/NX was considered. Hepatitis C seroconversion during follow-up was strongly associated with ALT events. Bilirubin elevations≥grade 2 occurred in 2% of subjects, with no significant difference between arms.
Over 52-week follow-up, the risk of hepatotoxicity was similar in opioid injectors receiving brief and prolonged treatment with BUP/NX. These data suggest that most hepatotoxic events observed during treatment with BUP/NX are due to other factors. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.
JF - Drug and alcohol dependence
AU - Lucas, Gregory M
AU - Young, Alicia
AU - Donnell, Deborah
AU - Richardson, Paul
AU - Aramrattana, Apinun
AU - Shao, Yiming
AU - Ruan, Yuhua
AU - Liu, Wei
AU - Fu, Liping
AU - Ma, Jun
AU - Celentano, David D
AU - Metzger, David
AU - Jackson, J Brooks
AU - Burns, David
AU - HPTN 058 study group
AD - Johns Hopkins University School of Medicine, Department of Medicine, 1830 E. Monument St., Room 435A, Baltimore, MD 21287, United States. Electronic address: glucas@jhmi.edu. ; Fred Hutchinson Cancer Research Center, Vaccine and Infectious Disease Division, 1100 Fairview Ave N, Seattle, WA 98109, United States. ; Johns Hopkins School of Medicine, Department of Pathology, 600North Wolfe St., Baltimore, MD 21287, United States. ; Chiang Mai University, Faculty of Medicine, Department of Family Medicine, 110 Intavaroros Road, Chiang Mai, Thailand. ; State Key Laboratory for Infectious Disease Prevention and Control, National Center for AIDS/STD Control and Prevention, Chinese Center for Disease Control and Prevention, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Beijing, China. ; Guangxi Centers for Disease Control and Prevention, Guangxi Center for HIV/AIDS Prevention and Control, No. 18 Jinzhou Road, Nanning 530028, Guangxi, China. ; Xinjiang Autonomous Region Center for Disease Control and Prevention, Jianquanyi Street no. 380, Urumqi 830002, Xinjiang, China. ; Johns Hopkins Bloomberg School of Public Health, Department of Epidemiology, 615 North Wolfe Street, Suite W6041, Baltimore, MD 21205, United States. ; Department of Psychiatry, University of Pennsylvania, 3535 Market Street, Suite 4000, Philadelphia, PA, 19104, United States. ; National Institute of Allergy and Infectious Diseases, Division of AIDS, Prevention Sciences Branch, 6700 B Rockledge Drive, Room 5121, Bethesda, MD 20892, United States. ; HPTN 058 study group
Y1 - 2014/09/01/
PY - 2014
DA - 2014 Sep 01
SP - 139
EP - 145
VL - 142
KW - Analgesics, Opioid
KW - 0
KW - Narcotic Antagonists
KW - Naloxone
KW - 36B82AMQ7N
KW - Buprenorphine
KW - 40D3SCR4GZ
KW - Alanine Transaminase
KW - EC 2.6.1.2
KW - Bilirubin
KW - RFM9X3LJ49
KW - Index Medicus
KW - Injection drug use
KW - Hepatitis C virus
KW - HIV prevention
KW - Buprenorphine/naloxone
KW - Safety
KW - Alanine aminotransferase
KW - Opioid dependence
KW - Hepatotoxicity
KW - Alanine Transaminase -- blood
KW - Thailand
KW - Humans
KW - Adult
KW - Treatment Outcome
KW - Middle Aged
KW - Bilirubin -- blood
KW - Male
KW - Female
KW - China
KW - Chemical and Drug Induced Liver Injury -- blood
KW - Buprenorphine -- therapeutic use
KW - Chemical and Drug Induced Liver Injury -- diagnosis
KW - Opioid-Related Disorders -- drug therapy
KW - Narcotic Antagonists -- adverse effects
KW - Narcotic Antagonists -- therapeutic use
KW - Opiate Substitution Treatment -- adverse effects
KW - Naloxone -- therapeutic use
KW - Analgesics, Opioid -- therapeutic use
KW - Buprenorphine -- adverse effects
KW - Analgesics, Opioid -- adverse effects
KW - Opioid-Related Disorders -- blood
KW - Naloxone -- adverse effects
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Drug+and+alcohol+dependence&rft.atitle=Hepatotoxicity+in+a+52-week+randomized+trial+of+short-term+versus+long-term+treatment+with+buprenorphine%2Fnaloxone+in+HIV-negative+injection+opioid+users+in+China+and+Thailand.&rft.au=Lucas%2C+Gregory+M%3BYoung%2C+Alicia%3BDonnell%2C+Deborah%3BRichardson%2C+Paul%3BAramrattana%2C+Apinun%3BShao%2C+Yiming%3BRuan%2C+Yuhua%3BLiu%2C+Wei%3BFu%2C+Liping%3BMa%2C+Jun%3BCelentano%2C+David+D%3BMetzger%2C+David%3BJackson%2C+J+Brooks%3BBurns%2C+David%3BHPTN+058+study+group&rft.aulast=Lucas&rft.aufirst=Gregory&rft.date=2014-09-01&rft.volume=142&rft.issue=&rft.spage=139&rft.isbn=&rft.btitle=&rft.title=Drug+and+alcohol+dependence&rft.issn=1879-0046&rft_id=info:doi/10.1016%2Fj.drugalcdep.2014.06.013
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-04-23
N1 - Date created - 2014-08-08
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Biol Psychiatry. 2000 Jun 15;47(12):1072-9 [10862807]
Am J Addict. 2000 Summer;9(3):265-9 [11000922]
Drug Alcohol Depend. 2001 Jan 1;61(2):173-81 [11137282]
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J Hepatol. 2001 Feb;34(2):346-50 [11281569]
Eur J Gastroenterol Hepatol. 2004 Oct;16(10):1033-7 [15371928]
Drug Alcohol Depend. 2013 Feb 1;128(1-2):71-6 [22921476]
Dig Liver Dis. 2005 Sep;37(9):674-80 [15951255]
Cochrane Database Syst Rev. 2008;(2):CD002207 [18425880]
Ann Intern Med. 2008 May 6;148(9):662-70 [18458279]
Dig Liver Dis. 2009 Jul;41(7):e8-e10 [18294936]
J Acquir Immune Defic Syndr. 2011 Mar 1;56 Suppl 1:S62-7 [21317596]
Int J Drug Policy. 2012 Mar;23(2):162-5 [21852093]
Acta Clin Belg Suppl. 1999;1:29-31 [10216978]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.drugalcdep.2014.06.013
ER -
TY - JOUR
T1 - Influence of lipoic acid on testicular toxicity induced by bi-n-butyl phthalate in rats.
AN - 1551020834; 24912129
AB - Bi-n-butyl phthalate (BNBP) is an environmental pollutant. The aim of this study was to evaluate the protective effect of lipoic acid (LA) against testicular dysfunction associated with the intake of to BNBP- intoxicated rats. Adult male Wistar rats were divided into 4 groups of 6 animals each, and received medication orally for 14 days. Group I rats received 0.5 ml corn oil. Group II rats received LA (20 mg/kg B.W./day). Group III rats received BNBP (250 mg/kg B.W./day). Group IV rats received LA 24h prior to BNBP intake. Testes weight, cauda sperm count and sperm motility were decreased significantly by 18.15%, 13.83% and 13.5%, respectively, after BNBP treatment. Significant increase by 12.1%, 10.20% and 11.51%, respectively, was observed in LA-BNBP rats. Significant increase by 1.53%, 1.5% and 1.8%, for serum follicle stimulating hormone, testosterone and total antioxidant status, respectively, were observed in LA-BNBP rats. Testicular lipid peroxides and lactate dehydrogenase enzyme were significantly decreased by 1.5 and 1.6 folds, respectively, in LA-BNBP rats were decreased after BNBP treatment. Testicular superoxide dismutase, catalase and glutathione reductase enzymes were significantly increased in LA-BNBP rats. LA-BNBP rats, decreased the damage to seminiferous tubules produced by BNBP intake. In conclusion, LA mitigated BNBP-induced testicular toxicity through antioxidant mechanism and by direct free radical scavenging activity.
Copyright © 2014 Elsevier Ltd. All rights reserved.
JF - Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
AU - El-Beshbishy, Hesham A
AU - Mariah, Reham A
AU - Al-Azhary, Nevin M
AU - Aly, Hamdy A A
AU - Ozbak, Hani A
AU - Baghdadi, Hussam H
AD - Medical Laboratories Technology Department, Faculty of Applied Medical Sciences, Taibah University, Madinah, Saudi Arabia; Biochemistry Department, Al-Azhar University, Nasr City, Cairo 11751, Egypt. Electronic address: hesham_elbeshbishy@hotmail.com. ; Biochemistry and Molecular Medicine Department, College of Medicine, Taibah University, Saudi Arabia; Medical Biochemistry Department, Faculty of Medicine, Tanta University, Egypt. ; Biochemistry and Molecular Medicine Department, College of Medicine, Taibah University, Saudi Arabia; Clinical Pathology Department, National Cancer Institute, Cairo University, Egypt. ; Medical Biochemistry Department, Faculty of Medicine, Tanta University, Egypt; Pharmacology &Toxicology Department, King AbdulAziz University, Jeddah, Saudi Arabia. ; Medical Laboratories Technology Department, Faculty of Applied Medical Sciences, Taibah University, Madinah, Saudi Arabia. ; Biochemistry and Molecular Medicine Department, College of Medicine, Taibah University, Saudi Arabia.
Y1 - 2014/09//
PY - 2014
DA - September 2014
SP - 26
EP - 32
VL - 71
KW - Dibutyl Phthalate
KW - 2286E5R2KE
KW - Testosterone
KW - 3XMK78S47O
KW - Thioctic Acid
KW - 73Y7P0K73Y
KW - Follicle Stimulating Hormone
KW - 9002-68-0
KW - L-Lactate Dehydrogenase
KW - EC 1.1.1.27
KW - Catalase
KW - EC 1.11.1.6
KW - Superoxide Dismutase
KW - EC 1.15.1.1
KW - Glutathione Reductase
KW - EC 1.8.1.7
KW - Index Medicus
KW - Testes
KW - Oxidative stress
KW - Bi-n-butyl phthalate
KW - Antioxidant
KW - Lipoic acid
KW - Rats
KW - Catalase -- metabolism
KW - Animals
KW - Sperm Count
KW - Glutathione Reductase -- metabolism
KW - Testosterone -- blood
KW - Rats, Wistar
KW - Lipid Peroxidation -- drug effects
KW - Superoxide Dismutase -- metabolism
KW - Sperm Motility -- drug effects
KW - Male
KW - L-Lactate Dehydrogenase -- metabolism
KW - Follicle Stimulating Hormone -- blood
KW - Testis -- drug effects
KW - Thioctic Acid -- pharmacology
KW - Testis -- enzymology
KW - Dibutyl Phthalate -- toxicity
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-04-06
N1 - Date created - 2014-08-01
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.fct.2014.05.024
ER -
TY - JOUR
T1 - The effects of acute alcohol administration on the human brain: insights from neuroimaging.
AN - 1548630089; 23978384
AB - Over the last quarter century, researchers have peered into the living human brain to develop and refine mechanistic accounts of alcohol-induced behavior, as well as neurobiological mechanisms for development and maintenance of addiction. These in vivo neuroimaging studies generally show that acute alcohol administration affects brain structures implicated in motivation and behavior control, and that chronic intoxication is correlated with structural and functional abnormalities in these same structures, where some elements of these decrements normalize with extended sobriety. In this review, we will summarize recent findings about acute human brain responses to alcohol using neuroimaging techniques, and how they might explain behavioral effects of alcohol intoxication. We then briefly address how chronic alcohol intoxication (as inferred from cross-sectional differences between various drinking populations and controls) may yield individual brain differences between drinking subjects that may confound interpretation of acute alcohol administration effects. This article is part of the Special Issue Section entitled 'Neuroimaging in Neuropharmacology'.
Published by Elsevier Ltd.
JF - Neuropharmacology
AU - Bjork, James M
AU - Gilman, Jodi M
AD - Division of Clinical Neuroscience and Behavioral Research, National Institute on Drug Abuse, National Institutes of Health, 6001 Executive Blvd, Room 3163, Bethesda, MD 20892, USA. Electronic address: jbjork@mail.nih.gov. ; Laboratory of Neuroimaging and Genetics, MGH Division of Psychiatric Neuroscience, Martinos Center for Biomedical Imaging, Massachusetts General Hospital, USA.
Y1 - 2014/09//
PY - 2014
DA - September 2014
SP - 101
EP - 110
VL - 84
KW - Central Nervous System Depressants
KW - 0
KW - Ethanol
KW - 3K9958V90M
KW - Index Medicus
KW - Alcohol
KW - Neuroimaging
KW - Addiction
KW - Positron Emission Tomography
KW - fMRI
KW - Alcohol-Related Disorders -- physiopathology
KW - Alcohol-Related Disorders -- diagnostic imaging
KW - Cognition Disorders -- diagnostic imaging
KW - Humans
KW - Cerebrovascular Circulation -- physiology
KW - Cerebrovascular Circulation -- drug effects
KW - Cognition Disorders -- chemically induced
KW - Cognition Disorders -- physiopathology
KW - Radionuclide Imaging
KW - Brain -- drug effects
KW - Ethanol -- administration & dosage
KW - Brain -- physiology
KW - Brain -- diagnostic imaging
KW - Central Nervous System Depressants -- administration & dosage
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1548630089?accountid=14244
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-02-02
N1 - Date created - 2014-06-16
N1 - Date revised - 2017-01-13
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.neuropharm.2013.07.039
ER -
TY - JOUR
T1 - Phase II trial of pirfenidone in children and young adults with neurofibromatosis type 1 and progressive plexiform neurofibromas.
AN - 1547530917; 24753394
AB - Pirfenidone, an oral anti-inflammatory, antifibrotic agent with activity in idiopathic pulmonary fibrosis, may mediate anti-tumor activity in neurofibromatosis type 1 (NF1) and plexiform neurofibromas (PN) by inhibition of fibroblast proliferation and collagen synthesis. The primary objective of this open label, single arm phase II trial was to evaluate the activity of pirfenidone in children and young adults with inoperable PN.
Patients (3-21 years) with NF1-related progressive PN received pirfenidone at the previously determined optimal dose (500 mg/m(2) orally, q8h) on a continuous dosing schedule (one cycle = 28 days). Volumetric MRI analysis was used to assess response. Progression was defined as ≥ 20% PN volume increase compared to baseline. Pirfenidone would be considered active if it doubled the median time to progression (TTP) compared to the TTP on the placebo arm of a phase II trial with the farnesyltransferase inhibitor tipifarnib, which used near identical eligibility criteria. Toxicities, objective response rate, and quality of life (QOL) also were evaluated. Thirty-six patients were enrolled and tolerated pirfenidone well with intermittent nausea and vomiting as the most frequent toxicities. A dose reduction was required in only three patients. The median TTP for pirfenidone was 13.2 months compared to 10.6 months for the placebo control group from the tipifarnib trial (two-tailed P = 0.92; one-tailed P = 0.46). No objective responses were observed.
Pirfenidone was well tolerated, but did not demonstrate activity as defined in this trial and does not warrant further evaluation in children with NF1 and progressive PN. © 2014 Wiley Periodicals, Inc.
JF - Pediatric blood & cancer
AU - Widemann, Brigitte C
AU - Babovic-Vuksanovic, Dusica
AU - Dombi, Eva
AU - Wolters, Pamela L
AU - Goldman, Stewart
AU - Martin, Staci
AU - Goodwin, Anne
AU - Goodspeed, Wendy
AU - Kieran, Mark W
AU - Cohen, Bruce
AU - Blaney, Susan M
AU - King, Allison
AU - Solomon, Jeffrey
AU - Patronas, Nicholas
AU - Balis, Frank M
AU - Fox, Elizabeth
AU - Steinberg, Seth M
AU - Packer, Roger J
AD - Pediatric Oncology Branch, National Cancer Institute, Bethesda, Maryland.
Y1 - 2014/09//
PY - 2014
DA - September 2014
SP - 1598
EP - 1602
VL - 61
IS - 9
KW - Antineoplastic Agents
KW - 0
KW - Pyridones
KW - Tumor Necrosis Factor-alpha
KW - pirfenidone
KW - D7NLD2JX7U
KW - Index Medicus
KW - phase II trial
KW - neurofibromatosis type 1
KW - volumetric MRI analysis
KW - time to progression
KW - progression free survival
KW - plexiform neurofibroma
KW - Young Adult
KW - Neoplasm Staging
KW - Humans
KW - Disease Progression
KW - Prognosis
KW - Quality of Life
KW - Child
KW - Child, Preschool
KW - Survival Rate
KW - Adult
KW - Follow-Up Studies
KW - Adolescent
KW - Time Factors
KW - Female
KW - Male
KW - Neurofibromatosis 1 -- drug therapy
KW - Neurofibroma, Plexiform -- drug therapy
KW - Neurofibroma, Plexiform -- pathology
KW - Tumor Necrosis Factor-alpha -- antagonists & inhibitors
KW - Neurofibroma, Plexiform -- mortality
KW - Neurofibromatosis 1 -- mortality
KW - Antineoplastic Agents -- therapeutic use
KW - Neurofibromatosis 1 -- pathology
KW - Pyridones -- therapeutic use
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-11-18
N1 - Date created - 2014-07-21
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1002/pbc.25041
ER -
TY - JOUR
T1 - Prefrontal single-unit firing associated with deficient extinction in mice.
AN - 1534792411; 24231425
AB - The neural circuitry mediating fear extinction has been increasingly well studied and delineated. The rodent infralimbic subregion (IL) of the ventromedial prefrontal cortex (vmPFC) has been found to promote extinction, whereas the prelimbic cortex (PL) demonstrates an opposing, pro-fear, function. Studies employing in vivo electrophysiological recordings have observed that while increased IL single-unit firing and bursting predicts robust extinction retrieval, increased PL firing can correlate with sustained fear and poor extinction. These relationships between single-unit firing and extinction do not hold under all experimental conditions, however. In the current study, we further investigated the relationship between vmPFC and PL single-unit firing and extinction using inbred mouse models of intact (C57BL/6J, B6) and deficient (129S1/SvImJ, S1) extinction strains. Simultaneous single-unit recordings were made in the PL and vmPFC (encompassing IL) as B6 and S1 mice performed extinction training and retrieval. Impaired extinction retrieval in S1 mice was associated with elevated PL single-unit firing, as compared to firing in extinguishing B6 mice, consistent with the hypothesized pro-fear contribution of PL. Analysis of local field potentials also revealed significantly higher gamma power in the PL of S1 than B6 mice during extinction training and retrieval. In the vmPFC, impaired extinction in S1 mice was also associated with exaggerated single-unit firing, relative to B6 mice. This is in apparent contradiction to evidence that IL activity promotes extinction, but could reflect a (failed) compensatory effort by the vmPFC to mitigate fear-promoting activity in other regions, such as the PL or amygdala. In support of this hypothesis, augmenting IL activity via direct infusion of the GABAA receptor antagonist picrotoxin rescued impaired extinction retrieval in S1 mice. Chronic fluoxetine treatment produced modest reductions in fear during extinction retrieval and increased the number of Zif268-labeled cells in layer II of IL, but failed to increase vmPFC single-unit firing. Collectively, these findings further support the important contribution these cortical regions play in determining the balance between robust extinction on the one hand, and sustained fear on the other. Elucidating the precise nature of these roles could help inform understanding of the pathophysiology of fear-related anxiety disorders.
Published by Elsevier Inc.
JF - Neurobiology of learning and memory
AU - Fitzgerald, Paul J
AU - Whittle, Nigel
AU - Flynn, Shaun M
AU - Graybeal, Carolyn
AU - Pinard, Courtney R
AU - Gunduz-Cinar, Ozge
AU - Kravitz, Alexxai V
AU - Singewald, Nicolas
AU - Holmes, Andrew
AD - Laboratory of Behavioral and Genomic Neuroscience, National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, MD, USA. Electronic address: pfitz@mbi.mb.jhu.edu. ; Department of Pharmacology & Toxicology, Institute of Pharmacy and CMBI, University of Innsbruck, Innsbruck, Austria. ; Laboratory of Behavioral and Genomic Neuroscience, National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, MD, USA. ; National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD, USA.
Y1 - 2014/09//
PY - 2014
DA - September 2014
SP - 69
EP - 81
VL - 113
KW - Early Growth Response Protein 1
KW - 0
KW - Egr1 protein, mouse
KW - GABA Antagonists
KW - Serotonin Uptake Inhibitors
KW - Fluoxetine
KW - 01K63SUP8D
KW - Picrotoxin
KW - 124-87-8
KW - Index Medicus
KW - Prelimbic cortex
KW - C57BL/6J
KW - Retrieval
KW - Infralimbic cortex
KW - 129S1/SvImJ
KW - Fear extinction
KW - Patch-Clamp Techniques -- methods
KW - Mice, 129 Strain
KW - Animals
KW - Early Growth Response Protein 1 -- metabolism
KW - Mice, Inbred C57BL
KW - Mice
KW - Male
KW - Serotonin Uptake Inhibitors -- administration & dosage
KW - Fluoxetine -- pharmacology
KW - Prefrontal Cortex -- physiopathology
KW - Prefrontal Cortex -- physiology
KW - Fear -- drug effects
KW - GABA Antagonists -- administration & dosage
KW - Extinction, Psychological -- physiology
KW - GABA Antagonists -- pharmacology
KW - Prefrontal Cortex -- drug effects
KW - Fluoxetine -- administration & dosage
KW - Picrotoxin -- pharmacology
KW - Picrotoxin -- administration & dosage
KW - Extinction, Psychological -- drug effects
KW - Fear -- physiology
KW - Serotonin Uptake Inhibitors -- pharmacology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurobiology+of+learning+and+memory&rft.atitle=Prefrontal+single-unit+firing+associated+with+deficient+extinction+in+mice.&rft.au=Fitzgerald%2C+Paul+J%3BWhittle%2C+Nigel%3BFlynn%2C+Shaun+M%3BGraybeal%2C+Carolyn%3BPinard%2C+Courtney+R%3BGunduz-Cinar%2C+Ozge%3BKravitz%2C+Alexxai+V%3BSingewald%2C+Nicolas%3BHolmes%2C+Andrew&rft.aulast=Fitzgerald&rft.aufirst=Paul&rft.date=2014-09-01&rft.volume=113&rft.issue=&rft.spage=69&rft.isbn=&rft.btitle=&rft.title=Neurobiology+of+learning+and+memory&rft.issn=1095-9564&rft_id=info:doi/10.1016%2Fj.nlm.2013.11.002
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-02-09
N1 - Date created - 2014-06-10
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.nlm.2013.11.002
ER -
TY - JOUR
T1 - Multiwalled carbon nanotubes induce altered morphology and loss of barrier function in human bronchial epithelium at noncytotoxic doses
AN - 1566848829; 20693554
AB - Multiwalled carbon nanotubes (MWCNTs) have seen increasing application in consumer products over the past decade, resulting in an increasing risk of human exposure. While numerous toxicological studies have been performed using acute high doses of various carbonaceous nanomaterials, the effects of longer-term, low doses of MWCNTs remain relatively unexplored. This study examined bronchoscopy-derived healthy human bronchial epithelial cells exposed in submerged culture to noncytotoxic doses of MWCNTs over 7 days. Under these conditions, doses as low as 3 mu g/mL caused altered cell morphology, superficially resembling fibroblasts. Electrical impedance of the epithelial monolayer was greatly reduced following MWCNT exposure. However, Western blot and polymerase chain reaction showed no elevated expression of the fibroblast markers, vimentin, alpha -smooth muscle actin, or fibronectin, indicating that a mechanism other than epithelial-mesenchymal transition may be responsible for the changes. Phalloidin and tubulin immunostaining showed disruption of the cytoskeleton, and confocal imaging showed a reduction of the tight junction proteins, zona occludens 1 and occludin. We propose that MWCNTs interfere with the cytoskeleton of the lung epithelium, which can result in a harmful reduction in barrier function over time, even at noncytotoxic doses.
JF - International Journal of Nanomedicine
AU - Snyder, Ryan J
AU - Hussain, Salik
AU - Rice, Annette B
AU - Garantziotis, Stavros
AD - Clinical Research Unit, National Institute of Environmental Health Sciences/National Institutes of Health, Research Triangle Park, NC, USA
Y1 - 2014/08/25/
PY - 2014
DA - 2014 Aug 25
SP - 4093
EP - 4105
PB - Dove Medical Press Ltd, Beechfield House Macclesfield SK11 0JL United Kingdom
VL - 9
SN - 1176-9114, 1176-9114
KW - Biotechnology and Bioengineering Abstracts
KW - multiwalled carbon nanotubes
KW - bronchial epithelium
KW - transepithelial electrical resistance
KW - cytoskeleton
KW - morphology
KW - human
KW - Western blotting
KW - Epithelial cells
KW - Tight junctions
KW - Fibronectin
KW - Muscles
KW - Cell culture
KW - Electrical impedance
KW - Vimentin
KW - Fibroblasts
KW - Cytoskeleton
KW - Carbon
KW - Lung
KW - nanotubes
KW - Polymerase chain reaction
KW - Actin
KW - Epithelium
KW - Tubulin
KW - Toxicity testing
KW - nanotechnology
KW - W 30910:Imaging
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Nanomedicine&rft.atitle=Multiwalled+carbon+nanotubes+induce+altered+morphology+and+loss+of+barrier+function+in+human+bronchial+epithelium+at+noncytotoxic+doses&rft.au=Snyder%2C+Ryan+J%3BHussain%2C+Salik%3BRice%2C+Annette+B%3BGarantziotis%2C+Stavros&rft.aulast=Snyder&rft.aufirst=Ryan&rft.date=2014-08-25&rft.volume=9&rft.issue=&rft.spage=4093&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Nanomedicine&rft.issn=11769114&rft_id=info:doi/10.2147%2FIJN.S65567
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-09-01
N1 - Last updated - 2014-10-02
N1 - SubjectsTermNotLitGenreText - Epithelial cells; Western blotting; Tight junctions; Fibronectin; Muscles; Cell culture; Electrical impedance; Vimentin; Fibroblasts; Cytoskeleton; Carbon; Lung; Polymerase chain reaction; nanotubes; Epithelium; Actin; Tubulin; Toxicity testing; nanotechnology
DO - http://dx.doi.org/10.2147/IJN.S65567
ER -
TY - JOUR
T1 - Autophagic degradation of the inhibitory p53 isoform Δ133p53α as a regulatory mechanism for p53-mediated senescence.
AN - 1555620142; 25144556
AB - Δ133p53α, a p53 isoform that can inhibit full-length p53, is downregulated at replicative senescence in a manner independent of mRNA regulation and proteasome-mediated degradation. Here we demonstrate that, unlike full-length p53, Δ133p53α is degraded by autophagy during replicative senescence. Pharmacological inhibition of autophagy restores Δ133p53α expression levels in replicatively senescent fibroblasts, without affecting full-length p53. The siRNA-mediated knockdown of pro-autophagic proteins (ATG5, ATG7 and Beclin-1) also restores Δ133p53α expression. The chaperone-associated E3 ubiquitin ligase STUB1, which is known to regulate autophagy, interacts with Δ133p53α and is downregulated at replicative senescence. The siRNA knockdown of STUB1 in proliferating, early-passage fibroblasts induces the autophagic degradation of Δ133p53α and thereby induces senescence. Upon replicative senescence or STUB1 knockdown, Δ133p53α is recruited to autophagosomes, consistent with its autophagic degradation. This study reveals that STUB1 is an endogenous regulator of Δ133p53α degradation and senescence, and identifies a p53 isoform-specific protein turnover mechanism that orchestrates p53-mediated senescence.
JF - Nature communications
AU - Horikawa, Izumi
AU - Fujita, Kaori
AU - Jenkins, Lisa M Miller
AU - Hiyoshi, Yukiharu
AU - Mondal, Abdul M
AU - Vojtesek, Borivoj
AU - Lane, David P
AU - Appella, Ettore
AU - Harris, Curtis C
AD - 1] Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Bethesda, Maryland 20892-4258, USA [2]. ; 1] Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Bethesda, Maryland 20892-4258, USA [2] [3]. ; Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Bethesda, Maryland 20892-4258, USA. ; Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Bethesda, Maryland 20892-4258, USA. ; Regional Centre for Applied and Molecular Oncology, Masaryk Memorial Cancer Institute, Zluty Kopec 7, Brno 65653, Czech Republic. ; Institute of Molecular and Cell Biology, 61 Biopolis Drive, Proteos, Singapore 138673, Singapore.
Y1 - 2014/08/21/
PY - 2014
DA - 2014 Aug 21
SP - 4706
VL - 5
KW - Adaptor Proteins, Signal Transducing
KW - 0
KW - Androstadienes
KW - Apoptosis Regulatory Proteins
KW - BECN1 protein, human
KW - Beclin-1
KW - MAP1LC3B protein, human
KW - Membrane Proteins
KW - Microtubule-Associated Proteins
KW - Protein Isoforms
KW - RNA, Small Interfering
KW - SQSTM1 protein, human
KW - Sequestosome-1 Protein
KW - TP53 protein, human
KW - Tumor Suppressor Protein p53
KW - Cycloheximide
KW - 98600C0908
KW - STUB1 protein, human
KW - EC 2.3.2.27
KW - Ubiquitin-Protein Ligases
KW - wortmannin
KW - XVA4O219QW
KW - Index Medicus
KW - Fibroblasts -- drug effects
KW - Microtubule-Associated Proteins -- metabolism
KW - Apoptosis Regulatory Proteins -- genetics
KW - Protein Isoforms -- metabolism
KW - Membrane Proteins -- metabolism
KW - Humans
KW - Androstadienes -- pharmacology
KW - Membrane Proteins -- genetics
KW - Fibroblasts -- metabolism
KW - Adaptor Proteins, Signal Transducing -- metabolism
KW - Microtubule-Associated Proteins -- genetics
KW - Gene Knockdown Techniques
KW - Cells, Cultured
KW - Cycloheximide -- pharmacology
KW - Ubiquitin-Protein Ligases -- genetics
KW - Apoptosis Regulatory Proteins -- metabolism
KW - Adaptor Proteins, Signal Transducing -- genetics
KW - Ubiquitin-Protein Ligases -- metabolism
KW - Autophagy -- drug effects
KW - Cell Aging -- physiology
KW - Tumor Suppressor Protein p53 -- genetics
KW - Tumor Suppressor Protein p53 -- metabolism
KW - Autophagy -- physiology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+communications&rft.atitle=Autophagic+degradation+of+the+inhibitory+p53+isoform+%CE%94133p53%CE%B1+as+a+regulatory+mechanism+for+p53-mediated+senescence.&rft.au=Horikawa%2C+Izumi%3BFujita%2C+Kaori%3BJenkins%2C+Lisa+M+Miller%3BHiyoshi%2C+Yukiharu%3BMondal%2C+Abdul+M%3BVojtesek%2C+Borivoj%3BLane%2C+David+P%3BAppella%2C+Ettore%3BHarris%2C+Curtis+C&rft.aulast=Horikawa&rft.aufirst=Izumi&rft.date=2014-08-21&rft.volume=5&rft.issue=&rft.spage=4706&rft.isbn=&rft.btitle=&rft.title=Nature+communications&rft.issn=2041-1723&rft_id=info:doi/10.1038%2Fncomms5706
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2016-02-02
N1 - Date created - 2014-08-22
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1038/ncomms5706
ER -
TY - JOUR
T1 - Genistein Disrupts Glucocorticoid Receptor Signaling in Human Uterine Endometrial Ishikawa Cells
AN - 1654686363; PQ0001052570
AB - Background: The link between environmental estrogen exposure and defects in the female reproductive tract is well established. The phytoestrogen genistein is able to modulate uterine estrogen receptor (ER) activity, and dietary exposure is associated with uterine pathologies. Regulation of stress and immune functions by the glucocorticoid receptor (GR) is also an integral part of maintaining reproductive tract function; disruption of GR signaling by genistein may also have a role in the adverse effects of genistein. Objective: We evaluated the transcriptional response to genistein in Ishikawa cells and investigated the effects of genistein on GR-mediated target genes. Methods: We used Ishikawa cells as a model system to identify novel targets of genistein and the synthetic glucocorticoid dexamethasone through whole genome microarray analysis. Common gene targets were defined and response patterns verified by quantitative real-time reverse-transcription polymerase chain reaction. The mechanism of transcriptional antagonism was determined for select genes. Results: Genistein regulated numerous genes in Ishikawa cells independently of estradiol, and the response to coadministration of genistein and dexamethasone was unique compared with the response to either estradiol or dexamethasone alone. Furthermore, genistein altered glucocorticoid regulation of GR target genes. In a select set of genes, co-regulation by dexamethasone and genistein was found to require both GR and ER alpha signaling, respectively. Conclusions: Using Ishikawa cells, we observed that exposure to genistein resulted in distinct changes in gene expression and unique differences in the GR transcriptome. Citation: Whirledge S, Senbanjo LT, Cidlowski JA. 2015. Genistein disrupts glucocorticoid receptor signaling in human uterine endometrial Ishikawa cells. Environ Health Perspect 123:80-87; http://dx.doi.org/10.1289/ehp.1408437
JF - Environmental Health Perspectives
AU - Whirledge, Shannon
AU - Senbanjo, Linda T
AU - Cidlowski, John A
AD - Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA
Y1 - 2014/08/19/
PY - 2014
DA - 2014 Aug 19
SP - 80
EP - 87
PB - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States
VL - 123
IS - 1
SN - 0091-6765, 0091-6765
KW - Environment Abstracts; Health & Safety Science Abstracts
KW - Diets
KW - Estrogens
KW - Pathology
KW - Stress
KW - Immune response
KW - Antagonism
KW - Side effects
KW - H 6000:Natural Disasters/Civil Defense/Emergency Management
KW - ENA 02:Toxicology & Environmental Safety
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Health+Perspectives&rft.atitle=Genistein+Disrupts+Glucocorticoid+Receptor+Signaling+in+Human+Uterine+Endometrial+Ishikawa+Cells&rft.au=Whirledge%2C+Shannon%3BSenbanjo%2C+Linda+T%3BCidlowski%2C+John+A&rft.aulast=Whirledge&rft.aufirst=Shannon&rft.date=2014-08-19&rft.volume=123&rft.issue=1&rft.spage=80&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1408437
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-02-01
N1 - Last updated - 2015-05-13
N1 - SubjectsTermNotLitGenreText - Diets; Estrogens; Pathology; Stress; Antagonism; Immune response; Side effects
DO - http://dx.doi.org/10.1289/ehp.1408437
ER -
TY - JOUR
T1 - Toward a Drug Development Path That Targets Metastatic Progression in Osteosarcoma
AN - 1808673722; PQ0003441841
AB - Despite successful primary tumor treatment, the development of pulmonary metastasis continues to be the most common cause of mortality in patients with osteosarcoma. A conventional drug development path requiring drugs to induce regression of established lesions has not led to improvements for patients with osteosarcoma in more than 30 years. On the basis of our growing understanding of metastasis biology, it is now reasonable and essential that we focus on developing therapeutics that target metastatic progression. To advance this agenda, a meeting of key opinion leaders and experts in the metastasis and osteosarcoma communities was convened in Bethesda, Maryland. The goal of this meeting was to provide a "Perspective" that would establish a preclinical translational path that could support the early evaluation of potential therapeutic agents that uniquely target the metastatic phenotype. Although focused on osteosarcoma, the need for this perspective is shared among many cancer types. The consensus achieved from the meeting included the following: the biology of metastatic progression is associated with metastasis-specific targets/processes that may not influence grossly detectable lesions; targeting of metastasis-specific processes is feasible; rigorous preclinical data are needed to support translation of metastasis-specific agents into human trials where regression of measurable disease is not an expected outcome; preclinical data should include an understanding of mechanism of action, validation of pharmacodynamic markers of effective exposure and response, the use of several murine models of effectiveness, and where feasible the inclusion of the dog with naturally occurring osteosarcoma to define the activity of new drugs in the micrometastatic disease setting. Clin Cancer Res; 20(16); 4200-9. copyright 2014 AACR.
JF - Clinical Cancer Research
AU - Khanna, Chand
AU - Fan, Timothy M
AU - Gorlick, Richard
AU - Helman, Lee J
AU - Kleinerman, Eugenie S
AU - Adamson, Peter C
AU - Houghton, Peter J
AU - Tap, William D
AU - Welch, Danny R
AU - Steeg, Patricia S
AU - Merlino, Glenn
AU - Sorensen, Poul HB
AU - Meltzer, Paul
AU - Kirsch, David G
AU - Janeway, Katherine A
AU - Weigel, Brenda
AU - Randall, Lor
AU - Withrow, Stephen J
AU - Paoloni, Melissa
AU - Kaplan, Rosandra
AU - Teicher, Beverly A
AU - Seibel, Nita L
AU - Smith, Malcolm
AU - Ueren, Aykut
AU - Patel, Shreyaskumar R
AU - Trent, Jeffrey
AU - Savage, Sharon A
AU - Mirabello, Lisa
AU - Reinke, Denise
AU - Barkaukas, Donald A
AU - Krailo, Mark
AU - Bernstein, Mark
AD - National Cancer Institute, NIH, Bethesda, Maryland; , t-fan@illinois.edu
Y1 - 2014/08/15/
PY - 2014
DA - 2014 Aug 15
SP - 4200
EP - 4209
PB - American Association for Cancer Research, 615 Chestnut St., 17th Floor Philadelphia PA 19106-4404 United States
VL - 20
IS - 16
SN - 1078-0432, 1078-0432
KW - Biotechnology and Bioengineering Abstracts
KW - Translation
KW - Mortality
KW - Data processing
KW - Animal models
KW - Osteosarcoma
KW - Drug development
KW - Tumors
KW - Clinical trials
KW - Cancer
KW - Metastases
KW - Lung
KW - Pharmacodynamics
KW - W 30965:Miscellaneous, Reviews
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2016-07-01
N1 - Last updated - 2016-08-17
N1 - SubjectsTermNotLitGenreText - Metastases; Mortality; Translation; Data processing; Lung; Animal models; Osteosarcoma; Drug development; Tumors; Clinical trials; Pharmacodynamics; Cancer
DO - http://dx.doi.org/10.1158/1078-0432.CCR-13-2574
ER -
TY - JOUR
T1 - Aerosol Vaccination with AERAS-402 Elicits Robust Cellular Immune Responses in the Lungs of Rhesus Macaques but Fails To Protect against High-Dose Mycobacterium tuberculosis Challenge
AN - 1808631190; PQ0003441117
AB - Development of a vaccine against pulmonary tuberculosis may require immunization strategies that induce a high frequency of Ag-specific CD4 and CD8 T cells in the lung. The nonhuman primate model is essential for testing such approaches because it has predictive value for how vaccines elicit responses in humans. In this study, we used an aerosol vaccination strategy to administer AERAS-402, a replication-defective recombinant adenovirus (rAd) type 35 expressing Mycobacterium tuberculosis Ags Ag85A, Ag85B, and TB10.4, in bacillus Calmette-Guerin (BCG)-primed or unprimed rhesus macaques. Immunization with BCG generated low purified protein derivative-specific CD4 T cell responses in blood and bronchoalveolar lavage. In contrast, aerosolized AERAS-402 alone or following BCG induced potent and stable Ag85A/b-specific CD4 and CD8 effector T cells in bronchoalveolar lavage that largely produced IFN- gamma , as well as TNF and IL-2. Such responses induced by BCG, AERAS-402, or both failed to confer overall protection following challenge with 275 CFUs M. tuberculosis Erdman, although vaccine-induced responses associated with reduced pathology were observed in some animals. Anamnestic T cell responses to Ag85A/b were not detected in blood of immunized animals after challenge. Overall, our data suggest that a high M. tuberculosis challenge dose may be a critical factor in limiting vaccine efficacy in this model. However, the ability of aerosol rAd immunization to generate potent cellular immunity in the lung suggests that using different or more immunogens, alternative rAd serotypes with enhanced immunogenicity, and a physiological challenge dose may achieve protection against M. tuberculosis.
JF - Journal of Immunology
AU - Darrah, Patricia A
AU - Bolton, Diane L
AU - Lackner, Andrew A
AU - Kaushal, Deepak
AU - Aye, Pyone Pyone
AU - Mehra, Smriti
AU - Blanchard, James L
AU - Didier, Peter J
AU - Roy, Chad J
AU - Rao, Srinivas S
AU - Hokey, David A
AU - Scanga, Charles A
AU - Sizemore, Donata R
AU - Sadoff, Jerald C
AU - Roederer, Mario
AU - Seder, Robert A
AD - Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892
Y1 - 2014/08/15/
PY - 2014
DA - 2014 Aug 15
SP - 1799
EP - 1811
PB - American Association of Immunologists, 9650 Rockville Pike Bethesda MD 20814-3998 United States
VL - 193
IS - 4
SN - 0022-1767, 0022-1767
KW - Microbiology Abstracts B: Bacteriology; Immunology Abstracts
KW - gamma -Interferon
KW - Serotypes
KW - Interleukin 2
KW - Tumor necrosis factor
KW - CD4 antigen
KW - Bronchus
KW - Lymphocytes T
KW - Macaca mulatta
KW - Tuberculosis
KW - Aerosols
KW - Data processing
KW - Adenovirus
KW - CD8 antigen
KW - Alveoli
KW - Effector cells
KW - Blood
KW - Immunity (cell-mediated)
KW - BCG
KW - Lung
KW - Immunogenicity
KW - Colony-forming cells
KW - Vaccines
KW - Immune response
KW - Mycobacterium tuberculosis
KW - F 06905:Vaccines
KW - J 02350:Immunology
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2016-07-01
N1 - Last updated - 2016-10-12
N1 - SubjectsTermNotLitGenreText - gamma -Interferon; Aerosols; Data processing; Serotypes; Interleukin 2; Tumor necrosis factor; CD8 antigen; Alveoli; Effector cells; Blood; CD4 antigen; Bronchus; Immunity (cell-mediated); Immunogenicity; Lung; BCG; Colony-forming cells; Lymphocytes T; Tuberculosis; Immune response; Vaccines; Adenovirus; Macaca mulatta; Mycobacterium tuberculosis
DO - http://dx.doi.org/10.4049/jimmunol.1400676
ER -
TY - JOUR
T1 - Perfluorochemicals and Human Semen Quality: The LIFE Study
AN - 1654688775; PQ0001052566
AB - Background: The relation between persistent environmental chemicals and semen quality is evolving, although limited data exist for men recruited from general populations. Objectives: We examined the relation between perfluorinated chemicals (PFCs) and semen quality among 501 male partners of couples planning pregnancy. Methods: Using population-based sampling strategies, we recruited 501 couples discontinuing contraception from two U.S. geographic regions from 2005 through 2009. Baseline interviews and anthropometric assessments were conducted, followed by blood collection for the quantification of seven serum PFCs (perfluorosulfonates, perfluorocarboxylates, and perfluorosulfonamides) using tandem mass spectrometry. Men collected a baseline semen sample and another approximately 1 month later. Semen samples were shipped with freezer packs, and analyses were performed on the day after collection. We used linear regression to estimate the difference in each semen parameter associated with a one unit increase in the natural log-transformed PFC concentration after adjusting for confounders and modeling repeated semen samples. Sensitivity analyses included optimal Box-Cox transformation of semen quality end points. Results: Six PFCs [2-(N-methyl-perfluorooctane sulfonamido) acetate (Me-PFOSA-AcOH), perfluorodecanoate (PFDeA), perfluorononanoate (PFNA), perfluorooctane sulfonamide (PFOSA), perfluorooctane sulfonate (PFOS), and perfluorooctanoic acid (PFOA)] were associated with 17 semen quality end points before Box-Cox transformation. PFOSA was associated with smaller sperm head area and perimeter, a lower percentage of DNA stainability, and a higher percentage of bicephalic and immature sperm. PFDeA, PFNA, PFOA, and PFOS were associated with a lower percentage of sperm with coiled tails. Conclusions: Select PFCs were associated with certain semen end points, with the most significant associations observed for PFOSA but with results in varying directions. Citation: Buck Louis GM, Chen Z, Schisterman EF, Kim S, Sweeney AM, Sundaram R, Lynch CD, Gore-Langton RE, Barr DB. 2015. Perfluorochemicals and human semen quality: the LIFE Study. Environ Health Perspect 123:57-63; http://dx.doi.org/10.1289/ehp.1307621
JF - Environmental Health Perspectives
AU - Louis, Germaine MBuck
AU - Chen, Zhen
AU - Schisterman, Enrique F
AU - Kim, Sungduk
AU - Sweeney, Anne M
AU - Sundaram, Rajeshwari
AU - Lynch, Courtney D
AU - Gore-Langton, Robert E
AU - Barr, Dana Boyd
AD - Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Department of Health and Human Services, Rockville, Maryland, USA
Y1 - 2014/08/15/
PY - 2014
DA - 2014 Aug 15
SP - 57
EP - 63
PB - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States
VL - 123
IS - 1
SN - 0091-6765, 0091-6765
KW - Environment Abstracts; Health & Safety Science Abstracts
KW - Chemicals
KW - Sensitivity analysis
KW - Sulfonates
KW - DNA
KW - Mass spectrometry
KW - Cadmium
KW - Pregnancy
KW - ENA 13:Population Planning & Control
KW - H 4000:Food and Drugs
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-02-01
N1 - Last updated - 2015-05-13
N1 - SubjectsTermNotLitGenreText - Chemicals; Sensitivity analysis; Sulfonates; DNA; Mass spectrometry; Cadmium; Pregnancy
DO - http://dx.doi.org/10.1289/ehp.1307621
ER -
TY - JOUR
T1 - Mitochondria, Energetics, Epigenetics, and Cellular Responses to Stress
AN - 1642628401; 21201989
AB - Background: Cells respond to environmental stressors through several key pathways, including response to reactive oxygen species (ROS), nutrient and ATP sensing, DNA damage response (DDR), and epigenetic alterations. Mitochondria play a central role in these pathways not only through energetics and ATP production but also through metabolites generated in the tricarboxylic acid cycle, as well as mitochondria-nuclear signaling related to mitochondria morphology, biogenesis, fission/fusion, mitophagy, apoptosis, and epigenetic regulation. Objectives: We investigated the concept of bidirectional interactions between mitochondria and cellular pathways in response to environmental stress with a focus on epigenetic regulation, and we examined DNA repair and DDR pathways as examples of biological processes that respond to exogenous insults through changes in homeostasis and altered mitochondrial function. Methods: The National Institute of Environmental Health Sciences sponsored the Workshop on Mitochondria, Energetics, Epigenetics, Environment, and DNA Damage Response on 25-26 March 2013. Here, we summarize key points and ideas emerging from this meeting. Discussion: A more comprehensive understanding of signaling mechanisms (cross-talk) between the mitochondria and nucleus is central to elucidating the integration of mitochondrial functions with other cellular response pathways in modulating the effects of environmental agents. Recent studies have highlighted the importance of mitochondrial functions in epigenetic regulation and DDR with environmental stress. Development and application of novel technologies, enhanced experimental models, and a systems-type research approach will help to discern how environmentally induced mitochondrial dysfunction affects key mechanistic pathways. Conclusions: Understanding mitochondria-cell signaling will provide insight into individual responses to environmental hazards, improving prediction of hazard and susceptibility to environmental stressors. Citation: Shaughnessy DT, McAllister K, Worth L, Haugen AC, Meyer JN, Domann FE, Van Houten B, Mostoslavsky R, Bultman SJ, Baccarelli AA, Begley TJ, Sobol RW, Hirschey MD, Ideker T, Santos JH, Copeland WC, Tice RR, Balshaw DM, Tyson FL. 2014. Mitochondria, energetics, epigenetics, and cellular responses to stress. Environ Health Perspect 122:1271-1278; http://dx.doi.org/10.1289/ehp.1408418
JF - Environmental Health Perspectives
AU - Shaughnessy, Daniel T
AU - McAllister, Kimberly
AU - Worth, Leroy
AU - Haugen, Astrid C
AU - Meyer, Joel N
AU - Domann, Frederick E
AU - Van Houten, Bennett
AU - Mostoslavsky, Raul
AU - Bultman, Scott J
AU - Baccarelli, Andrea A
AU - Begley, Thomas J
AU - Sobol, Robert W
AU - Hirschey, Matthew D
AU - Ideker, Trey
AU - Santos, Janine H
AU - Copeland, William C
AU - Tice, Raymond R
AU - Balshaw, David M
AU - Tyson, Frederick L
AD - Division of Extramural Research and Training, National Institute of Environmental Health Sciences (NIEHS), National Institutes of Health (NIH), Department of Health and Human Services (DHHS), Research Triangle Park, North Carolina, USA
Y1 - 2014/08/15/
PY - 2014
DA - 2014 Aug 15
SP - 1271
EP - 1278
PB - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States
VL - 122
IS - 12
SN - 0091-6765, 0091-6765
KW - Biochemistry Abstracts 2: Nucleic Acids; Environment Abstracts
KW - Prediction
KW - Apoptosis
KW - Environmental health
KW - Mitochondria
KW - Nutrients
KW - Metabolites
KW - Homeostasis
KW - Integration
KW - Reactive oxygen species
KW - Environmental hazards
KW - epigenetics
KW - Environmental stress
KW - Tricarboxylic acid cycle
KW - Adenylate cyclase
KW - Brazil, Sao Paulo, Santos
KW - Conferences
KW - ATP
KW - DNA repair
KW - Oxygen
KW - DNA damage
KW - Reviews
KW - Morphology
KW - DNA
KW - Technology
KW - Signal transduction
KW - N 14820:DNA Metabolism & Structure
KW - ENA 21:Wildlife
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-01-01
N1 - Last updated - 2015-05-13
N1 - SubjectsTermNotLitGenreText - Apoptosis; Conferences; Mitochondria; ATP; Metabolites; Nutrients; Homeostasis; DNA repair; Integration; DNA damage; Reactive oxygen species; epigenetics; Reviews; Environmental stress; Tricarboxylic acid cycle; Signal transduction; Adenylate cyclase; Prediction; Oxygen; Environmental hazards; Morphology; DNA; Environmental health; Technology; Brazil, Sao Paulo, Santos
DO - http://dx.doi.org/10.1289/ehp.1408418
ER -
TY - JOUR
T1 - Med25 is required for estrogen receptor alpha (ERα)-mediated regulation of human CYP2C9 expression.
AN - 1547542790; 24960263
AB - The CYP2C subfamily of cytochrome P450 enzymes is an important class of drug metabolizing enzymes in human liver. CYP2C9 is the most abundant member of the human CYP2C subfamily in liver and metabolizes ~15% of the therapeutic drugs as well as other xenobiotics and endogenous compounds. A number of nuclear receptors including xenobiotic-sensing receptors such as the constitutive androstane receptor (CAR), pregnane X receptor (PXR), and glucocorticoid receptor (GR) as well as liver enriched receptors hepatic nuclear factor 4α (HNF4α) and the estrogen receptor α (ERα) regulate CYP2C9 expression. Here, we show that Med25, a variable component of Mediator complex, enhanced ligand dependent ERα-mediated transcriptional activation of CYP2C9 promoter and interacts with activated ERα by 17β-estradiol through its C-terminal LXXLL motif. In conclusion, Med25 is identified as a new coactivator of ERα that is required for ERα-mediated regulation of CYP2C9 expression.
Copyright © 2014 Elsevier Inc. All rights reserved.
JF - Biochemical pharmacology
AU - Shi, Zhe
AU - Yang, Wenjun
AU - Goldstein, Joyce A
AU - Zhang, Shu-Yun
AD - Department of Preventive Medicine, School of Environmental Science and Public Health, Wenzhou Medical University, Wenzhou, Zhejiang 325035, PR China. ; Department of Hepatobiliary Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325035, PR China. ; Human Metabolism Section, Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. ; Department of Preventive Medicine, School of Environmental Science and Public Health, Wenzhou Medical University, Wenzhou, Zhejiang 325035, PR China. Electronic address: shuyunzh@gmail.com.
Y1 - 2014/08/15/
PY - 2014
DA - 2014 Aug 15
SP - 425
EP - 431
VL - 90
IS - 4
KW - Estrogen Receptor alpha
KW - 0
KW - MED25 protein, human
KW - Mediator Complex
KW - CYP2C9 protein, human
KW - EC 1.14.13.-
KW - Cytochrome P-450 CYP2C9
KW - Aryl Hydrocarbon Hydroxylases
KW - EC 1.14.14.1
KW - Index Medicus
KW - Med25
KW - CYP2C9
KW - Transcription regulation
KW - ERα
KW - Real-Time Polymerase Chain Reaction
KW - Microscopy, Confocal
KW - Promoter Regions, Genetic
KW - Hep G2 Cells
KW - Humans
KW - Chromatin Immunoprecipitation
KW - Aryl Hydrocarbon Hydroxylases -- metabolism
KW - Mediator Complex -- physiology
KW - Gene Expression Regulation, Enzymologic -- physiology
KW - Aryl Hydrocarbon Hydroxylases -- genetics
KW - Estrogen Receptor alpha -- physiology
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-09-16
N1 - Date created - 2014-07-21
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.bcp.2014.06.016
ER -
TY - JOUR
T1 - Safety of cotrimoxazole in pregnancy: a systematic review and meta-analysis.
AN - 1544742922; 24853309
AB - Cotrimoxazole is widely prescribed to treat a range of infections, and for HIV-infected individuals it is administered as prophylaxis to protect against opportunistic infections. Some reports suggest that fetuses exposed to cotrimoxazole during early pregnancy may have an increased risk of congenital anomalies. We carried out this systematic review to update the evidence of cotrimoxazole safety in pregnancy.
Three databases and 1 conference abstract site were searched in duplicate up to October 31, 2013, for studies reporting adverse maternal and infant outcomes among women receiving cotrimoxazole during pregnancy. This search was updated in MEDLINE via PubMed to April 28, 2014. Studies were included irrespective of HIV infection status or the presence of other coinfections. Our primary outcome was birth defects of any kind. Secondary outcomes included spontaneous abortions, terminations of pregnancy, stillbirths, preterm deliveries, and drug-associated toxicity. Twenty-four studies were included for review. There were 232 infants with congenital anomalies among 4196 women receiving cotrimoxazole during pregnancy, giving an overall pooled prevalence of 3.5% (95% confidence interval: 1.8% to 5.1%; τ² = 0.03). Three studies reported 31 infants with neural tube defects associated with first trimester exposure to cotrimoxazole, giving a crude prevalence of 0.7% (95% confidence interval: 0.5% to 1.0%) with most data (29 neural tube defects) coming from a single study. The majority of adverse drug reactions were mild. The quality of the evidence was very low.
The findings of this review support continued recommendations for cotrimoxazole as a priority intervention for HIV-infected pregnant women. It is critical to improve data collection on maternal and infant outcomes.
JF - Journal of acquired immune deficiency syndromes (1999)
AU - Ford, Nathan
AU - Shubber, Zara
AU - Jao, Jennifer
AU - Abrams, Elaine J
AU - Frigati, Lisa
AU - Mofenson, Lynne
AD - *Department of HIV/AIDS, World Health Organization, Geneva, Switzerland; †Department of Infectious Disease Epidemiology, Faculty of Medicine, Imperial College, London, United Kingdom; ‡Department of Medicine, Divisions of Infectious Diseases and General Internal Medicine, Icahn School of Medicine at Mount Sinai, New York, NY; §ICAP, Mailman School of Public Health, and College of Physicians and Surgeons, Columbia University, New York, NY; ‖Department of Paediatrics and Child Health, Tygerberg Hospital, University of Stellenbosch, Cape Town South Africa; and ¶Maternal and Pediatric Infectious Disease Branch, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Rockville, MD.
Y1 - 2014/08/15/
PY - 2014
DA - 2014 Aug 15
SP - 512
EP - 521
VL - 66
IS - 5
KW - Anti-Bacterial Agents
KW - 0
KW - Trimethoprim, Sulfamethoxazole Drug Combination
KW - 8064-90-2
KW - Index Medicus
KW - AIDS/HIV
KW - HIV Infections
KW - Humans
KW - Female
KW - Pregnancy
KW - Trimethoprim, Sulfamethoxazole Drug Combination -- administration & dosage
KW - Abnormalities, Drug-Induced
KW - Anti-Bacterial Agents -- adverse effects
KW - Anti-Bacterial Agents -- administration & dosage
KW - Trimethoprim, Sulfamethoxazole Drug Combination -- adverse effects
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+acquired+immune+deficiency+syndromes+%281999%29&rft.atitle=Safety+of+cotrimoxazole+in+pregnancy%3A+a+systematic+review+and+meta-analysis.&rft.au=Ford%2C+Nathan%3BShubber%2C+Zara%3BJao%2C+Jennifer%3BAbrams%2C+Elaine+J%3BFrigati%2C+Lisa%3BMofenson%2C+Lynne&rft.aulast=Ford&rft.aufirst=Nathan&rft.date=2014-08-15&rft.volume=66&rft.issue=5&rft.spage=512&rft.isbn=&rft.btitle=&rft.title=Journal+of+acquired+immune+deficiency+syndromes+%281999%29&rft.issn=1944-7884&rft_id=info:doi/10.1097%2FQAI.0000000000000211
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-08-25
N1 - Date created - 2014-07-11
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Am J Clin Nutr. 2000 May;71(5 Suppl):1295S-303S [10799405]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1097/QAI.0000000000000211
ER -
TY - JOUR
T1 - Validation of a hypoxia-inducible factor-1 alpha specimen collection procedure and quantitative enzyme-linked immunosorbent assay in solid tumor tissues.
AN - 1542004524; 24799347
AB - Hypoxia-inducible factor-1 alpha (HIF-1α) is an important marker of hypoxia in human tumors and has been implicated in tumor progression. Drugs targeting HIF-1α are being developed, but the ability to measure drug-induced changes in HIF-1α is limited by the lability of the protein in normoxia. Our goal was to devise methods for specimen collection and processing that preserve HIF-1α in solid tumor tissues and to develop and validate a two-site chemiluminescent quantitative enzyme-linked immunosorbent assay (ELISA) for HIF-1α. We tested various strategies for HIF-1α stabilization in solid tumors, including nitrogen gas-purged lysis buffer, the addition of proteasome inhibitors or the prolyl hydroxylase inhibitor 2-hydroxyglutarate, and bead homogenization. Degassing and the addition of 2-hydroxyglutarate to the collection buffer significantly increased HIF-1α recovery, whereas bead homogenization in sealed tubes improved HIF-1α recovery and reduced sample variability. Validation of the ELISA demonstrated intra- and inter-assay variability of less than 15% and accuracy of 99.8±8.3% as assessed by spike recovery. Inter-laboratory reproducibility was also demonstrated (R(2)=0.999). Careful sample handling techniques allow us to quantitatively detect HIF-1α in samples as small as 2.5μg of total protein extract, and this method is currently being applied to analyze tumor biopsy specimens in early-phase clinical trials.
Copyright © 2014 Elsevier Inc. All rights reserved.
JF - Analytical biochemistry
AU - Park, Sook Ryun
AU - Kinders, Robert J
AU - Khin, Sonny
AU - Hollingshead, Melinda
AU - Antony, Smitha
AU - Parchment, Ralph E
AU - Tomaszewski, Joseph E
AU - Kummar, Shivaani
AU - Doroshow, James H
AD - Division of Cancer Treatment and Diagnosis, National Cancer Institute, Bethesda, MD 20892, USA. ; Laboratory of Human Toxicology and Pharmacology, Applied/Developmental Research Directorate, Leidos Biomedical Research, Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA. Electronic address: kindersr@mail.nih.gov. ; Laboratory of Human Toxicology and Pharmacology, Applied/Developmental Research Directorate, Leidos Biomedical Research, Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA. ; Biological Testing Branch, Developmental Therapeutics Program, Frederick National Laboratory for Cancer Research, Frederick, MD 20892, USA. ; Division of Cancer Treatment and Diagnosis, National Cancer Institute, Bethesda, MD 20892, USA; Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.
Y1 - 2014/08/15/
PY - 2014
DA - 2014 Aug 15
SP - 1
EP - 11
VL - 459
KW - Biomarkers, Tumor
KW - 0
KW - Hypoxia-Inducible Factor 1, alpha Subunit
KW - Index Medicus
KW - HIF-1α
KW - Solid tumors
KW - Hypoxia-inducible factor
KW - Quantitative ELISA
KW - Pharmacodynamics
KW - Biomarkers, Tumor -- metabolism
KW - Animals
KW - Humans
KW - Mice
KW - Cell Line, Tumor
KW - Female
KW - Cell Transformation, Neoplastic
KW - Neoplasms -- pathology
KW - Enzyme-Linked Immunosorbent Assay
KW - Specimen Handling -- methods
KW - Hypoxia-Inducible Factor 1, alpha Subunit -- metabolism
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Analytical+biochemistry&rft.atitle=Validation+of+a+hypoxia-inducible+factor-1+alpha+specimen+collection+procedure+and+quantitative+enzyme-linked+immunosorbent+assay+in+solid+tumor+tissues.&rft.au=Park%2C+Sook+Ryun%3BKinders%2C+Robert+J%3BKhin%2C+Sonny%3BHollingshead%2C+Melinda%3BAntony%2C+Smitha%3BParchment%2C+Ralph+E%3BTomaszewski%2C+Joseph+E%3BKummar%2C+Shivaani%3BDoroshow%2C+James+H&rft.aulast=Park&rft.aufirst=Sook&rft.date=2014-08-15&rft.volume=459&rft.issue=&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Analytical+biochemistry&rft.issn=1096-0309&rft_id=info:doi/10.1016%2Fj.ab.2014.04.025
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-02-04
N1 - Date created - 2014-06-28
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Proc Natl Acad Sci U S A. 2011 Mar 1;108(9):3749-54 [21321221]
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Clin Cancer Res. 2011 Aug 1;17(15):5123-31 [21673063]
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Cancer Cell. 2011 Jan 18;19(1):17-30 [21251613]
Proc Natl Acad Sci U S A. 1998 Jul 7;95(14):7987-92 [9653127]
Am J Physiol. 1998 Oct;275(4 Pt 1):L818-26 [9755115]
Cancer Res. 2005 Apr 1;65(7):2825-31 [15805283]
Cancer Res. 2006 Apr 1;66(7):3639-48 [16585189]
J Biol Chem. 2006 Nov 3;281(44):33095-106 [16954218]
Nat Rev Cancer. 2007 Feb;7(2):131-9 [17251919]
Cancer Metastasis Rev. 2007 Jun;26(2):225-39 [17440684]
Blood. 2008 Mar 15;111(6):3131-6 [18174379]
Mol Cell. 2008 May 23;30(4):393-402 [18498744]
Clin Cancer Res. 2008 Jun 15;14(12):3658-63 [18559579]
Clin Cancer Res. 2008 Nov 1;14(21):6877-85 [18980982]
Nat Rev Cancer. 2008 Dec;8(12):967-75 [18987634]
Mol Cancer Ther. 2009 Jul;8(7):1878-84 [19584232]
Clin Cancer Res. 2009 Nov 1;15(21):6619-29 [19843666]
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Drug Resist Updat. 2011 Jun;14(3):191-201 [21466972]
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Cancer Res. 1999 Nov 15;59(22):5830-5 [10582706]
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Cell Growth Differ. 2001 Jul;12(7):363-9 [11457733]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.ab.2014.04.025
ER -
TY - JOUR
T1 - Identification by digital immunohistochemistry of intratumoral changes of immune infiltrates after vaccine in the absence of modifications of PBMC immune cell subsets.
AN - 1534794068; 24474335
AB - Preclinical studies have demonstrated that the combination of systemic subcutaneous (s.c.) vaccination with intratumoral (i.t.) vaccination was superior in the induction of antitumor activity vs. vaccination with either route alone. A subsequent phase I study employing i.t.-s.c. vaccination was carried out in men with locally recurrent or progressive prostate cancer. rF-PSA-TRICOM (PROSTVAC) vaccine was administered intraprostatically and rV-PSA-TRICOM followed by rF-PSA-TRICOM vaccine was administered systemically. In that study no dose limiting toxicities were observed, 19/21 patients had stable or improved prostate-specific antigen (PSA) values and tumor-infiltrating lymphocytes (TILs) increased in post- vs. pre-treatment tumor biopsies, analyzed employing conventional immunohistochemistry (IHC). In the studies reported here, 31 phenotypes of peripheral blood mononuclear cells (PBMCs) were analyzed prevaccination and postvaccination as well as the functions of PBMC regulatory T cells (Tregs) and natural killer cells. A trend was observed in decreases in serum PSA with the reduction of circulating Tregs postvaccination. Digital IHC was employed prevaccination and postvaccination to measure CD4 and CD8 TILs, as well as Treg TILs by conventional IHC. Few correlations were observed with CD4, CD8 or Treg in TILs vs. PBMCs. However, patients with lower levels of CD4 TILs prevaccination showed the greatest increases in CD4 TILs postvaccine, while Treg TILs decreased postvaccine. There was also a strong correlation between decreases in serum PSA and increases in CD8 TILs postvaccine. These studies provide additional rationale for the use of i.t.-s.c. vaccinations and demonstrate a noncoordinate expression of specific immune subsets in PBMCs vs. tumor. Published 2014. This article is a US Government work and, as such, is in the public domain of the United States of America.
JF - International journal of cancer
AU - Farsaci, Benedetto
AU - Jochems, Caroline
AU - Grenga, Italia
AU - Donahue, Renee N
AU - Tucker, Jo A
AU - Pinto, Peter A
AU - Merino, Maria J
AU - Heery, Christopher R
AU - Madan, Ravi A
AU - Gulley, James L
AU - Schlom, Jeffrey
AD - Laboratory of Tumor Immunology and Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD.
Y1 - 2014/08/15/
PY - 2014
DA - 2014 Aug 15
SP - 862
EP - 870
VL - 135
IS - 4
KW - Cancer Vaccines
KW - 0
KW - Vaccines, Synthetic
KW - rF-TRICOM vaccine
KW - rV-Tricom
KW - Prostate-Specific Antigen
KW - EC 3.4.21.77
KW - Index Medicus
KW - tumor-infiltrating lymphocytes
KW - intratumoral vaccine
KW - cancer vaccine
KW - digital immunohistochemistry
KW - PROSTVAC
KW - Phenotype
KW - Humans
KW - Prostate-Specific Antigen -- blood
KW - Cohort Studies
KW - Biopsy
KW - Vaccines, Synthetic -- therapeutic use
KW - Neoplasm Recurrence, Local
KW - Male
KW - Lymphocytes, Tumor-Infiltrating -- cytology
KW - Killer Cells, Natural -- immunology
KW - Prostatic Neoplasms -- immunology
KW - Prostatic Neoplasms -- blood
KW - Cancer Vaccines -- therapeutic use
KW - Leukocytes, Mononuclear -- immunology
KW - Immunohistochemistry -- methods
KW - Prostatic Neoplasms -- therapy
KW - Leukocytes, Mononuclear -- cytology
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-08-08
N1 - Date created - 2014-06-10
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1002/ijc.28743
ER -
TY - JOUR
T1 - Preconception Maternal and Paternal Exposure to Persistent Organic Pollutants and Birth Size: The LIFE Study
AN - 1660066280; PQ0001052575
AB - Background: Persistent organic pollutants (POPs) are developmental toxicants, but the impact of both maternal and paternal exposures on offspring birth size is largely unexplored. Objective: We examined associations between maternal and paternal serum concentrations of 63 POPs, comprising five major classes of pollutants, with birth size measures. Methods: Parental serum concentrations of 9 organochlorine pesticides, 1 polybrominated biphenyl (PBB), 7 perfluoroalkyl chemicals (PFCs), 10 polybrominated diphenyl ethers (PBDEs), and 36 polychlorinated biphenyls (PCBs) were measured before conception for 234 couples. Differences in birth weight, length, head circumference, and ponderal index were estimated using multiple linear regression per 1-SD increase in natural log-transformed (ln-transformed) chemicals. Models were estimated separately for each parent and adjusted for maternal age, maternal prepregnancy body mass index (kilograms per meter squared) and other confounders, and all models included an interaction term between infant sex and each chemical. Results: Among girls (n = 117), birth weight was significantly lower (range, 84-195 g) in association with a 1-SD increase in ln-transformed maternal serum concentrations of DDT, PBDE congeners 28 and 183, and paternal serum concentrations of PBDE-183 and PCB-167. Among boys (n = 113), maternal (PCBs 138, 153, 167, 170, 195, and 209 and perfluorooctane sulfonamide) and paternal (PCBs 172 and 195) serum concentrations of several POPs were statistically associated with lower birth weight (range, 98-170 g), whereas paternal concentrations of PBDEs (66, 99) were associated with higher birth weight. Differences in offspring head circumference, length, and ponderal index were also associated with parental exposures. Conclusions: Preconceptional maternal and paternal concentrations of several POPs were associated with statistically significant differences in birth size among offspring. Citation: Robledo CA, Yeung E, Mendola P, Sundaram R, Maisog J, Sweeney AM, Barr DB, Buck Louis GM. 2015. Preconception maternal and paternal exposure to persistent organic pollutants and birth size: the LIFE Study. Environ Health Perspect 123:88-94; http://dx.doi.org/10.1289/ehp.1308016
JF - Environmental Health Perspectives
AU - Robledo, Candace A
AU - Yeung, Edwina
AU - Mendola, Pauline
AU - Sundaram, Rajeshwari
AU - Maisog, Jose
AU - Sweeney, Anne M
AU - Barr, Dana Boyd
AU - Louis, Germaine MBuck
AD - Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Department of Health and Human Services, Rockville, Maryland, USA
Y1 - 2014/08/05/
PY - 2014
DA - 2014 Aug 05
SP - 88
EP - 94
PB - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States
VL - 123
IS - 1
SN - 0091-6765, 0091-6765
KW - Environmental Engineering Abstracts (EN); CSA / ASCE Civil Engineering Abstracts (CE)
KW - Birth
KW - Pollutants
KW - Exposure
KW - Circumferences
KW - Health
KW - Serums
KW - Perfluoroalkyls
KW - Infants
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aenvironmentalengabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Health+Perspectives&rft.atitle=Preconception+Maternal+and+Paternal+Exposure+to+Persistent+Organic+Pollutants+and+Birth+Size%3A+The+LIFE+Study&rft.au=Robledo%2C+Candace+A%3BYeung%2C+Edwina%3BMendola%2C+Pauline%3BSundaram%2C+Rajeshwari%3BMaisog%2C+Jose%3BSweeney%2C+Anne+M%3BBarr%2C+Dana+Boyd%3BLouis%2C+Germaine+MBuck&rft.aulast=Robledo&rft.aufirst=Candace&rft.date=2014-08-05&rft.volume=123&rft.issue=1&rft.spage=88&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1308016
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-03-01
N1 - Last updated - 2015-05-04
DO - http://dx.doi.org/10.1289/ehp.1308016
ER -
TY - JOUR
T1 - Uptake of compounds that selectively kill multidrug-resistant cells: the copper transporter SLC31A1 (CTR1) increases cellular accumulation of the thiosemicarbazone NSC73306.
AN - 1551331709; 24800945
AB - Acquired drug resistance in cancer continues to be a challenge in cancer therapy, in part due to overexpression of the drug efflux transporter P-glycoprotein (P-gp, MDR1, ABCB1). NSC73306 is a thiosemicarbazone compound that displays greater toxicity against cells expressing functional P-gp than against other cells. Here, we investigate the cellular uptake of NSC73306, and examine its interaction with P-gp and copper transporter 1 (CTR1, SLC31A1). Overexpression of P-gp sensitizes LLC-PK1 cells to NSC73306. Cisplatin (IC50 = 77 μM), cyclosporin A (IC50 = 500 μM), and verapamil (IC50 = 700 μM) inhibited cellular accumulation of [(3)H]NSC73306. Cellular hypertoxicity of NSC73306 to P-gp-expressing cells was inhibited by cisplatin in a dose-dependent manner. Cells transiently expressing the cisplatin uptake transporter CTR1 (SLC31A1) showed increased [(3)H]NSC73306 accumulation. In contrast, CTR1 knockdown decreased [(3)H]NSC73306 accumulation. The presence of NSC73306 reduced CTR1 levels, similar to the negative feedback of CTR1 levels by copper or cisplatin. Surprisingly, although cisplatin is a substrate of CTR1, we found that CTR1 protein was overexpressed in high-level cisplatin-resistant KB-CP20 and BEL7404-CP20 cell lines. We confirmed that the CTR1 protein was functional, as uptake of NSC73306 was increased in KB-CP20 cells compared to their drug-sensitive parental cells, and downregulation of CTR1 in KB-CP20 cells reduced [(3)H]NSC73306 accumulation. These results suggest that NSC73306 is a transport substrate of CTR1.
JF - Molecular pharmaceutics
AU - Fung, King Leung
AU - Tepede, Abisola K
AU - Pluchino, Kristen M
AU - Pouliot, Lynn M
AU - Pixley, Jessica N
AU - Hall, Matthew D
AU - Gottesman, Michael M
AD - Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health , Bethesda, Maryland 20892, United States.
Y1 - 2014/08/04/
PY - 2014
DA - 2014 Aug 04
SP - 2692
EP - 2702
VL - 11
IS - 8
KW - Cation Transport Proteins
KW - 0
KW - Indoles
KW - NSC73306
KW - P-Glycoprotein
KW - RNA, Small Interfering
KW - SLC31A1 protein, human
KW - Thiosemicarbazones
KW - Copper
KW - 789U1901C5
KW - Cyclosporine
KW - 83HN0GTJ6D
KW - Verapamil
KW - CJ0O37KU29
KW - Cisplatin
KW - Q20Q21Q62J
KW - Index Medicus
KW - Swine
KW - Animals
KW - Cisplatin -- chemistry
KW - Reproducibility of Results
KW - COS Cells
KW - HEK293 Cells
KW - Humans
KW - Thiosemicarbazones -- chemistry
KW - Cyclosporine -- chemistry
KW - RNA, Small Interfering -- metabolism
KW - Copper -- chemistry
KW - Cisplatin -- administration & dosage
KW - Verapamil -- administration & dosage
KW - P-Glycoprotein -- metabolism
KW - Cercopithecus aethiops
KW - LLC-PK1 Cells
KW - Inhibitory Concentration 50
KW - Indoles -- pharmacokinetics
KW - Drug Resistance, Multiple -- drug effects
KW - Cation Transport Proteins -- metabolism
KW - Drug Resistance, Neoplasm -- drug effects
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+pharmaceutics&rft.atitle=Uptake+of+compounds+that+selectively+kill+multidrug-resistant+cells%3A+the+copper+transporter+SLC31A1+%28CTR1%29+increases+cellular+accumulation+of+the+thiosemicarbazone+NSC73306.&rft.au=Fung%2C+King+Leung%3BTepede%2C+Abisola+K%3BPluchino%2C+Kristen+M%3BPouliot%2C+Lynn+M%3BPixley%2C+Jessica+N%3BHall%2C+Matthew+D%3BGottesman%2C+Michael+M&rft.aulast=Fung&rft.aufirst=King&rft.date=2014-08-04&rft.volume=11&rft.issue=8&rft.spage=2692&rft.isbn=&rft.btitle=&rft.title=Molecular+pharmaceutics&rft.issn=1543-8392&rft_id=info:doi/10.1021%2Fmp500114e
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-05-14
N1 - Date created - 2014-08-04
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1021/mp500114e
ER -
TY - JOUR
T1 - Protective effect of Selenium nanoparticle against cyclophosphamide induced hepatotoxicity and genotoxicity in Swiss albino mice.
AN - 1826591683; 24522241
AB - Cyclophosphamide (CP) is the most commonly used chemotherapeutic drug for various types of cancer. However, its use causes severe cytotoxicity to normal cells in human. It is well known that the undesirable side effects are caused due to the formation of reactive oxygen species. Selenium is an essential micronutrient for both animals and humans and has antioxidant and membrane stabilizing property, but selenium is also toxic above certain level. Nano selenium has been well proved to be less toxic than inorganic selenium as well as certain organoselenium compounds. The objective of the study is to evaluate the protective role of Nano-Se against CP-induced hepatotoxicity and genotoxicity in Swiss albino mice. CP was administered intraperitoneally (25 mg/kg b.w.) and Nano-Se was given by oral gavages (2 mg Se/kg b.w.) in concomitant and pretreatment scheme. Intraperitoneal administration of CP induced hepatic damage as indicated by the serum marker enzymes aspartate and alanine transaminases and increased the malonaldehyde level, depleted the glutathione content and antioxidant enzyme activity (glutathione peroxidase, glutathione-s-transferase, superoxide dismutase and catalase), and induced DNA damage and chromosomal aberration. Oral administration of Nano-Se caused a significant reduction in malonaldehyde, ROS level and glutathione levels, restoration of antioxidant enzyme activity, reduction in chromosomal aberration in bone marrow, and DNA damage in lymphocytes and also in bone marrow. Moreover, the chemoprotective efficiency of Nano-Se against CP induced toxicity was confirmed by histopathological evaluation. The results support the protective effect of Nano-Se against CP-induced hepatotoxicity and genotoxicity. © The Author(s) 2014 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav.
JF - Journal of biomaterials applications
AU - Bhattacharjee, Arin
AU - Basu, Abhishek
AU - Ghosh, Prosenjit
AU - Biswas, Jaydip
AU - Bhattacharya, Sudin
AD - Chittaranjan National Cancer Institute, Department of Cancer Chemoprevention, Kolkata, West Bengal, India. ; Chittaranjan National Cancer Institute, Department of Translational Research, Kolkata, West Bengal, India. ; Chittaranjan National Cancer Institute, Department of Cancer Chemoprevention, Kolkata, West Bengal, India sudinb19572004@yahoo.co.in.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 303
EP - 317
VL - 29
IS - 2
KW - cyclophosphamide
KW - genotoxicity
KW - Nano-Se
KW - oxidative stress
KW - hepatotoxicity
KW - antioxidant enzyme
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1826591683?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+biomaterials+applications&rft.atitle=Protective+effect+of+Selenium+nanoparticle+against+cyclophosphamide+induced+hepatotoxicity+and+genotoxicity+in+Swiss+albino+mice.&rft.au=Bhattacharjee%2C+Arin%3BBasu%2C+Abhishek%3BGhosh%2C+Prosenjit%3BBiswas%2C+Jaydip%3BBhattacharya%2C+Sudin&rft.aulast=Bhattacharjee&rft.aufirst=Arin&rft.date=2014-08-01&rft.volume=29&rft.issue=2&rft.spage=303&rft.isbn=&rft.btitle=&rft.title=Journal+of+biomaterials+applications&rft.issn=1530-8022&rft_id=info:doi/
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date created - 2014-07-11
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
ER -
TY - JOUR
T1 - Short Communication: Serum-Based Assay Accurately Detects Single Nucleotide Polymorphisms of IL28B and SOCS3 in HIV/Hepatitis C Virus-Coinfected Subjects
AN - 1768584252; PQ0002687176
AB - Single nucleotide polymorphisms (SNPs) have become important in predicting treatment response to interferon containing anti-hepatitis C virus (HCV) therapy in HCV and HIV/HCV-infected patients. A reliable method for extracting host DNA from serum for genotyping assays would present a practical alternative for clinicians and investigators seeking to perform SNP analyses in HCV-infected patients, particularly in resource-limited settings. Human genomic DNA was extracted from peripheral blood mononuclear cells (PBMCs) and serum of 51 HIV/HCV coinfected patients using the QIAamp DNA Blood Mini Kit and QIAamp Min Elute Virus Spin Kit, respectively. Genotyping assays for the IL28B SNP (rs12979860) and SOCS3 SNP (rs4969170) were performed using the commercially available ABI Taqman allelic discrimination kit and reverse transcriptase-polymerase chain reaction (RT-PCR) was performed using 50 cycles. Results of the genotyping assays using DNA from both PBMCs and cell-free serum were determined separately and then analyzed for concurrence. Genotype analyses performed using DNA isolated from PBMCs or cell-free serum showed a 100% agreement between the IL28B genotyping results from the serum and PBMC isolates and 98% agreement for SOCS3 SNP. This novel serum-based assay to isolate DNA fragments from the serum of HIV/HCV-coinfected subjects can accurately determine a subject's genotype for IL28B (rs12979860) and SOCS3 (rs4969170). This assay could be immediately valuable for detecting clinically relevant SNPs from serum in cases in which PBMCs are not available.
JF - AIDS Research and Human Retroviruses
AU - Shaffer, Ashton
AU - Hubbard, Jon J
AU - Townsend, Kerry
AU - Kottilil, Shyam
AU - Polis, Michael A
AU - Masur, Henry
AU - Kohli, Anita
AD - Critical Care Medicine Department, Clinical Research Center, National Institutes of Health, Bethesda, Maryland.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 792
EP - 795
PB - Mary Ann Liebert, Inc., 140 Huguenot Street New Rochelle NY 10801 United States
VL - 30
IS - 8
SN - 0889-2229, 0889-2229
KW - Biochemistry Abstracts 2: Nucleic Acids; Health & Safety Science Abstracts; Virology & AIDS Abstracts
KW - Acquired immune deficiency syndrome
KW - Genotyping
KW - Assays
KW - Discrimination
KW - Genotypes
KW - Interferon
KW - Peripheral blood mononuclear cells
KW - Retrovirus
KW - Communications
KW - Hepatitis C virus
KW - Human immunodeficiency virus
KW - Single-nucleotide polymorphism
KW - DNA
KW - Polymerase chain reaction
KW - genomics
KW - Hepatitis C
KW - H 6000:Natural Disasters/Civil Defense/Emergency Management
KW - V 22360:AIDS and HIV
KW - N 14810:Methods
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1768584252?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS+Research+and+Human+Retroviruses&rft.atitle=Short+Communication%3A+Serum-Based+Assay+Accurately+Detects+Single+Nucleotide+Polymorphisms+of+IL28B+and+SOCS3+in+HIV%2FHepatitis+C+Virus-Coinfected+Subjects&rft.au=Shaffer%2C+Ashton%3BHubbard%2C+Jon+J%3BTownsend%2C+Kerry%3BKottilil%2C+Shyam%3BPolis%2C+Michael+A%3BMasur%2C+Henry%3BKohli%2C+Anita&rft.aulast=Shaffer&rft.aufirst=Ashton&rft.date=2014-08-01&rft.volume=30&rft.issue=8&rft.spage=792&rft.isbn=&rft.btitle=&rft.title=AIDS+Research+and+Human+Retroviruses&rft.issn=08892229&rft_id=info:doi/10.1089%2Faid.2014.0028
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2016-02-01
N1 - Number of references - 14
N1 - Last updated - 2016-03-17
N1 - SubjectsTermNotLitGenreText - Interferon; Peripheral blood mononuclear cells; Single-nucleotide polymorphism; Genotyping; Polymerase chain reaction; Hepatitis C; genomics; Acquired immune deficiency syndrome; Communications; Human immunodeficiency virus; DNA; Discrimination; Assays; Genotypes; Retrovirus; Hepatitis C virus
DO - http://dx.doi.org/10.1089/aid.2014.0028
ER -
TY - JOUR
T1 - Phagocytosis and Killing of Staphylococcus aureus by Human Neutrophils
AN - 1768582624; PQ0002686528
AB - Neutrophils are essential for host defense against Staphylococcus aureus infections. Although significant progress has been made, our understanding of neutrophil interactions with S. aureus remains incomplete. To provide a more comprehensive view of this process, we investigated phagocytosis and killing of S. aureus by human neutrophils using varied assay conditions in vitro. A greater percentage of bacteria were internalized by adherent neutrophils compared to those in suspension, and, unexpectedly, uptake of S. aureus by adherent neutrophils occurred efficiently in the absence of opsonins. An antibody specific for S. aureus promoted uptake of unopsonized bacteria in suspension, but had little or no capacity to enhance phagocytosis of S. aureus opsonized with normal human serum or by adherent neutrophils. Collectively, these results indicate that assay conditions can have a significant influence on the phagocytosis and killing of S. aureus by neutrophils. More importantly, the results suggest a vaccine approach directed to enhance opsonophagocytosis alone is not sufficient to promote increased killing of S. aureus by human neutrophils. With the emergence and reemergence of antibiotic-resistant microorganisms, establishing parameters that are optimal for studying neutrophil-S. aureus interactions will pave the way towards developing immune-directed strategies for anti-staphylococcal therapies. copyright 2014 S. Karger AG, Basel
JF - Journal of Innate Immunity
AU - Lu, Thea
AU - Porter, Adeline R
AU - Kennedy, Adam D
AU - Kobayashi, Scott D
AU - DeLeo, Frank R
AD - Laboratory of Human Bacterial Pathogenesis, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Mont., USA
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 639
EP - 649
PB - S. Karger AG, P.O. Box Basel CH-4009 Switzerland
VL - 6
IS - 5
SN - 1662-811X, 1662-811X
KW - Microbiology Abstracts B: Bacteriology; Immunology Abstracts
KW - Neutrophils
KW - Phagocytosis
KW - Staphylococcus aureus
KW - Antibodies
KW - Leukocytes (neutrophilic)
KW - opsonophagocytosis
KW - Microorganisms
KW - Vaccines
KW - Infection
KW - Opsonins
KW - Opsonization
KW - F 06905:Vaccines
KW - J 02340:Antibiotics & Antimicrobials
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1768582624?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Innate+Immunity&rft.atitle=Phagocytosis+and+Killing+of+Staphylococcus+aureus+by+Human+Neutrophils&rft.au=Lu%2C+Thea%3BPorter%2C+Adeline+R%3BKennedy%2C+Adam+D%3BKobayashi%2C+Scott+D%3BDeLeo%2C+Frank+R&rft.aulast=Lu&rft.aufirst=Thea&rft.date=2014-08-01&rft.volume=6&rft.issue=5&rft.spage=639&rft.isbn=&rft.btitle=&rft.title=Journal+of+Innate+Immunity&rft.issn=1662811X&rft_id=info:doi/10.1159%2F000360478
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2016-02-01
N1 - Last updated - 2016-03-17
N1 - SubjectsTermNotLitGenreText - Antibodies; Microorganisms; opsonophagocytosis; Leukocytes (neutrophilic); Vaccines; Opsonins; Infection; Phagocytosis; Opsonization; Staphylococcus aureus
DO - http://dx.doi.org/10.1159/000360478
ER -
TY - JOUR
T1 - Interleukin-23 Promotes Interferon- alpha Responsiveness in Hepatitis C Virus/HIV-Coinfected Patients
AN - 1768572982; PQ0002687166
AB - Patients coinfected with HIV and hepatitis C virus (HCV) have poor to modest rates of response with interferon-based therapies, which remain a backbone of the treatment in HIV/HCV-coinfected patients. The mechanisms responsible for poor responsiveness to interferon are not well described. In this study a targeted proteomic analysis of plasma from 42 patients infected with both HIV and HCV and undergoing therapy for HCV with peginterferon and ribavirin was performed. Higher baseline plasma levels of interleukin (IL)-23 were associated with sustained virologic response. Further investigation of how IL-23 facilitates interferon (IFN) responsiveness, as evidenced by a >2-fold increase in most interferon-stimulated genes (ISGs), revealed that IL-23 indirectly enhances IFN signaling in peripheral blood mononuclear cells and HCV continuous culture system by preventing the down-regulation of the IFNAR2 receptor after exposure to IFN- alpha . These findings suggest a unique role of the IL-23 pathway in enhancing host response to type I interferons, thereby facilitating eradication of HCV. Low levels of IL-23 present in plasma of nonresponders may reflect an impaired immune state that in the case of HIV/HCV-coinfected subjects could potentially lead to disruption of TH17 CD4+ T cells. This study suggests a major role for HIV-associated immune dysregulation present in HIV-infected subjects that subsequently determines the overall responsiveness to exogenous interferon- alpha -based HCV therapy.
JF - AIDS Research and Human Retroviruses
AU - Odigie, Madeline
AU - Osinusi, Anu
AU - Barrett, Lisa
AU - Townsend, Kerry
AU - Wang, Honghui
AU - Suffredini, Anthony F
AU - Masur, Henry
AU - Polis, Michael A
AU - Kottilil, Shyam
AD - Immunopathogenesis Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 775
EP - 782
PB - Mary Ann Liebert, Inc., 140 Huguenot Street New Rochelle NY 10801 United States
VL - 30
IS - 8
SN - 0889-2229, 0889-2229
KW - Immunology Abstracts; Health & Safety Science Abstracts; Virology & AIDS Abstracts
KW - Acquired immune deficiency syndrome
KW - Helper cells
KW - Ribavirin
KW - Interferon
KW - CD4 antigen
KW - Peripheral blood mononuclear cells
KW - Plasma levels
KW - Retrovirus
KW - Interleukin 23
KW - Continuous culture
KW - Hepatitis C virus
KW - Human immunodeficiency virus
KW - alpha -Interferon
KW - Lymphocytes T
KW - Hepatitis C
KW - proteomics
KW - Signal transduction
KW - H 6000:Natural Disasters/Civil Defense/Emergency Management
KW - V 22360:AIDS and HIV
KW - F 06910:Microorganisms & Parasites
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1768572982?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS+Research+and+Human+Retroviruses&rft.atitle=Interleukin-23+Promotes+Interferon-+alpha+Responsiveness+in+Hepatitis+C+Virus%2FHIV-Coinfected+Patients&rft.au=Odigie%2C+Madeline%3BOsinusi%2C+Anu%3BBarrett%2C+Lisa%3BTownsend%2C+Kerry%3BWang%2C+Honghui%3BSuffredini%2C+Anthony+F%3BMasur%2C+Henry%3BPolis%2C+Michael+A%3BKottilil%2C+Shyam&rft.aulast=Odigie&rft.aufirst=Madeline&rft.date=2014-08-01&rft.volume=30&rft.issue=8&rft.spage=775&rft.isbn=&rft.btitle=&rft.title=AIDS+Research+and+Human+Retroviruses&rft.issn=08892229&rft_id=info:doi/10.1089%2Faid.2014.0003
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2016-02-01
N1 - Number of references - 22
N1 - Last updated - 2016-03-17
N1 - SubjectsTermNotLitGenreText - Interferon; Plasma levels; Peripheral blood mononuclear cells; CD4 antigen; Continuous culture; Interleukin 23; Helper cells; Ribavirin; alpha -Interferon; Lymphocytes T; proteomics; Signal transduction; Acquired immune deficiency syndrome; Human immunodeficiency virus; Hepatitis C; Retrovirus; Hepatitis C virus
DO - http://dx.doi.org/10.1089/aid.2014.0003
ER -
TY - JOUR
T1 - Chromatin Properties of Regulatory DNA Probed by Manipulation of Transcription Factors
AN - 1712777382; PQ0001969343
AB - Transcription factors (TFs) bind to DNA and regulate the transcription of nearby genes. However, only a small fraction of TF binding sites have such regulatory effects. Here we search for the predictors of functional binding sites by carrying out a systematic computational screening of a variety of contextual factors (histone modifications, nuclear lamin-bindings, and cofactor bindings). We used regression analysis to test if contextual factors are associated with upregulation or downregulation of neighboring genes following the induction or knockdown of the 9 TFs in mouse embryonic stem (ES) cells. Functional TF binding sites appeared to be either active (i.e., bound by P300, CHD7, mediator, cohesin, and SWI/SNF) or repressed (i.e., with H3K27me3 histone marks and bound by Polycomb factors). Active binding sites mediated the downregulation of nearby genes upon knocking down the activating TFs or inducing repressors. Repressed TF binding sites mediated the upregulation of nearby genes (e.g., poised developmental regulators) upon inducing TFs. In addition, repressed binding sites mediated repressive effects of TFs, identified by the downregulation of target genes after the induction of TFs or by the upregulation of target genes after the knockdown of TFs. The contextual factors associated with functions of DNA-bound TFs were used to improve the identification of candidate target genes regulated by TFs.
JF - Journal of Computational Biology
AU - Sharov, Alexei A
AU - Nishiyama, Akira
AU - Qian, Yong
AU - Dudekula, Dawood B
AU - Longo, Dan L
AU - Schlessinger, David
AU - Ko, Minoru SH
AD - National Institute on Aging, National Institutes of Health, Baltimore, Maryland.
PY - 2014
SP - 569
EP - 577
PB - Mary Ann Liebert, Inc., 2 Madison Ave Larchmont NY 10538 United States
VL - 21
IS - 8
SN - 1066-5277, 1066-5277
KW - Biochemistry Abstracts 2: Nucleic Acids; Biotechnology and Bioengineering Abstracts
KW - chromatin modification
KW - cis-regulatory module
KW - embryonic stem cells
KW - enhancer
KW - target genes
KW - transcription factor binding site
KW - Histones
KW - Cofactors
KW - Chromatin
KW - polycomb group proteins
KW - Transcription factors
KW - DNA
KW - Regression analysis
KW - Embryos
KW - Computer applications
KW - cohesin
KW - Repressors
KW - N 14820:DNA Metabolism & Structure
KW - W 30960:Bioinformatics & Computer Applications
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1712777382?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Computational+Biology&rft.atitle=Chromatin+Properties+of+Regulatory+DNA+Probed+by+Manipulation+of+Transcription+Factors&rft.au=Sharov%2C+Alexei+A%3BNishiyama%2C+Akira%3BQian%2C+Yong%3BDudekula%2C+Dawood+B%3BLongo%2C+Dan+L%3BSchlessinger%2C+David%3BKo%2C+Minoru+SH&rft.aulast=Sharov&rft.aufirst=Alexei&rft.date=2014-08-01&rft.volume=21&rft.issue=8&rft.spage=569&rft.isbn=&rft.btitle=&rft.title=Journal+of+Computational+Biology&rft.issn=10665277&rft_id=info:doi/10.1089%2Fcmb.2013.0126
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-09-01
N1 - Number of references - 41
N1 - Last updated - 2016-01-21
N1 - SubjectsTermNotLitGenreText - Cofactors; Histones; polycomb group proteins; Chromatin; Transcription factors; Regression analysis; DNA; Embryos; Computer applications; Repressors; cohesin
DO - http://dx.doi.org/10.1089/cmb.2013.0126
ER -
TY - JOUR
T1 - A Symmetrical Fluorous Dendron-Cyanine Dye-Conjugated Bimodal Nanoprobe for Quantitative super(19)F MRI and NIR Fluorescence Bioimaging
AN - 1701480790; PQ0001666976
AB - super(19)F MRI and optical imaging are two powerful noninvasive molecular imaging modalities in biomedical applications. super(19)F MRI has great potential for high resolution in vivo imaging, while fluorescent probes enable ultracontrast cellular/tissue imaging with high accuracy and sensitivity. A bimodal nanoprobe is developed, integrating the merits of super(19)F MRI and fluorescence imaging into a single synthetic molecule, which is further engineered into nanoprobe, by addressing shortcomings of conventional contrast agents to explore the quantitative super(19)F MRI and fluorescence imaging and cell tracking. Results show that this bimodal imaging nanoprobe presents high correlation of super(19)F MR signal and NIR fluorescence intensity in vitro and in vivo. Additionally, this nanoprobe enables quantitative super(19)F MR analysis, confirmed by a complementary fluorescence analysis. This unique feature can hardly be obtained by traditional super(19)F MRI contrast agents. It is envisioned that this nanoprobe can hold great potential for quantitative and sensitive multi-modal molecular imaging. super(19)F MRI and optical imaging are two powerful noninvasive molecular imaging modalities in biomedical applications. A bimodal nanoprobe incorporating a symmetrical fluorous dendron-cyanine dye single molecule is developed by addressing shortcomings of conventional contrast agents to explore the quantitative super(19)F MRI and fluorescent imaging. This nanoprobe can hold great potential for quantitative and sensitive multi-modal bioimaging.
JF - Advanced Healthcare Materials
AU - Wang, Zhe
AU - Yue, Xuyi
AU - Wang, Yu
AU - Qian, Chunqi
AU - Huang, Peng
AU - Lizak, Marty
AU - Niu, Gang
AU - Wang, Fu
AU - Rong, Pengfei
AU - Kiesewetter, Dale O
AU - Ma, Ying
AU - Chen, Xiaoyuan
AD - Laboratory of Molecular Imaging and Nanomedicine, National Institute of Biomedical Imaging and Bioengineering (NIBIB), National Institutes of Health, Bethesda, MD, 20892, USA.
Y1 - 2014/08//
PY - 2014
DA - Aug 2014
SP - 1326
EP - 1333
PB - John Wiley & Sons, Ltd., Baffins Lane Chichester W. Sussex PO19 1UD United Kingdom
VL - 3
IS - 8
SN - 2192-2640, 2192-2640
KW - Biotechnology and Bioengineering Abstracts
KW - Fluorescence
KW - Magnetic resonance imaging
KW - Computed tomography
KW - Contrast media
KW - Fluorescent indicators
KW - W 30910:Imaging
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Advanced+Healthcare+Materials&rft.atitle=A+Symmetrical+Fluorous+Dendron-Cyanine+Dye-Conjugated+Bimodal+Nanoprobe+for+Quantitative+super%2819%29F+MRI+and+NIR+Fluorescence+Bioimaging&rft.au=Wang%2C+Zhe%3BYue%2C+Xuyi%3BWang%2C+Yu%3BQian%2C+Chunqi%3BHuang%2C+Peng%3BLizak%2C+Marty%3BNiu%2C+Gang%3BWang%2C+Fu%3BRong%2C+Pengfei%3BKiesewetter%2C+Dale+O%3BMa%2C+Ying%3BChen%2C+Xiaoyuan&rft.aulast=Wang&rft.aufirst=Zhe&rft.date=2014-08-01&rft.volume=3&rft.issue=8&rft.spage=1326&rft.isbn=&rft.btitle=&rft.title=Advanced+Healthcare+Materials&rft.issn=21922640&rft_id=info:doi/10.1002%2Fadhm.201400088
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-08-01
N1 - Last updated - 2015-11-16
N1 - SubjectsTermNotLitGenreText - Fluorescence; Computed tomography; Magnetic resonance imaging; Contrast media; Fluorescent indicators
DO - http://dx.doi.org/10.1002/adhm.201400088
ER -
TY - JOUR
T1 - Teaching Genomic Counseling: Preparing the Genetic Counseling Workforce for the Genomic Era
AN - 1665160282
AB - Genetic counselors have a long-standing history of working on the clinical forefront of implementing new genetic technology. Genomic sequencing is no exception. The rapid advancement of genomic sequencing technologies, including but not limited to next generation sequencing approaches, across all subspecialties of genetic counseling mandates attention to genetic counselor training at both the graduate and continuing education levels. The current era provides a tremendous opportunity for counselors to become actively involved in making genomics more accessible, engaging the population in decisions to undergo sequencing and effectively translating genomic information to promote health and well-being. In this commentary, we explore reasons why genomic sequencing warrants particular consideration and put forward strategies for training program curricula and continuing education programs to meet this need.
JF - Journal of Genetic Counseling
AU - Hooker, Gillian W
AU - Ormond, Kelly E
AU - Sweet, Kevin
AU - Biesecker, Barbara B
AD - Social and Behavioral Research Branch, Genetic Counseling Training Program, The Johns Hopkins School of Public Health, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA, Social and Behavioral Research Branch, National Human Genome Research Institute, 31 Center Dr., Room B1B36K, MSC 2073, Bethesda, MD, 20892, USA ; Department of Genetics, MS Human Genetics and Genetic Counseling Program and Stanford Center for Biomedical Ethics, Stanford University, Stanford, CA, USA ; Division of Human Genetics, Ohio State University Wexner Medical Center, Columbus, OH, USA ; Social and Behavioral Research Branch, Genetic Counseling Training Program, The Johns Hopkins School of Public Health, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA ; Social and Behavioral Research Branch, Genetic Counseling Training Program, The Johns Hopkins School of Public Health, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA; Social and Behavioral Research Branch, National Human Genome Research Institute, 31 Center Dr., Room B1B36K, MSC 2073, Bethesda, MD, 20892, USA
Y1 - 2014/08//
PY - 2014
DA - Aug 2014
SP - 445
EP - 451
CY - New York
PB - Springer Science & Business Media
VL - 23
IS - 4
SN - 1059-7700
KW - Psychology
KW - Continuing education
KW - Counselling
KW - Curriculum
KW - Educational programmes
KW - Genetic counselling
KW - Health promotion
KW - Labour force
KW - Teaching
KW - Technology
KW - Wellbeing
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Genetic+Counseling&rft.atitle=Teaching+Genomic+Counseling%3A+Preparing+the+Genetic+Counseling+Workforce+for+the+Genomic+Era&rft.au=Hooker%2C+Gillian+W%3BOrmond%2C+Kelly+E%3BSweet%2C+Kevin%3BBiesecker%2C+Barbara+B&rft.aulast=Hooker&rft.aufirst=Gillian&rft.date=2014-08-01&rft.volume=23&rft.issue=4&rft.spage=445&rft.isbn=&rft.btitle=&rft.title=Journal+of+Genetic+Counseling&rft.issn=10597700&rft_id=info:doi/10.1007%2Fs10897-014-9689-4
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Date revised - 2015-01-09
N1 - Last updated - 2016-05-24
DO - http://dx.doi.org/10.1007/s10897-014-9689-4
ER -
TY - JOUR
T1 - Choice of method for endotoxin detection depends on nanoformulation
AN - 1635024782; 21021821
AB - Aims: Many nanoparticles interfere with traditional tests to quantify endotoxin. The aim of this study was to compare the performance of limulus amoebocyte lysate (LAL) formats on clinical-grade nanoformulations, to determine whether there were disparate results among formats and to test the applicability of an alternative bioassay (the macrophage activation test [MAT]) for resolving discrepancies, if observed. Materials & methods: Clinical-grade nanoformulations were tested using turbidimetric, gel-clot and chromogenic LAL. Formulations that cause a discrepancy among LAL tests were also tested by the MAT. Results & conclusion: The gel-clot LAL method cannot be relied upon to resolve discrepancies among LAL tests for certain nanoformulations. No one LAL format was shown to be optimal for all the tested clinical-grade nanoformulations. The tested alternative bioassay (the MAT) was useful for verifying LAL findings, but only for those nanoformulations not carrying/including cytotoxic drugs. Original submitted 1 March 2013; Revised submitted 13 August 2013
JF - Nanomedicine
AU - Dobrovolskaia, Marina A
AU - Neun, Barry W
AU - Clogston, Jeffrey D
AU - Grossman, Jennifer H
AU - McNeil, Scott E
AD - super(1)Nanotechnology Characterization Laboratory, Leidos Biomedical Research Inc., Frederick National Laboratory for Cancer Research, 1050 Boyles Street, Frederick, MD 21702, USA., marina@mail.nih.gov
Y1 - 2014/08//
PY - 2014
DA - Aug 2014
SP - 1847
EP - 1856
PB - Future Science Group (FSG), Unitec House, 2 Albert Place London N3 1QB United Kingdom
VL - 9
IS - 12
SN - 1743-5889, 1743-5889
KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Biotechnology and Bioengineering Abstracts
KW - endotoxin
KW - interference
KW - in vitro assay
KW - limulus amoebocyte lysate
KW - lipopolysaccharide nanoparticles
KW - rabbit pyrogen test
KW - Endotoxins
KW - Macrophages
KW - Cytotoxicity
KW - Limulus
KW - nanoparticles
KW - Drugs
KW - nanotechnology
KW - Cell activation
KW - A 01490:Miscellaneous
KW - W 30900:Methods
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nanomedicine&rft.atitle=Choice+of+method+for+endotoxin+detection+depends+on+nanoformulation&rft.au=Dobrovolskaia%2C+Marina+A%3BNeun%2C+Barry+W%3BClogston%2C+Jeffrey+D%3BGrossman%2C+Jennifer+H%3BMcNeil%2C+Scott+E&rft.aulast=Dobrovolskaia&rft.aufirst=Marina&rft.date=2014-08-01&rft.volume=9&rft.issue=12&rft.spage=1847&rft.isbn=&rft.btitle=&rft.title=Nanomedicine&rft.issn=17435889&rft_id=info:doi/
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-12-01
N1 - Number of references - 29
N1 - Last updated - 2015-04-02
N1 - SubjectsTermNotLitGenreText - Macrophages; Endotoxins; Cytotoxicity; Drugs; nanoparticles; Cell activation; nanotechnology; Limulus
ER -
TY - JOUR
T1 - Farm residence and lymphohematopoietic cancers in the Iowa Women super(3)s Health Study
AN - 1627967146; 20956907
AB - Background Cancer incidence in male farmers has been studied extensively; however, less is known about risk among women residing on farms or in agricultural areas, who may be exposed to pesticides by their proximity to crop fields. We extended a previous follow-up of the Iowa Women super(3)s Health Study cohort to examine farm residence and the incidence of lymphohematopoietic cancers. Further, we investigated crop acreage within 750m of residences, which has been associated with higher herbicide levels in Iowa homes. Methods We analyzed data for a cohort of 37,099 Iowa women aged 55-69 years who reported their residence location (farm, rural (not a farm), town size based on population) at enrollment in 1986. We identified incident lymphohematopoietic cancers (1986-2009) by linkage with the Iowa Cancer Registry. Using a geographic information system, we geocoded addresses and calculated acreage of pasture and row crops within 750m of homes using the 1992 National Land Cover Database. Cox regression was used to estimate hazard ratios (HR) and 95% confidence intervals (CI) in multivariate analyses of cancer risk in relation to both residence location and crop acreage. Results As found in an earlier analysis of residence location, risk of acute myeloid leukemia (AML) was higher among women living on farms (HR=2.23, 95%CI: 1.25-3.99) or rural areas (but not on a farm) (HR=1.95, 95%CI: 0.89-4.29) compared with women living in towns of >10,000 population. We observed no association between farm or rural residence and non-Hodgkin lymphoma (NHL; overall or for major subtypes) or multiple myeloma. In analyses of crop acreage, we observed no association between pasture or row crop acreage within 750m of homes and risk of leukemia overall or for the AML subtype. Chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma (SLL) risk was nonsignificantly elevated among women with pasture acreage within 750m of their home (HRs for increasing tertiles=1.8, 1.8 and 1.5) and with row crop acreage within 750m (HRs for increasing tertiles of acreage=1.4, 1.5 and 1.6) compared to women with no pasture or row crop acreage, respectively. Conclusions Iowa women living on a farm or in a rural area were at increased risk of developing AML, which was not related to crop acreage near the home. Living near pasture or row crops may confer an increased risk of CLL/SLL regardless of residence location. Further investigation of specific farm-related exposures and these cancers among women living on farms and in agricultural areas is warranted.
JF - Environmental Research
AU - Jones, Rena R
AU - Yu, Chu-Ling
AU - Nuckols, John R
AU - Cerhan, James R
AU - Airola, Matthew
AU - Ross, Julie A
AU - Robien, Kim
AU - Ward, Mary H
AD - Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, USA
Y1 - 2014/08//
PY - 2014
DA - Aug 2014
SP - 353
EP - 361
PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands
VL - 133
SN - 0013-9351, 0013-9351
KW - Risk Abstracts; Environment Abstracts
KW - Farm residence
KW - Pesticides
KW - Iowa Women super(3)s Health Study
KW - GIS
KW - Land use
KW - Farms
KW - Crop fields
KW - Remote sensing
KW - Herbicides
KW - Pasture
KW - Towns
KW - Cancer
KW - Crops
KW - Leukemia
KW - Health risks
KW - Multiple myeloma
KW - USA, Iowa
KW - Geographic information systems
KW - Lymphoma
KW - Rural areas
KW - ENA 06:Food & Drugs
KW - R2 23050:Environment
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Research&rft.atitle=Farm+residence+and+lymphohematopoietic+cancers+in+the+Iowa+Women+super%283%29s+Health+Study&rft.au=Jones%2C+Rena+R%3BYu%2C+Chu-Ling%3BNuckols%2C+John+R%3BCerhan%2C+James+R%3BAirola%2C+Matthew%3BRoss%2C+Julie+A%3BRobien%2C+Kim%3BWard%2C+Mary+H&rft.aulast=Jones&rft.aufirst=Rena&rft.date=2014-08-01&rft.volume=133&rft.issue=&rft.spage=353&rft.isbn=&rft.btitle=&rft.title=Environmental+Research&rft.issn=00139351&rft_id=info:doi/10.1016%2Fj.envres.2014.05.028
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-11-01
N1 - Last updated - 2015-04-16
N1 - SubjectsTermNotLitGenreText - Farms; Crop fields; Remote sensing; Herbicides; Pasture; Crops; Cancer; Towns; Health risks; Leukemia; Multiple myeloma; Geographic information systems; Lymphoma; Rural areas; USA, Iowa
DO - http://dx.doi.org/10.1016/j.envres.2014.05.028
ER -
TY - JOUR
T1 - Polycyclic aromatic hydrocarbons in residential dust and risk of childhood acute lymphoblastic leukemia
AN - 1627961892; 20956908
AB - Several polycyclic aromatic hydrocarbons (PAHs) are known or probable human carcinogens. We evaluated the relationship between PAH exposure and risk of childhood acute lymphoblastic leukemia (ALL) using concentrations in residential dust as an exposure indicator. We conducted a population-based case-control study (251 ALL cases, 306 birth-certificate controls) in Northern and Central California from 2001 to 2007. We collected residential dust using a high volume small surface sampler (HVS3) (n=185 cases, 212 controls) or by sampling from participants' household vacuum cleaners (n=66 cases, 94 controls). We evaluated log-transformed concentrations of 9 individual PAHs, the summed PAHs, and the summed PAHs weighted by their carcinogenic potency (the toxic equivalence). We calculated odds ratios (ORs) and 95% confidence intervals (CI) using logistic regression adjusting for demographic characteristics and duration between diagnosis/reference date and dust collection. Among participants with HVS3 dust, risk of ALL was not associated with increasing concentration of any PAHs based on OR perln(ng/g). Among participants with vacuum dust, we observed positive associations between ALL risk and increasing concentrations of benzo[a]pyrene (OR perln[ng/g]=1.42, 95% CI=0.95, 2.12), dibenzo[a,h]anthracene (OR=1.98, 95% CI=1.11, 3.55), benzo[k]fluoranthene (OR=1.71, 95% CI=0.91, 3.22), indeno[1,2,3-cd]pyrene (OR=1.81, 95% CI=1.04, 3.16), and the toxic equivalence (OR=2.35, 95% CI=1.18, 4.69). The increased ALL risk among participants with vacuum dust suggests that PAH exposure may increase the risk of childhood ALL; however, reasons for the different results based on HVS3 dust samples deserve further study.
JF - Environmental Research
AU - Deziel, N C
AU - Rull, R P
AU - Colt, J S
AU - Reynolds, P
AU - Whitehead, T P
AU - Gunier, R B
AU - Month
AU - Taggart
AU - Buffler, P
AU - Ward, M H
AU - Metayer, C
AD - Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, USA
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 388
EP - 395
PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands
VL - 133
SN - 0013-9351, 0013-9351
KW - Toxicology Abstracts; Risk Abstracts; Environment Abstracts; Meteorological & Geoastrophysical Abstracts
KW - ALL acute lymphoblastic leukemia
KW - PAHs polycyclic aromatic hydrocarbons
KW - HVS3 high volume small surface sampler
KW - TEQ toxic equivalence
KW - OR odds ratio
KW - 95% CI 95% confidence interval
KW - Polycyclic aromatic hydrocarbons
KW - Childhood leukemia
KW - Dust
KW - Environmental exposures
KW - Environmental epidemiology
KW - Statistical analysis
KW - Vacuum
KW - Environmental research
KW - Carcinogens
KW - Children
KW - Samplers
KW - Demography
KW - Leukemia
KW - Carcinogenicity
KW - Households
KW - Acute lymphatic leukemia
KW - Benzo(a)pyrene
KW - USA, California
KW - Sampling
KW - M2 551.510.42:Air Pollution (551.510.42)
KW - X 24350:Industrial Chemicals
KW - R2 23050:Environment
KW - ENA 02:Toxicology & Environmental Safety
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-11-01
N1 - Last updated - 2016-11-23
N1 - SubjectsTermNotLitGenreText - Demography; Polycyclic aromatic hydrocarbons; Acute lymphatic leukemia; Vacuum; Benzo(a)pyrene; Carcinogens; Sampling; Children; Samplers; Dust; Statistical analysis; Environmental research; Leukemia; Carcinogenicity; Households; USA, California
DO - http://dx.doi.org/10.1016/j.envres.2014.04.033
ER -
TY - JOUR
T1 - The root of reduced fertility in aged women and possible therapentic options: current status and future perspects.
AN - 1561979190; 23796757
AB - It is well known that maternal ageing not only causes increased spontaneous abortion and reduced fertility, but it is also a high genetic disease risk. Although assisted reproductive technologies (ARTs) have been widely used to treat infertility, the overall success is still low. The main reasons for age-related changes include reduced follicle number, compromised oocyte quality especially aneuploidy, altered reproductive endocrinology, and increased reproductive tract defect. Various approaches for improving or treating infertility in aged women including controlled ovarian hyperstimulation with intrauterine insemination (IUI), IVF/ICSI-ET, ovarian reserve testing, preimplantation genetic diagnosis and screening (PGD/PGS), oocyte selection and donation, oocyte and ovary tissue cryopreservation before ageing, miscarriage prevention, and caloric restriction are summarized in this review. Future potential reproductive techniques for infertile older women including oocyte and zygote micromanipulations, derivation of oocytes from germ stem cells, ES cells, and iPS cells, as well as through bone marrow transplantation are discussed.
Copyright © 2013 Elsevier Ltd. All rights reserved.
JF - Molecular aspects of medicine
AU - Qiao, Jie
AU - Wang, Zhen-Bo
AU - Feng, Huai-Liang
AU - Miao, Yi-Liang
AU - Wang, Qiang
AU - Yu, Yang
AU - Wei, Yan-Chang
AU - Yan, Jie
AU - Wang, Wei-Hua
AU - Shen, Wei
AU - Sun, Shao-Chen
AU - Schatten, Heide
AU - Sun, Qing-Yuan
AD - Center of Reproductive Medicine, Department of Obstetrics and Gynecology, Peking University Third Hospital, Beijing 100191, People's Republic of China. ; State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, People's Republic of China. ; Department of Laboratory Medicine, and Obstetrics and Gynecology, New York Hospital Queens, Weill Medical College of Cornell University, New York, NY, USA. ; Reproductive Medicine Group, Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. ; Department of Obstetrics and Gynecology, Washington University School of Medicine, 660 South Euclid Ave., St. Louis, MO 63110, USA. ; Houston Fertility Institute, Tomball Regional Hospital, Tomball, TX 77375, USA. ; Laboratory of Germ Cell Biology, Department of Animal Science, Qingdao Agricultural University, Qingdao 266109, People's Republic of China. ; Department of Animal Science, Nanjing Agricultural University, Nanjing 210095, People's Republic of China. ; Department of Veterinary Pathobiology, University of Missouri, Columbia, MO 65211, USA. ; State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, People's Republic of China. Electronic address: sunqy@ioz.ac.cn.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 54
EP - 85
VL - 38
KW - Index Medicus
KW - Infertility
KW - Maternal age
KW - Assited reproductive technology
KW - Ovary
KW - Oocyte
KW - Maternal Age
KW - Humans
KW - Female
KW - Bone Marrow Transplantation
KW - Aging -- physiology
KW - Infertility, Female -- therapy
KW - Reproductive Techniques
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+aspects+of+medicine&rft.atitle=The+root+of+reduced+fertility+in+aged+women+and+possible+therapentic+options%3A+current+status+and+future+perspects.&rft.au=Qiao%2C+Jie%3BWang%2C+Zhen-Bo%3BFeng%2C+Huai-Liang%3BMiao%2C+Yi-Liang%3BWang%2C+Qiang%3BYu%2C+Yang%3BWei%2C+Yan-Chang%3BYan%2C+Jie%3BWang%2C+Wei-Hua%3BShen%2C+Wei%3BSun%2C+Shao-Chen%3BSchatten%2C+Heide%3BSun%2C+Qing-Yuan&rft.aulast=Qiao&rft.aufirst=Jie&rft.date=2014-08-01&rft.volume=38&rft.issue=&rft.spage=54&rft.isbn=&rft.btitle=&rft.title=Molecular+aspects+of+medicine&rft.issn=1872-9452&rft_id=info:doi/10.1016%2Fj.mam.2013.06.001
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-03-30
N1 - Date created - 2014-08-01
N1 - Date revised - 2017-01-13
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.mam.2013.06.001
ER -
TY - JOUR
T1 - Identification of Three Noncontiguous Regions on Bacillus anthracis Plasmid pXO1 That Are Important for Its Maintenance
AN - 1560139502; 20602765
AB - Bacillus anthracis pXO1 minireplicon (MR) plasmid consisting of open reading frames (ORFs) GBAA_pXO1_0020 to GBAA_pXO1_0023 is not stably maintained in B. anthracis, whereas the full-size parent pXO1 plasmid (having 181,677 bp and 217 ORFs) is extremely stable under the same growth conditions. Two genetic tools developed for DNA manipulation in B. anthracis (Cre-loxP and Flp-FRT systems) were used to identify pXO1 regions important for plasmid stability. We localized a large segment of pXO1 that enables stable plasmid maintenance during vegetative growth. Further genetic analysis identified three genes that are necessary for pXO1 maintenance: amsP (GBAA_pXO1_0069), minP (GBAA_pXO1_0082), and sojP (GBAA_pXO1_0084). Analysis of conserved domains in the corresponding proteins indicated that only AmsP (activator of maintenance system of pXO1) is predicted to bind DNA, due to its strong helix-turn-helix domain. Two conserved domains were found in the MinP protein (Min protein from pXO1): an N-terminal domain having some similarity to the B. anthracis septum site-determining protein MinD and a C-terminal domain that resembles a baculovirus single-stranded-DNA-binding protein. The SojP protein (Soj from pXO1) contains putative Walker box motifs and belongs to the ParA family of ATPases. No sequences encoding other components of type I plasmid partition systems, namely, cis-acting centromere parS and its binding ParB protein, were identified within the pXO1 genome. A model describing the role of the MinP protein in pXO1 distribution between daughter cells is proposed.
JF - Journal of Bacteriology
AU - Pomerantsev, Andrei P
AU - Chang, Zanetta
AU - Rappole, Catherine
AU - Leppla, Stephen H
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 2921
EP - 2933
PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL - 196
IS - 16
SN - 0021-9193, 0021-9193
KW - Genetics Abstracts; Microbiology Abstracts B: Bacteriology
KW - Genomes
KW - Adenosinetriphosphatase
KW - Min protein
KW - Growth conditions
KW - Genetic analysis
KW - ParB protein
KW - Bacillus anthracis
KW - Plasmids
KW - Centromeres
KW - DNA
KW - Septum
KW - Baculovirus
KW - Open reading frames
KW - J 02320:Cell Biology
KW - G 07770:Bacteria
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1560139502?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Bacteriology&rft.atitle=Identification+of+Three+Noncontiguous+Regions+on+Bacillus+anthracis+Plasmid+pXO1+That+Are+Important+for+Its+Maintenance&rft.au=Pomerantsev%2C+Andrei+P%3BChang%2C+Zanetta%3BRappole%2C+Catherine%3BLeppla%2C+Stephen+H&rft.aulast=Pomerantsev&rft.aufirst=Andrei&rft.date=2014-08-01&rft.volume=196&rft.issue=16&rft.spage=2921&rft.isbn=&rft.btitle=&rft.title=Journal+of+Bacteriology&rft.issn=00219193&rft_id=info:doi/10.1128%2FJB.01747-14
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-09-01
N1 - Number of references - 36
N1 - Last updated - 2016-08-03
N1 - SubjectsTermNotLitGenreText - Genomes; Adenosinetriphosphatase; Min protein; Growth conditions; Genetic analysis; DNA; ParB protein; Septum; Plasmids; Open reading frames; Centromeres; Baculovirus; Bacillus anthracis
DO - http://dx.doi.org/10.1128/JB.01747-14
ER -
TY - JOUR
T1 - Lysine ubiquitination and acetylation of human cardiac 20S proteasomes
AN - 1560119237; 20584499
AB - Purpose Altered proteasome functions are associated with multiple cardiomyopathies. While the proteasome targets polyubiquitinated proteins for destruction, it itself is modifiable by ubiquitination. We aim to identify the exact ubiquitination sites on cardiac proteasomes and examine whether they are also subject to acetylations. Experimental design Assembled cardiac 20S proteasome complexes were purified from five human hearts with ischemic cardiomyopathy, then analyzed by high-resolution MS to identify ubiquitination and acetylation sites. We developed a library search strategy that may be used to complement database search in identifying PTM in different samples. Results We identified 63 ubiquitinated lysines from intact human cardiac 20S proteasomes. In parallel, 65 acetylated residues were also discovered, 39 of which shared with ubiquitination sites. Conclusion and clinical relevance This is the most comprehensive characterization of cardiac proteasome ubiquitination to date. There are significant overlaps between the discovered ubiquitination and acetylation sites, permitting potential crosstalk in regulating proteasome functions. The information presented here will aid future therapeutic strategies aimed at regulating the functions of cardiac proteasomes.
JF - Proteomics Clinical Applications
AU - Zong, Nobel
AU - Ping, Peipei
AU - Lau, Edward
AU - Choi, Howard JH
AU - Ng, Dominic CM
AU - Meyer, David
AU - Fang, Caiyun
AU - Li, Haomin
AU - Wang, Ding
AU - Zelaya, Ivette M
AU - Yates, John R
AU - Lam, Maggie PY
AD - The NHLBI Proteomics Center at UCLA, Los Angeles, CA, USA.
Y1 - 2014/08//
PY - 2014
DA - Aug 2014
SP - 590
EP - 594
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 8
IS - 7-8
SN - 1862-8346, 1862-8346
KW - Biotechnology and Bioengineering Abstracts
KW - Heart
KW - ubiquitination
KW - Acetylation
KW - Cardiomyopathy
KW - Databases
KW - proteasomes
KW - Lysine
KW - Therapeutic applications
KW - Ischemia
KW - proteomics
KW - W 30960:Bioinformatics & Computer Applications
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proteomics+Clinical+Applications&rft.atitle=Lysine+ubiquitination+and+acetylation+of+human+cardiac+20S+proteasomes&rft.au=Zong%2C+Nobel%3BPing%2C+Peipei%3BLau%2C+Edward%3BChoi%2C+Howard+JH%3BNg%2C+Dominic+CM%3BMeyer%2C+David%3BFang%2C+Caiyun%3BLi%2C+Haomin%3BWang%2C+Ding%3BZelaya%2C+Ivette+M%3BYates%2C+John+R%3BLam%2C+Maggie+PY&rft.aulast=Zong&rft.aufirst=Nobel&rft.date=2014-08-01&rft.volume=8&rft.issue=7-8&rft.spage=590&rft.isbn=&rft.btitle=&rft.title=Proteomics+Clinical+Applications&rft.issn=18628346&rft_id=info:doi/10.1002%2Fprca.201400029
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-09-01
N1 - Last updated - 2014-09-05
N1 - SubjectsTermNotLitGenreText - Heart; Databases; Cardiomyopathy; Acetylation; ubiquitination; proteasomes; Therapeutic applications; Lysine; proteomics; Ischemia
DO - http://dx.doi.org/10.1002/prca.201400029
ER -
TY - JOUR
T1 - Characterization of human plasma proteome dynamics using deuterium oxide
AN - 1560117667; 20584495
AB - Purpose High-throughput quantification of human protein turnover via in vivo administration of deuterium oxide ( super(2)H sub(2)O) is a powerful new approach to examine potential disease mechanisms. Its immediate clinical translation is contingent upon characterizations of the safety and hemodynamic effects of in vivo administration of super(2)H sub(2)O to human subjects. Experimental design We recruited ten healthy human subjects with a broad demographic variety to evaluate the safety, feasibility, efficacy, and reproducibility of super(2)H sub(2)O intake for studying protein dynamics. We designed a protocol where each subject orally consumed weight-adjusted doses of 70% super(2)H sub(2)O daily for 14 days to enrich body water and proteins with deuterium. Plasma proteome dynamics was measured using a high-resolution MS method we recently developed. Results This protocol was successfully applied in ten human subjects to characterize the endogenous turnover rates of 542 human plasma proteins, the largest such human dataset to-date. Throughout the study, we did not detect physiological effects or signs of discomfort from super(2)H sub(2)O consumption. Conclusions and clinical relevance Our investigation supports the utility of a super(2)H sub(2)O intake protocol that is safe, accessible, and effective for clinical investigations of large-scale human protein turnover dynamics. This workflow shows promising clinical translational value for examining plasma protein dynamics in human diseases.
JF - Proteomics Clinical Applications
AU - Wang, Ding
AU - Liem, David A
AU - Lau, Edward
AU - Ng, Dominic CM
AU - Bleakley, Brian J
AU - Cadeiras, Martin
AU - Deng, Mario C
AU - Lam, Maggie PY
AU - Ping, Peipei
AD - The NHLBI Proteomics Center at UCLA, Los Angeles, CA, USA.
Y1 - 2014/08//
PY - 2014
DA - Aug 2014
SP - 610
EP - 619
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 8
IS - 7-8
SN - 1862-8346, 1862-8346
KW - Biotechnology and Bioengineering Abstracts
KW - Plasma proteins
KW - Demography
KW - Translation
KW - Protein turnover
KW - oxides
KW - Hemodynamics
KW - Therapeutic applications
KW - Body water
KW - proteomics
KW - W 30960:Bioinformatics & Computer Applications
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1560117667?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proteomics+Clinical+Applications&rft.atitle=Characterization+of+human+plasma+proteome+dynamics+using+deuterium+oxide&rft.au=Wang%2C+Ding%3BLiem%2C+David+A%3BLau%2C+Edward%3BNg%2C+Dominic+CM%3BBleakley%2C+Brian+J%3BCadeiras%2C+Martin%3BDeng%2C+Mario+C%3BLam%2C+Maggie+PY%3BPing%2C+Peipei&rft.aulast=Wang&rft.aufirst=Ding&rft.date=2014-08-01&rft.volume=8&rft.issue=7-8&rft.spage=610&rft.isbn=&rft.btitle=&rft.title=Proteomics+Clinical+Applications&rft.issn=18628346&rft_id=info:doi/10.1002%2Fprca.201400038
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-09-01
N1 - Last updated - 2014-09-05
N1 - SubjectsTermNotLitGenreText - Demography; Plasma proteins; Translation; Therapeutic applications; Hemodynamics; oxides; Protein turnover; Body water; proteomics
DO - http://dx.doi.org/10.1002/prca.201400038
ER -
TY - JOUR
T1 - A Rapid Matrix-Assisted Laser Desorption Ionization-Time of Flight Mass Spectrometry-Based Method for Single-Plasmid Tracking in an Outbreak of Carbapenem-Resistant Enterobacteriaceae
AN - 1560115334; 20602801
AB - Carbapenem-resistant Enterobacteriaceae (CRE) have spread globally and represent a serious and growing threat to public health. Rapid methods for tracking plasmids carrying carbapenemase genes could greatly benefit infection control efforts. Here, we demonstrate that real-time, direct tracking of a single plasmid in a bacterial strain responsible for an outbreak is possible using a commercial matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS) system. In this case, we retrospectively tracked the blaKPC carbapenemase gene-bearing pKpQIL plasmid responsible for a CRE outbreak that occurred at the NIH Clinical Center in 2011. An similar to 11,109-Da MS peak corresponding to a gene product of the blaKPC pKpQIL plasmid was identified and characterized using a combination of proteomics and molecular techniques. This plasmid peak was present in spectra from retrospectively analyzed K. pneumoniae outbreak isolates, concordant with results from whole-genome sequencing, and absent from a diverse control set of blaKPC-negative clinical Enterobacteriaceae isolates. Notably, the gene characterized here is located adjacent to the blaKPC Tn4401 transposon on the pKpQIL plasmid. Sequence analysis demonstrates the presence of this gene in other blaKPC Tn4401-containing plasmids and suggests that this signature MS peak may be useful in tracking other plasmids conferring carbapenem resistance. Plasmid identification using this MALDI-TOF MS method was accomplished in as little as 10 min from isolated colonies and 30 min from positive (spiked) blood cultures, demonstrating the potential clinical utility for real-time plasmid tracking in an outbreak.
JF - Journal of Clinical Microbiology
AU - Lau, Anna F
AU - Wang, Honghui
AU - Weingarten, Rebecca A
AU - Drake, Steven K
AU - Suffredini, Anthony F
AU - Garfield, Mark K
AU - Chen, Yong
AU - Gucek, Marjan
AU - Youn, Jung-Ho
AU - Stock, Frida
AD - Microbiology Service, Department of Laboratory Medicine, Clinical Center, National Institutes of Health, Bethesda, Maryland, USA, john.dekker@nih.gov.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 2804
EP - 2812
PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL - 52
IS - 8
SN - 0095-1137, 0095-1137
KW - Health & Safety Science Abstracts; Microbiology Abstracts B: Bacteriology
KW - Blood culture
KW - Mass spectrometry
KW - Carbapenems
KW - carbapenemase
KW - Plasmids
KW - Infection
KW - Mass spectroscopy
KW - Public health
KW - Flight
KW - Transposons
KW - Colonies
KW - Lasers
KW - Outbreaks
KW - proteomics
KW - Enterobacteriaceae
KW - Klebsiella pneumoniae
KW - H 12000:Epidemiology and Public Health
KW - J 02400:Human Diseases
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1560115334?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Clinical+Microbiology&rft.atitle=A+Rapid+Matrix-Assisted+Laser+Desorption+Ionization-Time+of+Flight+Mass+Spectrometry-Based+Method+for+Single-Plasmid+Tracking+in+an+Outbreak+of+Carbapenem-Resistant+Enterobacteriaceae&rft.au=Lau%2C+Anna+F%3BWang%2C+Honghui%3BWeingarten%2C+Rebecca+A%3BDrake%2C+Steven+K%3BSuffredini%2C+Anthony+F%3BGarfield%2C+Mark+K%3BChen%2C+Yong%3BGucek%2C+Marjan%3BYoun%2C+Jung-Ho%3BStock%2C+Frida&rft.aulast=Lau&rft.aufirst=Anna&rft.date=2014-08-01&rft.volume=52&rft.issue=8&rft.spage=2804&rft.isbn=&rft.btitle=&rft.title=Journal+of+Clinical+Microbiology&rft.issn=00951137&rft_id=info:doi/10.1128%2FJCM.00694-14
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-09-01
N1 - Number of references - 45
N1 - Last updated - 2016-07-20
N1 - SubjectsTermNotLitGenreText - Transposons; Flight; Blood culture; Colonies; Carbapenems; carbapenemase; Lasers; proteomics; Infection; Plasmids; Mass spectroscopy; Public health; Mass spectrometry; Outbreaks; Enterobacteriaceae; Klebsiella pneumoniae
DO - http://dx.doi.org/10.1128/JCM.00694-14
ER -
TY - JOUR
T1 - Plasmodium falciparum Founder Populations in Western Cambodia Have Reduced Artemisinin Sensitivity In Vitro
AN - 1560113395; 20602567
AB - Reduced Plasmodium falciparum sensitivity to short-course artemisinin (ART) monotherapy manifests as a long parasite clearance half-life. We recently defined three parasite founder populations with long half-lives in Pursat, western Cambodia, where reduced ART sensitivity is prevalent. Using the ring-stage survival assay, we show that these founder populations have reduced ART sensitivity in vitro at the early ring stage of parasite development and that a genetically admixed population contains subsets of parasites with normal or reduced ART sensitivity.
JF - Antimicrobial Agents & Chemotherapy
AU - Amaratunga, Chanaki
AU - Witkowski, Benoit
AU - Dek, Dalin
AU - Try, Vorleak
AU - Khim, Nimol
AU - Miotto, Olivo
AU - Menard, Didier
AU - Fairhurst, Rick M
AD - Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA, rfairhurst@niaid.nih.gov.
Y1 - 2014/08//
PY - 2014
DA - Aug 2014
SP - 4935
EP - 4937
PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL - 58
IS - 8
SN - 0066-4804, 0066-4804
KW - Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts A: Industrial & Applied Microbiology
KW - Parasites
KW - Population genetics
KW - Developmental stages
KW - Survival
KW - artemisinin
KW - Plasmodium falciparum
KW - K 03340:Effects of Physical & Chemical Factors
KW - A 01340:Antibiotics & Antimicrobials
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1560113395?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Antimicrobial+Agents+%26+Chemotherapy&rft.atitle=Plasmodium+falciparum+Founder+Populations+in+Western+Cambodia+Have+Reduced+Artemisinin+Sensitivity+In+Vitro&rft.au=Amaratunga%2C+Chanaki%3BWitkowski%2C+Benoit%3BDek%2C+Dalin%3BTry%2C+Vorleak%3BKhim%2C+Nimol%3BMiotto%2C+Olivo%3BMenard%2C+Didier%3BFairhurst%2C+Rick+M&rft.aulast=Amaratunga&rft.aufirst=Chanaki&rft.date=2014-08-01&rft.volume=58&rft.issue=8&rft.spage=4935&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+Agents+%26+Chemotherapy&rft.issn=00664804&rft_id=info:doi/10.1128%2FAAC.03055-14
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-09-01
N1 - Number of references - 19
N1 - Last updated - 2014-10-30
N1 - SubjectsTermNotLitGenreText - Population genetics; Parasites; Survival; Developmental stages; artemisinin; Plasmodium falciparum
DO - http://dx.doi.org/10.1128/AAC.03055-14
ER -
TY - JOUR
T1 - Retirement of Hugh A. Tilson
AN - 1560113185; 20594452
JF - Environmental Health Perspectives
AU - Birnbaum, Linda S
AU - Woychik, Rick
AD - National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA
Y1 - 2014/08/01/
PY - 2014
DA - 2014 Aug 01
SP - A202
PB - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States
VL - 122
IS - 8
SN - 0091-6765, 0091-6765
KW - Environment Abstracts; Health & Safety Science Abstracts
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1560113185?accountid=14244
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-09-01
N1 - Last updated - 2014-09-05
DO - http://dx.doi.org/10.1289/ehp.1408939
ER -
TY - JOUR
T1 - Flow Cytometry-Based Analysis of Artemisinin-Resistant Plasmodium falciparum in the Ring-Stage Survival Assay
AN - 1560112058; 20602558
AB - The ring-stage survival assay (RSA) is a powerful tool for phenotyping artemisinin-resistant Plasmodium falciparum but requires experienced microscopists to count viable parasites among 10,000 erythrocytes in Giemsa-stained thin blood smears. Here we describe a rapid flow cytometric assay that accurately counts viable parasites among 250,000 erythrocytes in suspension. This method performs as well as light microscopy and can be used to standardize the collection of RSA data between research groups in laboratory and field settings.
JF - Antimicrobial Agents & Chemotherapy
AU - Amaratunga, Chanaki
AU - Neal, Aaron T
AU - Fairhurst, Rick M
Y1 - 2014/08//
PY - 2014
DA - Aug 2014
SP - 4938
EP - 4940
PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL - 58
IS - 8
SN - 0066-4804, 0066-4804
KW - Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts A: Industrial & Applied Microbiology
KW - Flow cytometry
KW - Parasites
KW - Blood
KW - Phenotyping
KW - Data processing
KW - Erythrocytes
KW - Survival
KW - Plasmodium falciparum
KW - A 01340:Antibiotics & Antimicrobials
KW - K 03420:Plant Diseases
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1560112058?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Antimicrobial+Agents+%26+Chemotherapy&rft.atitle=Flow+Cytometry-Based+Analysis+of+Artemisinin-Resistant+Plasmodium+falciparum+in+the+Ring-Stage+Survival+Assay&rft.au=Amaratunga%2C+Chanaki%3BNeal%2C+Aaron+T%3BFairhurst%2C+Rick+M&rft.aulast=Amaratunga&rft.aufirst=Chanaki&rft.date=2014-08-01&rft.volume=58&rft.issue=8&rft.spage=4938&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+Agents+%26+Chemotherapy&rft.issn=00664804&rft_id=info:doi/10.1128%2FAAC.02902-14
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-09-01
N1 - Number of references - 14
N1 - Last updated - 2014-10-30
N1 - SubjectsTermNotLitGenreText - Flow cytometry; Phenotyping; Blood; Parasites; Data processing; Erythrocytes; Survival; Plasmodium falciparum
DO - http://dx.doi.org/10.1128/AAC.02902-14
ER -
TY - JOUR
T1 - Repurposing of Clinically Developed Drugs for Treatment of Middle East Respiratory Syndrome Coronavirus Infection
AN - 1560106868; 20602565
AB - Outbreaks of emerging infections present health professionals with the unique challenge of trying to select appropriate pharmacologic treatments in the clinic with little time available for drug testing and development. Typically, clinicians are left with general supportive care and often untested convalescent-phase plasma as available treatment options. Repurposing of approved pharmaceutical drugs for new indications presents an attractive alternative to clinicians, researchers, public health agencies, drug developers, and funding agencies. Given the development times and manufacturing requirements for new products, repurposing of existing drugs is likely the only solution for outbreaks due to emerging viruses. In the studies described here, a library of 290 compounds was screened for antiviral activity against Middle East respiratory syndrome coronavirus (MERS-CoV) and severe acute respiratory syndrome coronavirus (SARS-CoV). Selection of compounds for inclusion in the library was dependent on current or previous FDA approval or advanced clinical development. Some drugs that had a well-defined cellular pathway as target were included. In total, 27 compounds with activity against both MERS-CoV and SARS-CoV were identified. The compounds belong to 13 different classes of pharmaceuticals, including inhibitors of estrogen receptors used for cancer treatment and inhibitors of dopamine receptor used as antipsychotics. The drugs identified in these screens provide new targets for in vivo studies as well as incorporation into ongoing clinical studies.
JF - Antimicrobial Agents & Chemotherapy
AU - Dyall, Julie
AU - Coleman, Christopher M
AU - Hart, Brit J
AU - Venkataraman, Thiagarajan
AU - Holbrook, Michael R
AU - Kindrachuk, Jason
AU - Johnson, Reed F
AU - Olinger, Gene G, Jr
AU - Jahrling, Peter B
AU - Laidlaw, Monique
AD - Integrated Research Facility, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Frederick, Maryland, USA, MFrieman@som.umaryland.edu.
Y1 - 2014/08//
PY - 2014
DA - Aug 2014
SP - 4885
EP - 4893
PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL - 58
IS - 8
SN - 0066-4804, 0066-4804
KW - Virology & AIDS Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology
KW - Severe acute respiratory syndrome
KW - Drug development
KW - Infection
KW - Dopamine receptors
KW - Antiviral activity
KW - Cancer
KW - Public health
KW - Antiviral agents
KW - Neuroleptics
KW - Pharmaceuticals
KW - Estrogen receptors
KW - SARS coronavirus
KW - A 01340:Antibiotics & Antimicrobials
KW - V 22410:Animal Diseases
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1560106868?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Antimicrobial+Agents+%26+Chemotherapy&rft.atitle=Repurposing+of+Clinically+Developed+Drugs+for+Treatment+of+Middle+East+Respiratory+Syndrome+Coronavirus+Infection&rft.au=Dyall%2C+Julie%3BColeman%2C+Christopher+M%3BHart%2C+Brit+J%3BVenkataraman%2C+Thiagarajan%3BHolbrook%2C+Michael+R%3BKindrachuk%2C+Jason%3BJohnson%2C+Reed+F%3BOlinger%2C+Gene+G%2C+Jr%3BJahrling%2C+Peter+B%3BLaidlaw%2C+Monique&rft.aulast=Dyall&rft.aufirst=Julie&rft.date=2014-08-01&rft.volume=58&rft.issue=8&rft.spage=4885&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+Agents+%26+Chemotherapy&rft.issn=00664804&rft_id=info:doi/10.1128%2FAAC.03036-14
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-09-01
N1 - Number of references - 48
N1 - Last updated - 2014-12-11
N1 - SubjectsTermNotLitGenreText - Antiviral agents; Neuroleptics; Severe acute respiratory syndrome; Pharmaceuticals; Drug development; Antiviral activity; Dopamine receptors; Infection; Estrogen receptors; Cancer; Public health; SARS coronavirus
DO - http://dx.doi.org/10.1128/AAC.03036-14
ER -
TY - JOUR
T1 - Threshold and subthreshold generalized anxiety disorder among US adolescents: prevalence, sociodemographic, and clinical characteristics
AN - 1558992596; 201428182
AB - Threshold and subthreshold forms of generalized anxiety disorder (GAD) are highly prevalent and impairing conditions among adults. However, there are few general population studies that have examined these conditions during the early life course. The primary objectives of this study were to: (1) examine the prevalence, and sociodemographic and clinical characteristics of threshold and subthreshold forms of GAD in a nationally representative sample of US youth; and (2) test differences in sociodemographic and clinical characteristics between threshold and subthreshold forms of the disorder. The National Comorbidity Survey-Adolescent Supplement is a nationally representative face-to-face survey of 10 123 adolescents 13 to 18 years of age in the continental USA. Approximately 3% of adolescents met criteria for threshold GAD. Reducing the required duration from 6 months to 3 months resulted in a 65.7% increase in prevalence (5.0%); further relaxing the uncontrollability criterion led to an additional 20.7% increase in prevalence (6.1%). Adolescents with all forms of GAD displayed a recurrent clinical course marked by substantial impairment and co-morbidity with other psychiatric disorders. There were few significant differences in sociodemographic and clinical characteristics between threshold and subthreshold cases of GAD. Results also revealed age-related differences in the associated symptoms and clinical course of GAD. Findings demonstrate the clinical significance of subthreshold forms of GAD among adolescent youth, highlighting the continuous nature of the GAD construct. Age-related differences in the associated symptoms and clinical course of GAD provide further support for criteria that capture variation in clinical features across development. Adapted from the source document.
JF - Psychological Medicine
AU - Burstein, M
AU - Beesdo-Baum, K
AU - He, J.-P.
AU - Merikangas, K R
AD - Genetic Epidemiology Research Branch, National Institute of Mental Health, Bethesda, MD, USA
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 2351
EP - 2362
PB - Cambridge University Press, UK
VL - 44
IS - 11
SN - 0033-2917, 0033-2917
KW - Generalized anxiety disorders
KW - Sociodemographic aspects
KW - Comorbidity
KW - Adolescents
KW - Thresholds
KW - Prevalence
KW - article
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Psychological+Medicine&rft.atitle=Threshold+and+subthreshold+generalized+anxiety+disorder+among+US+adolescents%3A+prevalence%2C+sociodemographic%2C+and+clinical+characteristics&rft.au=Burstein%2C+M%3BBeesdo-Baum%2C+K%3BHe%2C+J.-P.%3BMerikangas%2C+K+R&rft.aulast=Burstein&rft.aufirst=M&rft.date=2014-08-01&rft.volume=44&rft.issue=11&rft.spage=2351&rft.isbn=&rft.btitle=&rft.title=Psychological+Medicine&rft.issn=00332917&rft_id=info:doi/10.1017%2FS0033291713002997
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Date revised - 2014-09-01
N1 - Number of references - 43
N1 - Last updated - 2016-09-27
N1 - CODEN - PSMDCO
N1 - SubjectsTermNotLitGenreText - Generalized anxiety disorders; Thresholds; Adolescents; Prevalence; Sociodemographic aspects; Comorbidity
DO - http://dx.doi.org/10.1017/S0033291713002997
ER -
TY - JOUR
T1 - Longitudinal relationship between drinking with peers, descriptive norms, and adolescent alcohol use
AN - 1556285609; 4591076
AB - Descriptive norms are consistently found to predict adolescent alcohol use but less is known about the factors that predict descriptive norms. The objective of this study is to test if drinking with peers predicts later alcohol consumption and if this relationship is mediated by a change in the descriptive norms of peer alcohol use. Data are from a nationally representative cohort of high school students surveyed in the 10th and 11th grade ( Italic N = 2,162). Structural equation modeling was used to test a mediation model of the relationship between drinking with peers (T1) on later alcohol use (T2) and mediation of the relationship by descriptive norms (T2). Descriptive norms significantly mediated the relationship between drinking with peers and alcohol use for both males and females with a somewhat larger effect for males compared to females. These results support a continued focus on the development and evaluation of interventions to alter descriptive norms of alcohol use. Reprinted by permission of Springer
JF - Prevention science
AU - Brooks-Russell, Ashley
AU - Simons-Morton, Bruce
AU - Haynie, Denise
AU - Farhat, Tilda
AU - Wang, Jing
AD - Eunice Kennedy Shriver National Institute of Child Health and Human Development
Y1 - 2014/08//
PY - 2014
DA - Aug 2014
SP - 497
EP - 505
VL - 15
IS - 4
SN - 1389-4986, 1389-4986
KW - Sociology
KW - Alcohol
KW - Peer groups
KW - Structural analysis
KW - Adolescents
KW - Interventionism
KW - Mediation
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1556285609?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Prevention+science&rft.atitle=Longitudinal+relationship+between+drinking+with+peers%2C+descriptive+norms%2C+and+adolescent+alcohol+use&rft.au=Brooks-Russell%2C+Ashley%3BSimons-Morton%2C+Bruce%3BHaynie%2C+Denise%3BFarhat%2C+Tilda%3BWang%2C+Jing&rft.aulast=Brooks-Russell&rft.aufirst=Ashley&rft.date=2014-08-01&rft.volume=15&rft.issue=4&rft.spage=497&rft.isbn=&rft.btitle=&rft.title=Prevention+science&rft.issn=13894986&rft_id=info:doi/10.1007%2Fs11121-013-0391-9
LA - English
DB - International Bibliography of the Social Sciences (IBSS)
N1 - Date revised - 2014-08-26
N1 - Last updated - 2014-08-27
N1 - SubjectsTermNotLitGenreText - 7869 2703 2698; 909; 9347; 12320 971; 6828 7869 2703 2698 5200 5574 10472; 593
DO - http://dx.doi.org/10.1007/s11121-013-0391-9
ER -
TY - JOUR
T1 - Estimating the burden of pertussis in Mexican adolescents from paired serological data by using a bivariate mixture model
AN - 1556285182; 4591115
AB - In recent decades there has been an increase in the reported incidence of clinical pertussis in many countries. Estimation of the true circulation of the bacterium Bordetella pertussis is most reliably made on the basis of studies that measure antibody concentrations against pertussis toxin. Antibody levels decay over time and provide a fading memory of the infection. We develop a discrete bivariate mixture model for paired antibody levels in a cohort of 1002 Mexican adolescents who were followed over the 2008-2009 school year. This model postulates three groups of children based on past pertussis infection; never, prior and new. On the basis of this model we directly estimate incidence and prevalence, and select a diagnostic cut-off for classifying children as recently infected. We also discuss a relatively simple approach that uses only 'discordant' children who test positively on one visit and negatively on the other. The discordant approach provides inferences that are very similar to those of the full model when the data follow the assumed full model. Additionally, the discordant method is much more robust to model misspecification than the full model which has substantial problems with optimization. We estimate the school year incidence of pertussis to be about 3% and the prevalence to be about 8%. A cut-off of 50 was estimated to have about 99.5% specificity and 68% sensitvity. Reprinted by permission of Blackwell Publishers
JF - Journal of the Royal Statistical Society
AU - Gabrielle Breugelmans, J
AU - Rosales Pedraza, Gustave
AU - Gessner, Bradford D
AU - Ruiz-Palacios, Guillermo M
AU - Follmann, Dean
AU - Qin, Jing
AU - Lourdes Guerrero, M
AD - National Institute of Allergy and Infectious Diseases ; Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán
Y1 - 2014/08//
PY - 2014
DA - Aug 2014
SP - 621
EP - 637
VL - 63
IS - 4
SN - 0035-9254, 0035-9254
KW - Economics
KW - Memory
KW - Mexico
KW - Schools
KW - Estimation
KW - Children
KW - Serology
KW - Adolescents
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+Royal+Statistical+Society&rft.atitle=Estimating+the+burden+of+pertussis+in+Mexican+adolescents+from+paired+serological+data+by+using+a+bivariate+mixture+model&rft.au=Gabrielle+Breugelmans%2C+J%3BRosales+Pedraza%2C+Gustave%3BGessner%2C+Bradford+D%3BRuiz-Palacios%2C+Guillermo+M%3BFollmann%2C+Dean%3BQin%2C+Jing%3BLourdes+Guerrero%2C+M&rft.aulast=Gabrielle+Breugelmans&rft.aufirst=J&rft.date=2014-08-01&rft.volume=63&rft.issue=4&rft.spage=621&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+Royal+Statistical+Society&rft.issn=00359254&rft_id=info:doi/10.1111%2Frssc.12051
LA - English
DB - International Bibliography of the Social Sciences (IBSS)
N1 - Date revised - 2014-08-26
N1 - Last updated - 2014-08-27
N1 - SubjectsTermNotLitGenreText - 4403 7854; 2212; 7930; 593; 11324; 11525 9507 1077; 251 293 14
DO - http://dx.doi.org/10.1111/rssc.12051
ER -
TY - JOUR
T1 - Developing estimates of frequency and intensity of exposure to three types of metalworking fluids in a population-based case-control study of bladder cancer
AN - 1554955814; 20446176
AB - Background A systematic, transparent, and data-driven approach was developed to estimate frequency and intensity of exposure to straight, soluble, and synthetic/semi-synthetic metalworking fluids (MWFs) within a case-control study of bladder cancer in New England. Methods We assessed frequency using individual-level information from job-specific questionnaires wherever possible, then derived and applied job group-level patterns to likely exposed jobs with less information. Intensity estimates were calculated using a statistical model developed from measurements and determinants extracted from the published literature. Results For jobs with probabilities of exposure greater than or equal to 0.5, median frequencies were 8-10hr/week, depending on MWF type. Median intensities for these jobs were 2.5, 2.1, and 1.0mg/m super(3) for soluble, straight, and synthetic/semi-synthetic MWFs, respectively. Conclusions Compared to case-by-case assessment, these data-driven decision rules are transparent and reproducible and may result in less biased estimates. These rules can also aid future exposure assessments of MWFs in population-based studies. Am. J. Ind. Med. 57:915-927, 2014. copyright 2014 Wiley Periodicals, Inc.
JF - American Journal of Industrial Medicine
AU - Friesen, Melissa C
AU - Park, Dong-Uk
AU - Colt, Joanne S
AU - Baris, Dalsu
AU - Schwenn, Molly
AU - Karagas, Margaret R
AU - Armenti, Karla R
AU - Johnson, Alison
AU - Silverman, Debra T
AU - Stewart, Patricia A
AD - Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, DHHS, Rockville, Maryland.
Y1 - 2014/08//
PY - 2014
DA - Aug 2014
SP - 915
EP - 927
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 57
IS - 8
SN - 0271-3586, 0271-3586
KW - Toxicology Abstracts; Health & Safety Science Abstracts
KW - Inventories
KW - Mathematical models
KW - USA, New England
KW - Urinary bladder
KW - Statistical analysis
KW - Population studies
KW - Metal-working fluids
KW - Cancer
KW - Models
KW - X 24360:Metals
KW - H 1000:Occupational Safety and Health
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Industrial+Medicine&rft.atitle=Developing+estimates+of+frequency+and+intensity+of+exposure+to+three+types+of+metalworking+fluids+in+a+population-based+case-control+study+of+bladder+cancer&rft.au=Friesen%2C+Melissa+C%3BPark%2C+Dong-Uk%3BColt%2C+Joanne+S%3BBaris%2C+Dalsu%3BSchwenn%2C+Molly%3BKaragas%2C+Margaret+R%3BArmenti%2C+Karla+R%3BJohnson%2C+Alison%3BSilverman%2C+Debra+T%3BStewart%2C+Patricia+A&rft.aulast=Friesen&rft.aufirst=Melissa&rft.date=2014-08-01&rft.volume=57&rft.issue=8&rft.spage=915&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Industrial+Medicine&rft.issn=02713586&rft_id=info:doi/10.1002%2Fajim.22328
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-08-01
N1 - Last updated - 2014-11-12
N1 - SubjectsTermNotLitGenreText - Inventories; Mathematical models; Urinary bladder; Statistical analysis; Population studies; Cancer; Models; Metal-working fluids; USA, New England
DO - http://dx.doi.org/10.1002/ajim.22328
ER -
TY - JOUR
T1 - Lung tumors in mice induced by "whole-life" inorganic arsenic exposure at human-relevant doses
AN - 1554949668; 20489398
AB - In mice, inorganic arsenic in the drinking water in the parts per million range via the dam during in utero life or with whole-life exposure is a multi-site carcinogen in the offspring. However, human arsenic exposure is typically in the parts per billion (ppb) range. Thus, we studied "whole-life" inorganic arsenic carcinogenesis in mice at levels more relevant to humans. Breeder male and female CD1 mice were exposed to 0, 50, 500 or 5,000 ppb arsenic (as sodium arsenite) in the drinking water for 3 weeks prior to breeding, during pregnancy and lactation, and after weaning (at week 3) groups of male and female offspring (initial n = 40) were exposed for up to 2 years. Tumors were assessed in these offspring. Arsenic exposure had no effect on pregnant dam weights or water consumption, litter size, offspring birthweight or weight at weaning compared to control. In male offspring mice, arsenic exposure increased (p < 0.05) bronchiolo-alveolar tumor (adenoma or carcinoma) incidence at 50-ppb group (51 %) and 500-ppb group (54 %), but not at 5,000-ppb group (28 %) compared to control (22 %). These arsenic-induced bronchiolo-alveolar tumors included increased (p < 0.05) carcinoma at 50-ppb group (27 %) compared to controls (8 %). An increase (p < 0.05) in lung adenoma (25 %) in the 50-ppb group compared to control (11 %) occurred in female offspring. Thus, in CD1 mice whole-life arsenic exposure induced lung tumors at human-relevant doses (i.e., 50 and 500 ppb).
JF - Archives of Toxicology
AU - Waalkes, Michael P
AU - Qu, Wei
AU - Tokar, Erik J
AU - Kissling, Grace E
AU - Dixon, Darlene
AD - Inorganic Toxicology Group, National Toxicology Program Laboratory, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, 111 Alexander Drive, MD E1-07, P.O. Box 12233, Research Triangle Park, NC, 27709, USA, waalkes@niehs.nih.gov
Y1 - 2014/08//
PY - 2014
DA - Aug 2014
SP - 1619
EP - 1629
PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL - 88
IS - 8
SN - 0340-5761, 0340-5761
KW - Toxicology Abstracts
KW - Birth weight
KW - Litter
KW - Arsenic
KW - Sodium arsenite
KW - Weaning
KW - Tumors
KW - Carcinogens
KW - Pregnancy
KW - Carcinoma
KW - Lactation
KW - Breeding
KW - Lung
KW - Carcinogenesis
KW - Progeny
KW - Drinking water
KW - Adenoma
KW - X 24360:Metals
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+Toxicology&rft.atitle=Lung+tumors+in+mice+induced+by+%22whole-life%22+inorganic+arsenic+exposure+at+human-relevant+doses&rft.au=Waalkes%2C+Michael+P%3BQu%2C+Wei%3BTokar%2C+Erik+J%3BKissling%2C+Grace+E%3BDixon%2C+Darlene&rft.aulast=Waalkes&rft.aufirst=Michael&rft.date=2014-08-01&rft.volume=88&rft.issue=8&rft.spage=1619&rft.isbn=&rft.btitle=&rft.title=Archives+of+Toxicology&rft.issn=03405761&rft_id=info:doi/10.1007%2Fs00204-014-1305-8
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-08-01
N1 - Number of references - 35
N1 - Last updated - 2015-04-16
N1 - SubjectsTermNotLitGenreText - Birth weight; Arsenic; Litter; Sodium arsenite; Weaning; Carcinogens; Tumors; Lactation; Carcinoma; Pregnancy; Breeding; Lung; Carcinogenesis; Progeny; Drinking water; Adenoma
DO - http://dx.doi.org/10.1007/s00204-014-1305-8
ER -
TY - JOUR
T1 - Strain-specific properties and T cells regulate the susceptibility to papilloma induction by Mus musculus papillomavirus 1.
AN - 1553709212; 25121947
AB - The immunocytes that regulate papillomavirus infection and lesion development in humans and animals remain largely undefined. We found that immunocompetent mice with varying H-2 haplotypes displayed asymptomatic skin infection that produced L1 when challenged with 6×1010 MusPV1 virions, the recently identified domestic mouse papillomavirus (also designated "MmuPV1"), but were uniformly resistant to MusPV1-induced papillomatosis. Broad immunosuppression with cyclosporin A resulted in variable induction of papillomas after experimental infection with a similar dose, from robust in Cr:ORL SENCAR to none in C57BL/6 mice, with lesional outgrowth correlating with early viral gene expression and partly with reported strain-specific susceptibility to chemical carcinogens, but not with H-2 haplotype. Challenge with 1×1012 virions in the absence of immunosuppression induced small transient papillomas in Cr:ORL SENCAR but not in C57BL/6 mice. Antibody-induced depletion of CD3+ T cells permitted efficient virus replication and papilloma formation in both strains, providing experimental proof for the crucial role of T cells in controlling papillomavirus infection and associated disease. In Cr:ORL SENCAR mice, immunodepletion of either CD4+ or CD8+ T cells was sufficient for efficient infection and papillomatosis, although deletion of one subset did not inhibit the recruitment of the other subset to the infected epithelium. Thus, the functional cooperation of CD4+ and CD8+ T cells is required to protect this strain. In contrast, C57BL/6 mice required depletion of both CD4+ and CD8+ T cells for infection and papillomatosis, and separate CD4 knock-out and CD8 knock-out C57BL/6 were also resistant. Thus, in C57BL/6 mice, either CD4+ or CD8+ T cell-independent mechanisms exist that can protect this particular strain from MusPV1-associated disease. These findings may help to explain the diversity of pathological outcomes in immunocompetent humans after infection with a specific human papillomavirus genotype.
JF - PLoS pathogens
AU - Handisurya, Alessandra
AU - Day, Patricia M
AU - Thompson, Cynthia D
AU - Bonelli, Michael
AU - Lowy, Douglas R
AU - Schiller, John T
AD - Laboratory of Cellular Oncology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America. ; Lymphocyte Cell Biology Section, Molecular Immunology and Inflammation Branch, National Institute of Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, United States of America; Division of Rheumatology, Internal Medicine III, General Hospital of Vienna, Medical University of Vienna, Vienna, Austria.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 1
VL - 10
IS - 8
KW - Index Medicus
KW - Animals
KW - Mice, Inbred C57BL
KW - Papillomaviridae
KW - Mice
KW - Flow Cytometry
KW - Mice, Inbred SENCAR
KW - Fluorescent Antibody Technique
KW - Mice, Knockout
KW - CD8-Positive T-Lymphocytes -- immunology
KW - CD4-Positive T-Lymphocytes -- immunology
KW - Disease Susceptibility -- immunology
KW - Papillomavirus Infections -- immunology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PLoS+pathogens&rft.atitle=Strain-specific+properties+and+T+cells+regulate+the+susceptibility+to+papilloma+induction+by+Mus+musculus+papillomavirus+1.&rft.au=Handisurya%2C+Alessandra%3BDay%2C+Patricia+M%3BThompson%2C+Cynthia+D%3BBonelli%2C+Michael%3BLowy%2C+Douglas+R%3BSchiller%2C+John+T&rft.aulast=Handisurya&rft.aufirst=Alessandra&rft.date=2014-08-01&rft.volume=10&rft.issue=8&rft.spage=e1004314&rft.isbn=&rft.btitle=&rft.title=PLoS+pathogens&rft.issn=1553-7374&rft_id=info:doi/10.1371%2Fjournal.ppat.1004314
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-12-21
N1 - Date created - 2014-08-15
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1371/journal.ppat.1004314
ER -
TY - JOUR
T1 - Molecular genetics and cellular features of TFE3 and TFEB fusion kidney cancers.
AN - 1552804484; 25048860
AB - Despite nearly two decades passing since the discovery of gene fusions involving TFE3 or TFEB in sporadic renal cell carcinoma (RCC), the molecular mechanisms underlying the renal-specific tumorigenesis of these genes remain largely unclear. The recently published findings of The Cancer Genome Atlas Network reported that five of the 416 surveyed clear cell RCC tumours (1.2%) harboured SFPQ-TFE3 fusions, providing further evidence for the importance of gene fusions. A total of five TFE3 gene fusions (PRCC-TFE3, ASPSCR1-TFE3, SFPQ-TFE3, NONO-TFE3, and CLTC-TFE3) and one TFEB gene fusion (MALAT1-TFEB) have been identified in RCC tumours and characterized at the mRNA transcript level. A multitude of molecular pathways well-described in carcinogenesis are regulated in part by TFE3 or TFEB proteins, including activation of TGFβ and ETS transcription factors, E-cadherin expression, CD40L-dependent lymphocyte activation, mTORC1 signalling, insulin-dependent metabolism regulation, folliculin signalling, and retinoblastoma-dependent cell cycle arrest. Determining which pathways are most important to RCC oncogenesis will be critical in discovering the most promising therapeutic targets for this disease.
JF - Nature reviews. Urology
AU - Kauffman, Eric C
AU - Ricketts, Christopher J
AU - Rais-Bahrami, Soroush
AU - Yang, Youfeng
AU - Merino, Maria J
AU - Bottaro, Donald P
AU - Srinivasan, Ramaprasad
AU - Linehan, W Marston
AD - Urologic Oncology Branch, National Cancer Institute, National Institutes of Health, Building 10, CRC Room 1-5940, Bethesda, MD 20892, USA. ; Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Building 10, CRC Room 1-5940, Bethesda, MD 20892, USA.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 465
EP - 475
VL - 11
IS - 8
KW - Basic Helix-Loop-Helix Leucine Zipper Transcription Factors
KW - 0
KW - Biomarkers, Tumor
KW - TFE3 protein, human
KW - TFEB protein, human
KW - Index Medicus
KW - Gene Expression Regulation, Neoplastic
KW - Carcinogenesis -- metabolism
KW - Carcinogenesis -- genetics
KW - Base Sequence
KW - Humans
KW - Molecular Sequence Data
KW - Kidney Neoplasms -- genetics
KW - Biomarkers, Tumor -- metabolism
KW - Biomarkers, Tumor -- genetics
KW - Carcinoma, Renal Cell -- metabolism
KW - Kidney Neoplasms -- metabolism
KW - Gene Fusion
KW - Carcinoma, Renal Cell -- genetics
KW - Basic Helix-Loop-Helix Leucine Zipper Transcription Factors -- metabolism
KW - Basic Helix-Loop-Helix Leucine Zipper Transcription Factors -- genetics
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1552804484?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+reviews.+Urology&rft.atitle=Molecular+genetics+and+cellular+features+of+TFE3+and+TFEB+fusion+kidney+cancers.&rft.au=Kauffman%2C+Eric+C%3BRicketts%2C+Christopher+J%3BRais-Bahrami%2C+Soroush%3BYang%2C+Youfeng%3BMerino%2C+Maria+J%3BBottaro%2C+Donald+P%3BSrinivasan%2C+Ramaprasad%3BLinehan%2C+W+Marston&rft.aulast=Kauffman&rft.aufirst=Eric&rft.date=2014-08-01&rft.volume=11&rft.issue=8&rft.spage=465&rft.isbn=&rft.btitle=&rft.title=Nature+reviews.+Urology&rft.issn=1759-4820&rft_id=info:doi/10.1038%2Fnrurol.2014.162
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-09-30
N1 - Date created - 2014-08-11
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1038/nrurol.2014.162
ER -
TY - JOUR
T1 - In vitro and in vivo activity of the low-immunogenic antimesothelin immunotoxin RG7787 in pancreatic cancer.
AN - 1552377267; 24928849
AB - Pancreatic ductal adenocarcinoma (PDAC) has a dismal prognosis, and new therapies are needed. RG7787 is a novel low-immunogenic antimesothelin recombinant immunotoxin (RIT), engineered to overcome the limitations of SS1P, a RIT now in clinical trials. In vitro activity was evaluated on five established PDAC cell lines (KLM-1, AsPC-1, BxPC-3, Panc 3.014, and PK-1) and on PDAC cells directly established from a patient tumor (GUMC108). RG7787 had subnanomolar IC50s in most cell lines, and was significantly more active than SS1P in GUMC108, KLM-1, and Panc 3.014 cells. GUMC108 was most sensitive, with RG7787 killing >99% of the cells. In a subcutaneous KLM-1 xenograft mouse model, two cycles of 3 × 2.5 mg/kg RG7787 QOD combined with two cycles of 1 × 50 mg/kg paclitaxel induced near-complete responses, with all tumors regressing below 5 mm(3) within 30 days after therapy was initiated (>95% decrease) and no significant growth increase for at least another 3 weeks. RG7787 alone gave limited but significant regressions and paclitaxel by itself arrested tumor growth. Quantifying the uptake of Alexa Fluor 647-labeled RG7787 in tumors showed that the RIT reached only 45% of KLM-1 cells, accounting in part for the limited responses. Paclitaxel did not improve RG7787 uptake, which thus cannot explain the beneficial effect of the combination therapy. In conclusion, RG7787 has high cytotoxic activity on PDAC cell lines as well as on primary patient cells. In vivo, this novel RIT gives durable near-complete tumor responses when combined with paclitaxel. RG7787 merits further evaluation for the treatment of PDAC.
©2014 American Association for Cancer Research.
JF - Molecular cancer therapeutics
AU - Hollevoet, Kevin
AU - Mason-Osann, Emily
AU - Liu, Xiu-fen
AU - Imhof-Jung, Sabine
AU - Niederfellner, Gerhard
AU - Pastan, Ira
AD - Laboratory of Molecular Biology, Center for Cancer Research, NCI, NIH, Bethesda, Maryland; Laboratory for Therapeutic and Diagnostic Antibodies, Department of Pharmaceutical and Pharmacological Sciences, KU Leuven, Leuven, Belgium; and. ; Laboratory of Molecular Biology, Center for Cancer Research, NCI, NIH, Bethesda, Maryland; ; Pharmaceutical Research and Early Development (pRED), Roche Innovation Center Penzberg, Germany. ; Laboratory of Molecular Biology, Center for Cancer Research, NCI, NIH, Bethesda, Maryland; pastani@mail.nih.gov.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 2040
EP - 2049
VL - 13
IS - 8
KW - Antibodies, Monoclonal
KW - 0
KW - Antineoplastic Agents
KW - GPI-Linked Proteins
KW - Immunoconjugates
KW - Protein Synthesis Inhibitors
KW - RG7787
KW - SS1(dsFv)PE38
KW - mesothelin
KW - Index Medicus
KW - Animals
KW - Apoptosis
KW - Antibodies, Monoclonal -- metabolism
KW - Humans
KW - Cell Line, Tumor
KW - Mice, Nude
KW - Antibodies, Monoclonal -- pharmacology
KW - Cell Proliferation
KW - Cell Survival
KW - GPI-Linked Proteins -- metabolism
KW - Protein Synthesis Inhibitors -- pharmacology
KW - Xenograft Model Antitumor Assays
KW - Female
KW - GPI-Linked Proteins -- immunology
KW - Pancreatic Neoplasms -- metabolism
KW - Immunoconjugates -- pharmacokinetics
KW - Carcinoma, Pancreatic Ductal -- metabolism
KW - Carcinoma, Pancreatic Ductal -- drug therapy
KW - Antineoplastic Agents -- pharmacokinetics
KW - Pancreatic Neoplasms -- drug therapy
KW - Immunoconjugates -- pharmacology
KW - Antineoplastic Agents -- pharmacology
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1552377267?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+cancer+therapeutics&rft.atitle=In+vitro+and+in+vivo+activity+of+the+low-immunogenic+antimesothelin+immunotoxin+RG7787+in+pancreatic+cancer.&rft.au=Hollevoet%2C+Kevin%3BMason-Osann%2C+Emily%3BLiu%2C+Xiu-fen%3BImhof-Jung%2C+Sabine%3BNiederfellner%2C+Gerhard%3BPastan%2C+Ira&rft.aulast=Hollevoet&rft.aufirst=Kevin&rft.date=2014-08-01&rft.volume=13&rft.issue=8&rft.spage=2040&rft.isbn=&rft.btitle=&rft.title=Molecular+cancer+therapeutics&rft.issn=1538-8514&rft_id=info:doi/10.1158%2F1535-7163.MCT-14-0089-T
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-05-11
N1 - Date created - 2014-08-07
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Clin Cancer Res. 2009 Aug 15;15(16):5274-9 [19671873]
Cancer Res. 2014 Jun 1;74(11):2907-12 [24824231]
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J Mol Graph. 1996 Feb;14(1):33-8, 27-8 [8744570]
Semin Cancer Biol. 1996 Apr;7(2):87-95 [8740564]
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N Engl J Med. 2012 Sep 27;367(13):1220-7 [23013073]
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Erratum In:
Mol Cancer Ther. 2015 Jul;14(7):1763 [26018754]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1158/1535-7163.MCT-14-0089-T
ER -
TY - CONF
T1 - Achieving professional success in US government, academia, and industry: an EMGS commentary.
AN - 1552373627; 24788591
AB - One of the goals of the EMGS is to help members achieve professional success in the fields they have trained in. Today, there is greater competition for jobs in genetic toxicology, genomics, and basic research than ever before. In addition, job security and the ability to advance in one's career is challenging, regardless of whether one works in a regulatory, academic, or industry environment. At the EMGS Annual Meeting in Monterey, CA (September, 2013), the Women in EMGS Special Interest Group held a workshop to discuss strategies for achieving professional success. Presentations were given by three speakers, each representing a different employment environment: Government (Miriam C. Poirier), Academia (Jeffrey L. Schwartz), and Industry (Marilyn J. Aardema). Although some differences in factors or traits affecting success in the three employment sectors were noted by each of the speakers, common factors considered important for advancement included networking, seeking out mentors, and developing exceptional communication skills.
© 2014 Wiley Periodicals, Inc.
JF - Environmental and molecular mutagenesis
AU - Poirier, Miriam C
AU - Schwartz, Jeffrey L
AU - Aardema, Marilyn J
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 525
EP - 529
VL - 55
IS - 7
KW - Index Medicus
KW - career development
KW - Government
KW - industry
KW - academia
KW - United States
KW - Humans
KW - Career Choice
KW - Female
KW - Universities -- manpower
KW - Women
KW - Industry -- manpower
KW - Employment
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1552373627?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=Environmental+and+molecular+mutagenesis&rft.atitle=Achieving+professional+success+in+US+government%2C+academia%2C+and+industry%3A+an+EMGS+commentary.&rft.au=Poirier%2C+Miriam+C%3BSchwartz%2C+Jeffrey+L%3BAardema%2C+Marilyn+J&rft.aulast=Poirier&rft.aufirst=Miriam&rft.date=2014-08-01&rft.volume=55&rft.issue=7&rft.spage=525&rft.isbn=&rft.btitle=&rft.title=Environmental+and+molecular+mutagenesis&rft.issn=1098-2280&rft_id=info:doi/10.1002%2Fem.21871
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-09-29
N1 - Date created - 2014-08-07
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1002/em.21871
ER -
TY - JOUR
T1 - Selective protection of zidovudine-induced DNA-damage by the antioxidants WR-1065 and tempol.
AN - 1552373610; 24833597
AB - The cytokinesis-block micronucleus cytome (CBMN) assay, introduced by Fenech, was used to demonstrate different types of DNA damage in MOLT-3 human lymphoblastoid cells exposed to 10 μM zidovudine (AZT). In addition, we explored the cytoprotective potential of two antioxidants, WR-1065 and Tempol, to decrease AZT-induced genotoxicity. Binucleated cells, arrested by Cytochalasin B (Cyt B), were evaluated for micronuclei (MN), caused by DNA damage or chromosomal loss, and chromatin nucleoplasmic bridges (NPBs), caused by telomere attrition. Additionally, nuclear buds (NBUDs), caused by amplified DNA, and apoptotic and necrotic (A/N) cells were scored. We hypothesized that AZT exposure would increase the frequency of genotoxic end points, and that the antioxidants Tempol and WR-1065 would protect against AZT-induced genotoxicity. MOLT-3 cells were exposed to 0 or 10 µM AZT for a total of 76 hr. After the first 24 hr, 0 or 5 µM WR-1065 and/or 0 or 200 µM Tempol were added for the remainder of the experiment. For the last 28 hr (of 76 hr), Cyt B was added to arrest replication after one cell division, leaving a predominance of binucleated cells. The nuclear division index (NDI) was similar for all treatment groups, indicating that the exposures did not alter cell viability. MOLT-3 cells exposed to AZT alone had significant (P < 0.05) increases in MN and NBs, compared to unexposed cells. Both Tempol and WR-1065 protected against AZT-induced MN formation (P < 0.003 for both), and WR-1065, but not Tempol, reduced the levels of A/N (P = 0.041). In cells exposed to AZT/Tempol there were significantly reduced levels of NBUDs, compared to cells exposed to AZT alone (P = 0.015). Cells exposed to AZT/WR-1065 showed reduced levels of NPBs, compared to cells exposed to AZT alone (P = 0.037). Thus WR-1065 and Tempol protected MOLT-3 cells against specific types of AZT-induced DNA damage.
© 2014 Wiley Periodicals, Inc.
JF - Environmental and molecular mutagenesis
AU - Olivero, Ofelia A
AU - Ongele, Michael O
AU - Braun, Hannan M
AU - Marrogi, Ariadna
AU - Divi, Kathyiani
AU - Mitchell, James B
AU - Poirier, Miriam C
AD - Carcinogen-DNA Interactions Section, Laboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 566
EP - 572
VL - 55
IS - 7
KW - Antioxidants
KW - 0
KW - Chromatin
KW - Cyclic N-Oxides
KW - Mercaptoethylamines
KW - Mutagens
KW - Radiation-Protective Agents
KW - Spin Labels
KW - WR 1065
KW - 31098-42-7
KW - Cytochalasin B
KW - 3CHI920QS7
KW - Zidovudine
KW - 4B9XT59T7S
KW - tempol
KW - U78ZX2F65X
KW - Index Medicus
KW - nuclear buds
KW - chromatin neoplasmic bridges
KW - cytome assay
KW - apoptosis
KW - necrosis
KW - MOLT-3 cells
KW - CBMN assay
KW - micronuclei
KW - Apoptosis
KW - Radiation-Protective Agents -- chemistry
KW - Cell Nucleus -- metabolism
KW - Humans
KW - Cell Line, Tumor
KW - Cell Proliferation
KW - Cytochalasin B -- chemistry
KW - Cell Survival
KW - Necrosis
KW - Micronucleus Tests
KW - Chromosomes -- ultrastructure
KW - Mutagens -- chemistry
KW - Mercaptoethylamines -- chemistry
KW - DNA Damage
KW - Chromatin -- chemistry
KW - Zidovudine -- chemistry
KW - Cyclic N-Oxides -- chemistry
KW - Antioxidants -- chemistry
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1552373610?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+and+molecular+mutagenesis&rft.atitle=Selective+protection+of+zidovudine-induced+DNA-damage+by+the+antioxidants+WR-1065+and+tempol.&rft.au=Olivero%2C+Ofelia+A%3BOngele%2C+Michael+O%3BBraun%2C+Hannan+M%3BMarrogi%2C+Ariadna%3BDivi%2C+Kathyiani%3BMitchell%2C+James+B%3BPoirier%2C+Miriam+C&rft.aulast=Olivero&rft.aufirst=Ofelia&rft.date=2014-08-01&rft.volume=55&rft.issue=7&rft.spage=566&rft.isbn=&rft.btitle=&rft.title=Environmental+and+molecular+mutagenesis&rft.issn=1098-2280&rft_id=info:doi/10.1002%2Fem.21872
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-09-29
N1 - Date created - 2014-08-07
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1002/em.21872
ER -
TY - JOUR
T1 - Genome-wide interaction study of smoking and bladder cancer risk.
AN - 1552370757; 24662972
AB - Bladder cancer is a complex disease with known environmental and genetic risk factors. We performed a genome-wide interaction study (GWAS) of smoking and bladder cancer risk based on primary scan data from 3002 cases and 4411 controls from the National Cancer Institute Bladder Cancer GWAS. Alternative methods were used to evaluate both additive and multiplicative interactions between individual single nucleotide polymorphisms (SNPs) and smoking exposure. SNPs with interaction P values < 5 × 10(-) (5) were evaluated further in an independent dataset of 2422 bladder cancer cases and 5751 controls. We identified 10 SNPs that showed association in a consistent manner with the initial dataset and in the combined dataset, providing evidence of interaction with tobacco use. Further, two of these novel SNPs showed strong evidence of association with bladder cancer in tobacco use subgroups that approached genome-wide significance. Specifically, rs1711973 (FOXF2) on 6p25.3 was a susceptibility SNP for never smokers [combined odds ratio (OR) = 1.34, 95% confidence interval (CI) = 1.20-1.50, P value = 5.18 × 10(-) (7)]; and rs12216499 (RSPH3-TAGAP-EZR) on 6q25.3 was a susceptibility SNP for ever smokers (combined OR = 0.75, 95% CI = 0.67-0.84, P value = 6.35 × 10(-) (7)). In our analysis of smoking and bladder cancer, the tests for multiplicative interaction seemed to more commonly identify susceptibility loci with associations in never smokers, whereas the additive interaction analysis identified more loci with associations among smokers-including the known smoking and NAT2 acetylation interaction. Our findings provide additional evidence of gene-environment interactions for tobacco and bladder cancer. Published by Oxford University Press 2014.
JF - Carcinogenesis
AU - Figueroa, Jonine D
AU - Han, Summer S
AU - Garcia-Closas, Montserrat
AU - Baris, Dalsu
AU - Jacobs, Eric J
AU - Kogevinas, Manolis
AU - Schwenn, Molly
AU - Malats, Nuria
AU - Johnson, Alison
AU - Purdue, Mark P
AU - Caporaso, Neil
AU - Landi, Maria Teresa
AU - Prokunina-Olsson, Ludmila
AU - Wang, Zhaoming
AU - Hutchinson, Amy
AU - Burdette, Laurie
AU - Wheeler, William
AU - Vineis, Paolo
AU - Siddiq, Afshan
AU - Cortessis, Victoria K
AU - Kooperberg, Charles
AU - Cussenot, Olivier
AU - Benhamou, Simone
AU - Prescott, Jennifer
AU - Porru, Stefano
AU - Bueno-de-Mesquita, H Bas
AU - Trichopoulos, Dimitrios
AU - Ljungberg, Börje
AU - Clavel-Chapelon, Françoise
AU - Weiderpass, Elisabete
AU - Krogh, Vittorio
AU - Dorronsoro, Miren
AU - Travis, Ruth
AU - Tjønneland, Anne
AU - Brenan, Paul
AU - Chang-Claude, Jenny
AU - Riboli, Elio
AU - Conti, David
AU - Gago-Dominguez, Manuela
AU - Stern, Mariana C
AU - Pike, Malcolm C
AU - Van Den Berg, David
AU - Yuan, Jian-Min
AU - Hohensee, Chancellor
AU - Rodabough, Rebecca
AU - Cancel-Tassin, Geraldine
AU - Roupret, Morgan
AU - Comperat, Eva
AU - Chen, Constance
AU - De Vivo, Immaculata
AU - Giovannucci, Edward
AU - Hunter, David J
AU - Kraft, Peter
AU - Lindstrom, Sara
AU - Carta, Angela
AU - Pavanello, Sofia
AU - Arici, Cecilia
AU - Mastrangelo, Giuseppe
AU - Karagas, Margaret R
AU - Schned, Alan
AU - Armenti, Karla R
AU - Hosain, G M Monawar
AU - Haiman, Chris A
AU - Fraumeni, Joseph F
AU - Chanock, Stephen J
AU - Chatterjee, Nilanjan
AU - Rothman, Nathaniel
AU - Silverman, Debra T
AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, USA, Institute for Cancer Research, London, UK, Epidemiology Research Program, American Cancer Society, Atlanta, GA, USA, Centre for Research in Environmental Epidemiology (CREAL), Barcelona, Spain, Municipal Institute of Medical Research, Barcelona, Spain, CIBER Epidemiología y Salud Pública (CIBERESP), Barcelona, Spain, National School of Public Health, Athens, Greece, Maine Cancer Registry, Augusta, ME, USA, Spanish National Cancer Research Centre (CNIO), Madrid, Spain, Vermont Cancer Registry, Burlington, VT, USA, Center for Genomics Research, SAIC-Frederick, Inc., National Cancer Institute-Frederick, Frederick, MD, USA, Information Management Services, Inc., Rockville, MD, USA, Imperial College London, London, UK, Department of Preventive Medicine and Department of Obstetrics & Gynecology, Keck School of Medicine of USC, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA, USA, Fred Hutchinson Cancer Research Center, Division of Public Health Sciences, Seattle, WA, USA, Department of Urology, Assistance Publique-Hôpitaux de Paris, Tenon Hospital, Paris, France, Centre de Recherche sur les Pathologies Prostatiques, Paris, France, Institut national de la sante et de la recherche medicale, U946, Foundation Jean Dausset Centre d'Etude du Polymorphisme Humain (CEPH), Paris, France, Centre National de la Receherche Scientifique, UMR8200, Institut Gustave-Roussy, Villejuif, France, Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA, Program in Genetic Epidemiology and Statistical Genetics, Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA, Department of Medical and Surgical Specialties, Radiological Sciences and Public Health, University of Brescia, Brescia, Italy, National Institute for Public Health and the Environment (RIVM), Biltho ; Institute for Cancer Research, London, UK. ; Epidemiology Research Program, American Cancer Society, Atlanta, GA, USA. ; Maine Cancer Registry, Augusta, ME, USA. ; Spanish National Cancer Research Centre (CNIO), Madrid, Spain. ; Vermont Cancer Registry, Burlington, VT, USA. ; Center for Genomics Research, SAIC-Frederick, Inc., National Cancer Institute-Frederick, Frederick, MD, USA. ; Information Management Services, Inc., Rockville, MD, USA. ; Imperial College London, London, UK. ; Department of Preventive Medicine and Department of Obstetrics & Gynecology, Keck School of Medicine of USC, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA, USA. ; Fred Hutchinson Cancer Research Center, Division of Public Health Sciences, Seattle, WA, USA. ; Department of Urology, Assistance Publique-Hôpitaux de Paris, Tenon Hospital, Paris, France, Centre de Recherche sur les Pathologies Prostatiques, Paris, France. ; Institut national de la sante et de la recherche medicale, U946, Foundation Jean Dausset Centre d'Etude du Polymorphisme Humain (CEPH), Paris, France, Centre National de la Receherche Scientifique, UMR8200, Institut Gustave-Roussy, Villejuif, France. ; Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA, Program in Genetic Epidemiology and Statistical Genetics, Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA. ; Department of Medical and Surgical Specialties, Radiological Sciences and Public Health, University of Brescia, Brescia, Italy. ; Imperial College London, London, UK, National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands, Department of Gastroenterology and Hepatology, University Medical Centre, Utrecht, The Netherlands. ; Department of Surgical and Perioperative Sciences, Urology and Andrology, Umeå University, Umeå, Sweden. ; Fondazione IRCCS Istituto Nazionale dei Tumori, Milano, Italy. ; CIBER Epidemiología y Salud Pública (CIBERESP), Barcelona, Spain, Public Health Division of Gipuzkoa, BioDonostia Research Institute, Health Department of Basque Region, San Sebastian, Spain. ; Cancer Epidemiology Unit, University of Oxford, Oxford, UK. ; Danish Cancer Society Research Center, Copenhagen, Denmark. ; International Agency for Research on Cancer, Lyon, France. ; DKFZ, Heidelberg, Germany. ; Genomic Medicine Group, Galician Foundation of Genomic Medicine, Complejo Hospitalario Universitario de Santiago, Servicio Galego de Saude (SERGAS), Instituto de Investigación Sanitaria de Santiago (IDIS), Santiago de Compostela, Spain. ; Department of Epidemiology and Biostatistics, Memorial Sloan-Kettering Cancer Center, New York, NY, USA. ; UPMC Univ Paris 06, GRC n°5,ONCOTYPE-URO, Paris, France. ; Department of Urology, Assistance Publique-Hôpitaux de Paris, Tenon Hospital, Paris, France, Centre de Recherche sur les Pathologies Prostatiques, Paris, France, UPMC Univ Paris 06, GRC n°5,ONCOTYPE-URO, Paris, France. ; Program in Genetic Epidemiology and Statistical Genetics, Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA. ; Department of Nutrition and Epidemiology, Harvard School of Public Health, Boston, MA, USA. ; Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA, Program in Genetic Epidemiology and Statistical Genetics, Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA, Broad Institute of Harvard and MIT, Cambridge, MA, USA. ; Program in Genetic Epidemiology and Statistical Genetics, Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA, Department of Biostatistics, Harvard School of Public Health, Boston, MA, USA. ; Department of Cardiac, Thoracic and Vascular Sciences, University of Padova, Padova, Italy; ; Geisel School of Medicine at Dartmouth, Lebanon, NH, USA. ; New Hampshire Department of Health and Human Services, Concord, NH, USA and. ; Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA, USA.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 1737
EP - 1744
VL - 35
IS - 8
KW - Biomarkers, Tumor
KW - 0
KW - Index Medicus
KW - Risk Factors
KW - Humans
KW - Adult
KW - Prognosis
KW - Case-Control Studies
KW - Genetic Predisposition to Disease
KW - Meta-Analysis as Topic
KW - Biomarkers, Tumor -- genetics
KW - Urinary Bladder Neoplasms -- etiology
KW - Genome, Human
KW - Smoking -- adverse effects
KW - Gene-Environment Interaction
KW - Polymorphism, Single Nucleotide -- genetics
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Genome-wide+interaction+study+of+smoking+and+bladder+cancer+risk.&rft.au=Figueroa%2C+Jonine+D%3BHan%2C+Summer+S%3BGarcia-Closas%2C+Montserrat%3BBaris%2C+Dalsu%3BJacobs%2C+Eric+J%3BKogevinas%2C+Manolis%3BSchwenn%2C+Molly%3BMalats%2C+Nuria%3BJohnson%2C+Alison%3BPurdue%2C+Mark+P%3BCaporaso%2C+Neil%3BLandi%2C+Maria+Teresa%3BProkunina-Olsson%2C+Ludmila%3BWang%2C+Zhaoming%3BHutchinson%2C+Amy%3BBurdette%2C+Laurie%3BWheeler%2C+William%3BVineis%2C+Paolo%3BSiddiq%2C+Afshan%3BCortessis%2C+Victoria+K%3BKooperberg%2C+Charles%3BCussenot%2C+Olivier%3BBenhamou%2C+Simone%3BPrescott%2C+Jennifer%3BPorru%2C+Stefano%3BBueno-de-Mesquita%2C+H+Bas%3BTrichopoulos%2C+Dimitrios%3BLjungberg%2C+B%C3%B6rje%3BClavel-Chapelon%2C+Fran%C3%A7oise%3BWeiderpass%2C+Elisabete%3BKrogh%2C+Vittorio%3BDorronsoro%2C+Miren%3BTravis%2C+Ruth%3BTj%C3%B8nneland%2C+Anne%3BBrenan%2C+Paul%3BChang-Claude%2C+Jenny%3BRiboli%2C+Elio%3BConti%2C+David%3BGago-Dominguez%2C+Manuela%3BStern%2C+Mariana+C%3BPike%2C+Malcolm+C%3BVan+Den+Berg%2C+David%3BYuan%2C+Jian-Min%3BHohensee%2C+Chancellor%3BRodabough%2C+Rebecca%3BCancel-Tassin%2C+Geraldine%3BRoupret%2C+Morgan%3BComperat%2C+Eva%3BChen%2C+Constance%3BDe+Vivo%2C+Immaculata%3BGiovannucci%2C+Edward%3BHunter%2C+David+J%3BKraft%2C+Peter%3BLindstrom%2C+Sara%3BCarta%2C+Angela%3BPavanello%2C+Sofia%3BArici%2C+Cecilia%3BMastrangelo%2C+Giuseppe%3BKaragas%2C+Margaret+R%3BSchned%2C+Alan%3BArmenti%2C+Karla+R%3BHosain%2C+G+M+Monawar%3BHaiman%2C+Chris+A%3BFraumeni%2C+Joseph+F%3BChanock%2C+Stephen+J%3BChatterjee%2C+Nilanjan%3BRothman%2C+Nathaniel%3BSilverman%2C+Debra+T&rft.aulast=Figueroa&rft.aufirst=Jonine&rft.date=2014-08-01&rft.volume=35&rft.issue=8&rft.spage=1737&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgu064
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-02-18
N1 - Date created - 2014-08-07
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/carcin/bgu064
ER -
TY - JOUR
T1 - Clinical imaging in regenerative medicine.
AN - 1552369411; 25093889
AB - In regenerative medicine, clinical imaging is indispensable for characterizing damaged tissue and for measuring the safety and efficacy of therapy. However, the ability to track the fate and function of transplanted cells with current technologies is limited. Exogenous contrast labels such as nanoparticles give a strong signal in the short term but are unreliable long term. Genetically encoded labels are good both short- and long-term in animals, but in the human setting they raise regulatory issues related to the safety of genomic integration and potential immunogenicity of reporter proteins. Imaging studies in brain, heart and islets share a common set of challenges, including developing novel labeling approaches to improve detection thresholds and early delineation of toxicity and function. Key areas for future research include addressing safety concerns associated with genetic labels and developing methods to follow cell survival, differentiation and integration with host tissue. Imaging may bridge the gap between cell therapies and health outcomes by elucidating mechanisms of action through longitudinal monitoring.
JF - Nature biotechnology
AU - Naumova, Anna V
AU - Modo, Michel
AU - Moore, Anna
AU - Murry, Charles E
AU - Frank, Joseph A
AD - 1] Department of Radiology, University of Washington, Seattle, Washington, USA. [2] Center for Cardiovascular Biology, University of Washington, Seattle, Washington, USA. [3] Institute for Stem Cell and Regenerative Medicine, University of Washington, Seattle, Washington, USA. ; 1] McGowan Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA. [2] Centre for the Neural Basis of Cognition, University of Pittsburgh, Pittsburgh, Pennsylvania, USA. [3] Department of Radiology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA. [4] Department of Bioengineering, University of Pittsburgh, Pittsburgh, Pennsylvania, USA. ; Athinoula A. Martinos Center for Biomedical Imaging, Department of Radiology, Massachusetts General Hospital, Charlestown, Massachusetts, USA. ; 1] Center for Cardiovascular Biology, University of Washington, Seattle, Washington, USA. [2] Institute for Stem Cell and Regenerative Medicine, University of Washington, Seattle, Washington, USA. [3] Department of Pathology, University of Washington, Seattle, Washington, USA. [4] Department of Bioengineering, University of Washington, Seattle, Washington, USA. [5] Department of Medicine/Cardiology, University of Washington, Seattle, Washington, USA. ; 1] Radiology and Imaging Sciences, Clinical, National Institutes of Health, Bethesda, Maryland, USA. [2] National Institutes of Biomedical Imaging and Bioengineering, National Institutes of Health, Bethesda, Maryland, USA.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 804
EP - 818
VL - 32
IS - 8
KW - Index Medicus
KW - Animals
KW - Diagnostic Imaging
KW - Regenerative Medicine
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1552369411?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+biotechnology&rft.atitle=Clinical+imaging+in+regenerative+medicine.&rft.au=Naumova%2C+Anna+V%3BModo%2C+Michel%3BMoore%2C+Anna%3BMurry%2C+Charles+E%3BFrank%2C+Joseph+A&rft.aulast=Naumova&rft.aufirst=Anna&rft.date=2014-08-01&rft.volume=32&rft.issue=8&rft.spage=804&rft.isbn=&rft.btitle=&rft.title=Nature+biotechnology&rft.issn=1546-1696&rft_id=info:doi/10.1038%2Fnbt.2993
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-04-13
N1 - Date created - 2014-08-08
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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Comment In:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1038/nbt.2993
ER -
TY - JOUR
T1 - Inhibition of glutathione peroxidase mediates the collateral sensitivity of multidrug-resistant cells to tiopronin.
AN - 1551027856; 24930045
AB - Multidrug resistance (MDR) is a major obstacle to the successful chemotherapy of cancer. MDR is often the result of overexpression of ATP-binding cassette transporters following chemotherapy. A common ATP-binding cassette transporter that is overexpressed in MDR cancer cells is P-glycoprotein, which actively effluxes drugs against a concentration gradient, producing an MDR phenotype. Collateral sensitivity (CS), a phenomenon of drug hypersensitivity, is defined as the ability of certain compounds to selectively target MDR cells, but not the drug-sensitive parent cells from which they were derived. The drug tiopronin has been previously shown to elicit CS. However, unlike other CS agents, the mechanism of action was not dependent on the expression of P-glycoprotein in MDR cells. We have determined that the CS activity of tiopronin is mediated by the generation of reactive oxygen species (ROS) and that CS can be reversed by a variety of ROS-scavenging compounds. Specifically, selective toxicity of tiopronin toward MDR cells is achieved by inhibition of glutathione peroxidase (GPx), and the mode of inhibition of GPx1 by tiopronin is shown in this report. Why MDR cells are particularly sensitive to ROS is discussed, as is the difficulty in exploiting this hypersensitivity to tiopronin in the clinic. © 2014 by The American Society for Biochemistry and Molecular Biology, Inc.
JF - The Journal of biological chemistry
AU - Hall, Matthew D
AU - Marshall, Travis S
AU - Kwit, Alexandra D T
AU - Miller Jenkins, Lisa M
AU - Dulcey, Andrés E
AU - Madigan, James P
AU - Pluchino, Kristen M
AU - Goldsborough, Andrew S
AU - Brimacombe, Kyle R
AU - Griffiths, Gary L
AU - Gottesman, Michael M
AD - From the Laboratory of Cell Biology, Center for Cancer Research, NCI, National Institutes of Health, Bethesda, Maryland 20892 and. ; the Imaging Probe Development Center, NHLBI, National Institutes of Health, Rockville, Maryland 20850. ; From the Laboratory of Cell Biology, Center for Cancer Research, NCI, National Institutes of Health, Bethesda, Maryland 20892 and mgottesman@nih.gov.
Y1 - 2014/08/01/
PY - 2014
DA - 2014 Aug 01
SP - 21473
EP - 21489
VL - 289
IS - 31
KW - Enzyme Inhibitors
KW - 0
KW - Oligodeoxyribonucleotides
KW - Reactive Oxygen Species
KW - Thiomalates
KW - 2-thiomalic acid
KW - 94239W5L4H
KW - Tiopronin
KW - C5W04GO61S
KW - Glutathione Peroxidase
KW - EC 1.11.1.9
KW - Index Medicus
KW - Oxygen Radicals
KW - Enzyme Inhibitor
KW - Chemoresistance
KW - Reactive Oxygen Species (ROS)
KW - Cell Death
KW - Thiomalates -- pharmacology
KW - Reactive Oxygen Species -- metabolism
KW - Base Sequence
KW - Humans
KW - Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization
KW - Molecular Sequence Data
KW - Drug Resistance, Neoplasm
KW - Cell Line, Tumor
KW - Amino Acid Sequence
KW - Tandem Mass Spectrometry
KW - Drug Resistance, Multiple
KW - Glutathione Peroxidase -- chemistry
KW - Enzyme Inhibitors -- pharmacology
KW - Tiopronin -- pharmacology
KW - Glutathione Peroxidase -- antagonists & inhibitors
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551027856?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Inhibition+of+glutathione+peroxidase+mediates+the+collateral+sensitivity+of+multidrug-resistant+cells+to+tiopronin.&rft.au=Hall%2C+Matthew+D%3BMarshall%2C+Travis+S%3BKwit%2C+Alexandra+D+T%3BMiller+Jenkins%2C+Lisa+M%3BDulcey%2C+Andr%C3%A9s+E%3BMadigan%2C+James+P%3BPluchino%2C+Kristen+M%3BGoldsborough%2C+Andrew+S%3BBrimacombe%2C+Kyle+R%3BGriffiths%2C+Gary+L%3BGottesman%2C+Michael+M&rft.aulast=Hall&rft.aufirst=Matthew&rft.date=2014-08-01&rft.volume=289&rft.issue=31&rft.spage=21473&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M114.581702
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-12-15
N1 - Date created - 2014-08-02
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1074/jbc.M114.581702
ER -
TY - JOUR
T1 - Dual VEGF/VEGFR inhibition in advanced solid malignancies: clinical effects and pharmacodynamic biomarkers.
AN - 1551027207; 24842548
AB - Our prior phase I study of the combination of vascular endothelial growth factor (VEGF) antibody, bevacizumab, and VEGF receptor (VEGFR) inhibitor, sunitinib, in advanced solid tumors identified an encouraging response evaluation. An expansion phase of this study was thus undertaken to obtain further safety data, response assessment and characterization of pharmacodynamic biomarkers in melanoma, renal, and adrenal carcinoma patients. Patients with metastatic solid tumors received sunitinib (37.5 mg/d, 4 wk on/2 wk off) and bevacizumab (5 mg/kg intravenously every 2 wk). Responses were assessed every 2 cycles. Serum levels of angiogenic molecules were measured using ELISA assays. Twenty-two patients were enrolled, including 11 melanoma, 5 renal cell carcinoma (RCC), 5 adrenal cancer, and 1 angiosarcoma. Grade 3 or higher adverse events were observed in 15 patients, including hypertension (41%), thrombocytopenia (23%), and fatigue (14%). Three RCC patients, and 1 melanoma patient developed thrombotic microangiopathy (TMA). Partial response (PR) occurred in 21% patients, including melanoma (2), adrenal (1), and renal (1) carcinomas. Overall, 6 patients demonstrated some reduction in their tumor burden. Serum VEGF and several other proangiogenic proteins declined over the first 4 wk of treatment whereas the putative VEGF-resistant protein, prokineticin-2, increased over 10-fold. Occurrence of TMA related to dual VEGF/VEGFR inhibition can result from systemic or nephron specific injury even in non-renal malignancies. While the combination of sunitinib and bevacizumab was clinically efficacious in renal cell carcinoma and melanoma, the observance of microangiopathy, even in non-RCC patients, is a significant toxicity that precludes further clinical development.
JF - Cancer biology & therapy
AU - Mittal, Kriti
AU - Koon, Henry
AU - Elson, Paul
AU - Triozzi, Pierre
AU - Dowlati, Afshin
AU - Chen, Helen
AU - Borden, Ernest C
AU - Rini, Brian I
AD - Cleveland Clinic Taussig Cancer Institute; Cleveland, OH USA. ; Case Western University; Cleveland, OH USA. ; National Cancer Institute; Rockville, MD USA.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 975
EP - 981
VL - 15
IS - 8
KW - Antibodies, Monoclonal, Humanized
KW - 0
KW - Biomarkers, Pharmacological
KW - Gastrointestinal Hormones
KW - Indoles
KW - Neuropeptides
KW - PROK2 protein, human
KW - Pyrroles
KW - Vascular Endothelial Growth Factor A
KW - Bevacizumab
KW - 2S9ZZM9Q9V
KW - Receptors, Vascular Endothelial Growth Factor
KW - EC 2.7.10.1
KW - sunitinib
KW - V99T50803M
KW - Index Medicus
KW - VEGFR
KW - VEGF
KW - bevacizumab
KW - angiogenesis
KW - Neuropeptides -- metabolism
KW - Pyrroles -- administration & dosage
KW - Biomarkers, Pharmacological -- metabolism
KW - Gastrointestinal Hormones -- metabolism
KW - Humans
KW - Indoles -- administration & dosage
KW - Middle Aged
KW - Antibodies, Monoclonal, Humanized -- administration & dosage
KW - Male
KW - Female
KW - Vascular Endothelial Growth Factor A -- antagonists & inhibitors
KW - Neoplasms -- drug therapy
KW - Receptors, Vascular Endothelial Growth Factor -- antagonists & inhibitors
KW - Receptors, Vascular Endothelial Growth Factor -- metabolism
KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use
KW - Vascular Endothelial Growth Factor A -- metabolism
KW - Neoplasms -- metabolism
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551027207?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+biology+%26+therapy&rft.atitle=Dual+VEGF%2FVEGFR+inhibition+in+advanced+solid+malignancies%3A+clinical+effects+and+pharmacodynamic+biomarkers.&rft.au=Mittal%2C+Kriti%3BKoon%2C+Henry%3BElson%2C+Paul%3BTriozzi%2C+Pierre%3BDowlati%2C+Afshin%3BChen%2C+Helen%3BBorden%2C+Ernest+C%3BRini%2C+Brian+I&rft.aulast=Mittal&rft.aufirst=Kriti&rft.date=2014-08-01&rft.volume=15&rft.issue=8&rft.spage=975&rft.isbn=&rft.btitle=&rft.title=Cancer+biology+%26+therapy&rft.issn=1555-8576&rft_id=info:doi/10.4161%2Fcbt.29187
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-06-03
N1 - Date created - 2014-08-02
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.4161/cbt.29187
ER -
TY - JOUR
T1 - Predicted 25(OH)D score and colorectal cancer risk according to vitamin D receptor expression.
AN - 1551027056; 24920642
AB - Despite accumulating evidence for the preventive effect of vitamin D on colorectal carcinogenesis, its precise mechanisms remain unclear. We hypothesized that vitamin D was associated with a lower risk of colorectal cancer with high-level vitamin D receptor (VDR) expression, but not with risk of tumor with low-level VDR expression.
Among 140,418 participants followed from 1986 through 2008 in the Nurses' Health Study and the Health Professionals' Follow-up Study, we identified 1,059 incident colorectal cancer cases with tumor molecular data. The predicted 25-hydroxyvitamin D [25(OH)D] score was developed using the known determinants of plasma 25(OH)D. We estimated the HR for cancer subtypes using the duplication method Cox proportional hazards model.
A higher predicted 25(OH)D score was associated with a lower risk of colorectal cancer irrespective of VDR expression level (P(heterogeneity) for subtypes = 0.75). Multivariate HRs (95% confidence intervals) comparing the highest with the lowest quintile of predicted 25(OH)D scores were 0.48 (0.30-0.78) for VDR-negative tumor and 0.56 (0.42-0.75) for VDR-positive tumor. Similarly, the significant inverse associations of the predicted 25(OH)D score with colorectal cancer risk did not significantly differ by KRAS, BRAF, or PIK3CA status (P(heterogeneity) for subtypes ≥ 0.22). A higher predicted vitamin D score was significantly associated with a lower colorectal cancer risk, regardless of VDR status and other molecular features examined.
The preventive effect of vitamin D on colorectal carcinogenesis may not totally depend on tumor factors. Host factors (such as local and systemic immunity) may need to be considered. ©2014 American Association for Cancer Research.
JF - Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
AU - Jung, Seungyoun
AU - Qian, Zhi Rong
AU - Yamauchi, Mai
AU - Bertrand, Kimberly A
AU - Fitzgerald, Kathryn C
AU - Inamura, Kentaro
AU - Kim, Sun A
AU - Mima, Kosuke
AU - Sukawa, Yasutaka
AU - Zhang, Xuehong
AU - Wang, Molin
AU - Smith-Warner, Stephanie A
AU - Wu, Kana
AU - Fuchs, Charles S
AU - Chan, Andrew T
AU - Giovannucci, Edward L
AU - Ng, Kimmie
AU - Cho, Eunyoung
AU - Ogino, Shuji
AU - Nishihara, Reiko
AD - Channing Division of Network Medicine, Department of Medicine and. ; Department of Medical Oncology, Dana-Farber Cancer Institute; Departments of. ; Epidemiology. ; Department of Medical Oncology, Dana-Farber Cancer Institute; Departments of Laboratory of Human Carcinogenesis, National Cancer Institute, NIH, Bethesda, Maryland; and. ; Epidemiology, Biostatistics, and. ; Epidemiology, Nutrition, Harvard School of Public Health, Boston, Massachusetts; ; Nutrition, Harvard School of Public Health, Boston, Massachusetts; ; Channing Division of Network Medicine, Department of Medicine and Department of Medical Oncology, Dana-Farber Cancer Institute; Departments of. ; Channing Division of Network Medicine, Department of Medicine and Division of Gastroenterology, Massachusetts General Hospital, Harvard Medical School; ; Channing Division of Network Medicine, Department of Medicine and Epidemiology, Nutrition, Harvard School of Public Health, Boston, Massachusetts; ; Channing Division of Network Medicine, Department of Medicine and Department of Dermatology, The Warren Alpert Medical School of Brown University, Providence, Rhode Island. ; Department of Pathology, Brigham and Women's Hospital and Department of Medical Oncology, Dana-Farber Cancer Institute; Departments of Epidemiology, rnishiha@hsph.harvard.edu shuji_ogino@dfci.harvard.edu. ; Department of Medical Oncology, Dana-Farber Cancer Institute; Departments of Nutrition, Harvard School of Public Health, Boston, Massachusetts; rnishiha@hsph.harvard.edu shuji_ogino@dfci.harvard.edu.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 1628
EP - 1637
VL - 23
IS - 8
KW - Receptors, Calcitriol
KW - 0
KW - Vitamin D
KW - 1406-16-2
KW - 25-hydroxyvitamin D
KW - 64719-49-9
KW - Index Medicus
KW - Polymerase Chain Reaction
KW - Risk Factors
KW - Humans
KW - Adult
KW - Incidence
KW - Middle Aged
KW - Immunohistochemistry
KW - Male
KW - Female
KW - Receptors, Calcitriol -- biosynthesis
KW - Colorectal Neoplasms -- metabolism
KW - Receptors, Calcitriol -- analysis
KW - Vitamin D -- blood
KW - Vitamin D -- analogs & derivatives
KW - Colorectal Neoplasms -- epidemiology
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551027056?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+epidemiology%2C+biomarkers+%26+prevention+%3A+a+publication+of+the+American+Association+for+Cancer+Research%2C+cosponsored+by+the+American+Society+of+Preventive+Oncology&rft.atitle=Predicted+25%28OH%29D+score+and+colorectal+cancer+risk+according+to+vitamin+D+receptor+expression.&rft.au=Jung%2C+Seungyoun%3BQian%2C+Zhi+Rong%3BYamauchi%2C+Mai%3BBertrand%2C+Kimberly+A%3BFitzgerald%2C+Kathryn+C%3BInamura%2C+Kentaro%3BKim%2C+Sun+A%3BMima%2C+Kosuke%3BSukawa%2C+Yasutaka%3BZhang%2C+Xuehong%3BWang%2C+Molin%3BSmith-Warner%2C+Stephanie+A%3BWu%2C+Kana%3BFuchs%2C+Charles+S%3BChan%2C+Andrew+T%3BGiovannucci%2C+Edward+L%3BNg%2C+Kimmie%3BCho%2C+Eunyoung%3BOgino%2C+Shuji%3BNishihara%2C+Reiko&rft.aulast=Jung&rft.aufirst=Seungyoun&rft.date=2014-08-01&rft.volume=23&rft.issue=8&rft.spage=1628&rft.isbn=&rft.btitle=&rft.title=Cancer+epidemiology%2C+biomarkers+%26+prevention+%3A+a+publication+of+the+American+Association+for+Cancer+Research%2C+cosponsored+by+the+American+Society+of+Preventive+Oncology&rft.issn=1538-7755&rft_id=info:doi/10.1158%2F1055-9965.EPI-14-0229
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-06-18
N1 - Date created - 2014-08-02
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1158/1055-9965.EPI-14-0229
ER -
TY - JOUR
T1 - Vanadium as a chemoprotectant: effect of vanadium(III)-L-cysteine complex against cyclophosphamide-induced hepatotoxicity and genotoxicity in Swiss albino mice.
AN - 1551025005; 24777843
AB - Vanadium is an essential micronutrient for living systems and has antioxidant and genoprotective property. In the present study, the protective role of an organovanadium compound vanadium(III)-L-cysteine (VC-III) was evaluated against hepatotoxicity and genotoxicity induced by cyclophosphamide (CP) (25 mg/kg b.w., i.p.) in Swiss albino mice. Treatment with VC-III (1 mg/kg b.w., p.o.) mitigated CP-induced hepatic injury as indicated by reduction in activities of alanine transaminase, aspartate transaminase, alkaline phosphatase by 1.57-, 1.58- and 1.32-fold in concomitant treatment schedule and by 1.83-, 1.77- and 1.45-fold in pretreatment schedule, respectively, and confirmed by histopathological evidences. Parallel to these changes, VC-III ameliorated CP-induced oxidative stress in liver by 1.46-, 1.26-, 1.32- and 1.42-fold in concomitant treatment group and by 1.95-, 1.40-, 1.46- and 1.73-fold in pretreatment group at the level of H2O2, superoxide, nitric oxide and lipid peroxidation, respectively. VC-III also enhanced activities of antioxidant enzymes such as superoxide dismutase, catalase, glutathione peroxidase, glutathione S-transferase and glutathione (reduced) level in mice liver by 1.46-, 1.37-, 1.29-, 1.44- and 1.45-fold in concomitant treatment schedule and by 1.64-, 1.65-, 1.42-, 1.49- and 1.57-fold in pretreatment schedule, respectively. In addition, the organovanadium compound could efficiently attenuate CP-induced chromosomal aberrations, DNA fragmentation and apoptosis in bone marrow cells and DNA damage in lymphocytes by 1.49-, 1.43-, 1.48- and 1.59-fold in concomitant treatment group and by 1.76-, 1.92-, 1.99- and 2.15-fold in pretreatment group, respectively. Thus, the present study showed that VC-III could exert protection against CP-induced hepatotoxicity and genotoxicity.
JF - Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry
AU - Basu, Abhishek
AU - Bhattacharjee, Arin
AU - Roy, Somnath Singha
AU - Ghosh, Prosenjit
AU - Chakraborty, Pramita
AU - Das, Ila
AU - Bhattacharya, Sudin
AD - Department of Cancer Chemoprevention, Chittaranjan National Cancer Institute, 37, S. P. Mukherjee Road, Kolkata, 700 026, West Bengal, India.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 981
EP - 996
VL - 19
IS - 6
KW - Mutagens
KW - 0
KW - Organometallic Compounds
KW - Vanadium
KW - 00J9J9XKDE
KW - Cyclophosphamide
KW - 8N3DW7272P
KW - Cysteine
KW - K848JZ4886
KW - Index Medicus
KW - Animals
KW - DNA Damage
KW - Mutagens -- toxicity
KW - Mice
KW - Cytoprotection -- drug effects
KW - Mutagens -- administration & dosage
KW - Female
KW - Cyclophosphamide -- administration & dosage
KW - Organometallic Compounds -- pharmacology
KW - Liver -- injuries
KW - Cyclophosphamide -- antagonists & inhibitors
KW - Liver -- metabolism
KW - Cyclophosphamide -- toxicity
KW - Vanadium -- chemistry
KW - Organometallic Compounds -- chemistry
KW - Chromosome Aberrations -- chemically induced
KW - Chromosome Aberrations -- drug effects
KW - Cysteine -- chemistry
KW - Liver -- drug effects
KW - Organometallic Compounds -- chemical synthesis
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+biological+inorganic+chemistry+%3A+JBIC+%3A+a+publication+of+the+Society+of+Biological+Inorganic+Chemistry&rft.atitle=Vanadium+as+a+chemoprotectant%3A+effect+of+vanadium%28III%29-L-cysteine+complex+against+cyclophosphamide-induced+hepatotoxicity+and+genotoxicity+in+Swiss+albino+mice.&rft.au=Basu%2C+Abhishek%3BBhattacharjee%2C+Arin%3BRoy%2C+Somnath+Singha%3BGhosh%2C+Prosenjit%3BChakraborty%2C+Pramita%3BDas%2C+Ila%3BBhattacharya%2C+Sudin&rft.aulast=Basu&rft.aufirst=Abhishek&rft.date=2014-08-01&rft.volume=19&rft.issue=6&rft.spage=981&rft.isbn=&rft.btitle=&rft.title=Journal+of+biological+inorganic+chemistry+%3A+JBIC+%3A+a+publication+of+the+Society+of+Biological+Inorganic+Chemistry&rft.issn=1432-1327&rft_id=info:doi/10.1007%2Fs00775-014-1141-6
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-03-30
N1 - Date created - 2014-08-01
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1007/s00775-014-1141-6
ER -
TY - JOUR
T1 - Analysis of polychlorinated biphenyls and organochlorine pesticides in archived dried blood spots and its application to track temporal trends of environmental chemicals in newborns.
AN - 1551023706; 24968082
AB - Dried blood spots (DBS) collected from infants shortly after birth for the newborn screening program (NSP) in the United States are valuable resources for the assessment of exposure to environmental chemicals in newborns. The NSP was debuted as a public health program in the United States in the 1960s; and the DBS samples collected over a period of time can be used in tracking temporal trends in exposure to environmental chemicals by newborns. In this study, polychlorinated biphenyls (PCBs) and organochlorine pesticides (OCPs) were measured in DBS samples collected from newborns in Upstate New York from 1997 to 2011 by gas chromatography-high resolution mass spectrometry (GC-HRMS). Twelve PCBs and two OCPs were found in DBS samples at a detection rate above 50% (n=51). The mean whole blood concentration of ΣPCBs (sum of 12 congeners) over the 15-year period was 1.06 ng/mL, followed by p,p'-DDE (0.421 ng/mL) and HCB (0.065 ng/mL). The measured concentrations of PCBs and p,p'-DDE in infants'blood were comparable to those reported in cord blood, suggesting maternal/trans-placental transfer of these compounds from mothers to fetuses. The concentrations of ΣPCBs and p,p'-DDE in blood samples of infants decreased significantly between 1997 and 2001, and no significant reduction was found thereafter. This observation is consistent with the trends reported for these chemicals in other human tissues in the United States. Copyright © 2014 Elsevier Inc. All rights reserved.
JF - Environmental research
AU - Ma, Wan-Li
AU - Gao, Chongjing
AU - Bell, Erin M
AU - Druschel, Charlotte M
AU - Caggana, Michele
AU - Aldous, Kenneth M
AU - Louis, Germaine M Buck
AU - Kannan, Kurunthachalam
AD - Wadsworth Center, New York State Department of Health, and Department of Environmental Health Sciences, School of Public Health, State University of New York at Albany, Empire State Plaza, P.O. Box 509, Albany, NY 12201-0509, USA; International Joint Research Center for Persistent Toxic Substances, State Key Laboratory of Urban Water Resource and Environment, Harbin Institute of Technology, Harbin 150090, China. ; Department of Environmental Health Sciences, School of Public Health, State University of New York at Albany, Albany, NY, USA. ; New York State Department of Health, Bureau of Environmental & Occupational Epidemiology, Empire State Plaza-Corning Tower, Room 1203, Albany, NY 12237, USA; Department of Epidemiology and Biostatistics, School of Public Health, State University of New York at Albany, Albany, NY, USA. ; Wadsworth Center, New York State Department of Health, and Department of Environmental Health Sciences, School of Public Health, State University of New York at Albany, Empire State Plaza, P.O. Box 509, Albany, NY 12201-0509, USA. ; Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, the National Institutes of Health, 6100 Executive Blvd. Room 7B03, Rockville, MD 20852, USA. ; Wadsworth Center, New York State Department of Health, and Department of Environmental Health Sciences, School of Public Health, State University of New York at Albany, Empire State Plaza, P.O. Box 509, Albany, NY 12201-0509, USA; International Joint Research Center for Persistent Toxic Substances, State Key Laboratory of Urban Water Resource and Environment, Harbin Institute of Technology, Harbin 150090, China; Experimental Biochemistry Unit, King Fahd Medical Research Center, King Abdulaziz University, PO Box 80216, Jeddah 21589, Saudi Arabia. Electronic address: kkannan@wadsworth.org.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 204
EP - 210
VL - 133
KW - Environmental Pollutants
KW - 0
KW - Hydrocarbons, Chlorinated
KW - Pesticides
KW - Polychlorinated Biphenyls
KW - DFC2HB4I0K
KW - Index Medicus
KW - PCBs
KW - OCPs
KW - Temporal trend
KW - Dried blood spot
KW - Infants
KW - New York
KW - Humans
KW - Reference Standards
KW - Infant, Newborn
KW - Time Factors
KW - Quality Control
KW - Neonatal Screening -- trends
KW - Hydrocarbons, Chlorinated -- blood
KW - Polychlorinated Biphenyls -- blood
KW - Hydrocarbons, Chlorinated -- adverse effects
KW - Environmental Pollutants -- blood
KW - Pesticides -- adverse effects
KW - Environmental Pollutants -- adverse effects
KW - Polychlorinated Biphenyls -- adverse effects
KW - Pesticides -- blood
KW - Neonatal Screening -- methods
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+research&rft.atitle=Analysis+of+polychlorinated+biphenyls+and+organochlorine+pesticides+in+archived+dried+blood+spots+and+its+application+to+track+temporal+trends+of+environmental+chemicals+in+newborns.&rft.au=Ma%2C+Wan-Li%3BGao%2C+Chongjing%3BBell%2C+Erin+M%3BDruschel%2C+Charlotte+M%3BCaggana%2C+Michele%3BAldous%2C+Kenneth+M%3BLouis%2C+Germaine+M+Buck%3BKannan%2C+Kurunthachalam&rft.aulast=Ma&rft.aufirst=Wan-Li&rft.date=2014-08-01&rft.volume=133&rft.issue=&rft.spage=204&rft.isbn=&rft.btitle=&rft.title=Environmental+research&rft.issn=1096-0953&rft_id=info:doi/10.1016%2Fj.envres.2014.05.029
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-10-03
N1 - Date created - 2014-08-01
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Arch Environ Health. 1999 Jan-Feb;54(1):40-7 [10025415]
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Environ Sci Technol. 2008 Sep 15;42(18):6991-6 [18853821]
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Anal Chem. 2009 Mar 1;81(5):1931-6 [19199567]
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J Chromatogr B Analyt Technol Biomed Life Sci. 2012 May 15;897:72-9 [22552005]
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Chemosphere. 2013 Jun;91(10):1426-33 [23453434]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.envres.2014.05.029
ER -
TY - JOUR
T1 - Research resource: comparison of gene profiles from wild-type ERα and ERα hinge region mutants.
AN - 1551019542; 24947674
AB - We showed previously that the hinge region of estrogen receptor (ER) α is involved in mediating its actions. The hinge 1 (H1) ERα mutant has disrupted nuclear localization and has lost interaction with c-JUN, but retains estrogen response element (ERE)-mediated functions. The hinge 2 + nuclear export sequence (H2NES) ERα mutant does not maintain nuclear translocation with hormone and no longer activates ERE target genes but does retain a nongenomic, nonnuclear, rapid-action response. Herein, we used the human endometrial cancer Ishikawa stable cell lines (Ishikawa/vector, Ishikawa/wild-type [WT] ERα, Ishikawa/H1 ERα, or Ishikawa/H2NES ERα) to characterize the biological activities of these 2 ERα hinge region mutants. We confirmed by confocal microscopy increased cytoplasmic ERα in the H1 ERα cell line and full cytoplasmic ERα localization in the H2NES ERα cell line. Luciferase assays using the 3xERE reporter showed activation of H1 ERα and H2NES ERα by estradiol (E2) treatment, but using the endogenous pS2 reporter, luciferase activity was only seen with the H1 ERα cell line. Examining cell proliferation revealed that only the WT ERα and H1 ERα cell lines increased proliferation after treatment. Using microarrays, we found that WT ERα and H1 ERα cluster together, whereas vector and H2NES ERα are most similar and cluster independently of E2 treatment. These studies revealed that the nongenomic activities of ERα are unable to mediate proliferative changes or the transcriptional profile after treatment and demonstrate the importance of genomic action for ERα/E2-mediated responses with the nongenomic actions of ERα being complementary to elicit the full biological actions of ERα.
JF - Molecular endocrinology (Baltimore, Md.)
AU - Burns, Katherine A
AU - Li, Yin
AU - Liu, Liwen
AU - Korach, Kenneth S
AD - Receptor Biology (K.A.B., Y.L., K.S.K.), Laboratory of Reproductive and Developmental Toxicology and Molecular Genomics Core Facility (L.L.), National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 1352
EP - 1361
VL - 28
IS - 8
KW - Estrogen Receptor alpha
KW - 0
KW - estrogen receptor alpha, human
KW - Estradiol
KW - 4TI98Z838E
KW - Index Medicus
KW - Oligonucleotide Array Sequence Analysis
KW - HeLa Cells
KW - Cell Nucleus -- metabolism
KW - Humans
KW - Estradiol -- physiology
KW - Gene Expression Regulation
KW - Protein Structure, Tertiary
KW - Cell Proliferation
KW - Protein Transport
KW - Estrogen Receptor alpha -- genetics
KW - Transcriptome
KW - Estrogen Receptor alpha -- physiology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+endocrinology+%28Baltimore%2C+Md.%29&rft.atitle=Research+resource%3A+comparison+of+gene+profiles+from+wild-type+ER%CE%B1+and+ER%CE%B1+hinge+region+mutants.&rft.au=Burns%2C+Katherine+A%3BLi%2C+Yin%3BLiu%2C+Liwen%3BKorach%2C+Kenneth+S&rft.aulast=Burns&rft.aufirst=Katherine&rft.date=2014-08-01&rft.volume=28&rft.issue=8&rft.spage=1352&rft.isbn=&rft.btitle=&rft.title=Molecular+endocrinology+%28Baltimore%2C+Md.%29&rft.issn=1944-9917&rft_id=info:doi/10.1210%2Fme.2014-1122
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-03-30
N1 - Date created - 2014-08-02
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1210/me.2014-1122
ER -
TY - JOUR
T1 - Whole-exome and targeted gene sequencing of gallbladder carcinoma identifies recurrent mutations in the ErbB pathway.
AN - 1549632568; 24997986
AB - Individuals with gallbladder carcinoma (GBC), the most aggressive malignancy of the biliary tract, have a poor prognosis. Here we report the identification of somatic mutations for GBC in 57 tumor-normal pairs through a combination of exome sequencing and ultra-deep sequencing of cancer-related genes. The mutation pattern is defined by a dominant prevalence of C>T mutations at TCN sites. Genes with a significant frequency (false discovery rate (FDR)<0.05) of non-silent mutations include TP53 (47.1%), KRAS (7.8%) and ERBB3 (11.8%). Moreover, ErbB signaling (including EGFR, ERBB2, ERBB3, ERBB4 and their downstream genes) is the most extensively mutated pathway, affecting 36.8% (21/57) of the GBC samples. Multivariate analyses further show that cases with ErbB pathway mutations have a worse outcome (P=0.001). These findings provide insight into the somatic mutational landscape in GBC and highlight the key role of the ErbB signaling pathway in GBC pathogenesis.
JF - Nature genetics
AU - Li, Maolan
AU - Zhang, Zhou
AU - Li, Xiaoguang
AU - Ye, Junyi
AU - Wu, Xiangsong
AU - Tan, Zhujun
AU - Liu, Chang
AU - Shen, Baiyong
AU - Wang, Xu-An
AU - Wu, Wenguang
AU - Zhou, Daizhan
AU - Zhang, Di
AU - Wang, Ting
AU - Liu, Bingya
AU - Qu, Kai
AU - Ding, Qichen
AU - Weng, Hao
AU - Ding, Qian
AU - Mu, Jiasheng
AU - Shu, Yijun
AU - Bao, Runfa
AU - Cao, Yang
AU - Chen, Peizhan
AU - Liu, Tianyu
AU - Jiang, Lin
AU - Hu, Yunping
AU - Dong, Ping
AU - Gu, Jun
AU - Lu, Wei
AU - Shi, Weibin
AU - Lu, Jianhua
AU - Gong, Wei
AU - Tang, Zhaohui
AU - Zhang, Yong
AU - Wang, Xuefeng
AU - Chin, Y Eugene
AU - Weng, Xiaoling
AU - Zhang, Hong
AU - Tang, Wei
AU - Zheng, Yonglan
AU - He, Lin
AU - Wang, Hui
AU - Liu, Yun
AU - Liu, Yingbin
AD - 1] Department of General Surgery, Xinhua Hospital affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China. [2] Institute of Biliary Tract Disease, Shanghai Jiao Tong University School of Medicine, Shanghai, China. [3]. ; 1] Department of General Surgery, Xinhua Hospital affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China. [2] Institute of Biliary Tract Disease, Shanghai Jiao Tong University School of Medicine, Shanghai, China. [3] Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Bio-X Center, Shanghai Jiao Tong University, Shanghai, China. [4]. ; 1] Key Laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China. [2]. ; Institutes of Biomedical Sciences, Fudan University, Shanghai, China. ; 1] Department of General Surgery, Xinhua Hospital affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China. [2] Institute of Biliary Tract Disease, Shanghai Jiao Tong University School of Medicine, Shanghai, China. ; Department of Hepatobiliary Surgery, The First Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an, China. ; Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. ; Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Bio-X Center, Shanghai Jiao Tong University, Shanghai, China. ; Key Laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China. ; Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China. ; Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, US National Institutes of Health, Bethesda, Maryland, USA. ; Department of Medicine, The University of Chicago, Chicago, Illinois, USA. ; 1] Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Bio-X Center, Shanghai Jiao Tong University, Shanghai, China. [2] Institutes of Biomedical Sciences, Fudan University, Shanghai, China. [3] Women's Hospital, Zhejiang University School of Medicine, Hangzhou, China. ; 1] Key Laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China. [2] Key Laboratory of Food Safety Risk Assessment, Ministry of Health, Beijing, China. [3]. ; 1] Institutes of Biomedical Sciences, Fudan University, Shanghai, China. [2].
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 872
EP - 876
VL - 46
IS - 8
KW - EGFR protein, human
KW - EC 2.7.10.1
KW - Receptor, Epidermal Growth Factor
KW - Index Medicus
KW - High-Throughput Nucleotide Sequencing -- methods
KW - Aged, 80 and over
KW - Humans
KW - HEK293 Cells
KW - Adult
KW - Signal Transduction -- genetics
KW - Aged
KW - Middle Aged
KW - Cell Line, Tumor
KW - Male
KW - Female
KW - Cell Line
KW - Gallbladder Neoplasms -- enzymology
KW - Receptor, Epidermal Growth Factor -- genetics
KW - Exome
KW - Neoplasm Recurrence, Local -- enzymology
KW - Carcinoma -- enzymology
KW - Gallbladder Neoplasms -- genetics
KW - Mutation
KW - Neoplasm Recurrence, Local -- genetics
KW - Carcinoma -- genetics
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1549632568?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+genetics&rft.atitle=Whole-exome+and+targeted+gene+sequencing+of+gallbladder+carcinoma+identifies+recurrent+mutations+in+the+ErbB+pathway.&rft.au=Li%2C+Maolan%3BZhang%2C+Zhou%3BLi%2C+Xiaoguang%3BYe%2C+Junyi%3BWu%2C+Xiangsong%3BTan%2C+Zhujun%3BLiu%2C+Chang%3BShen%2C+Baiyong%3BWang%2C+Xu-An%3BWu%2C+Wenguang%3BZhou%2C+Daizhan%3BZhang%2C+Di%3BWang%2C+Ting%3BLiu%2C+Bingya%3BQu%2C+Kai%3BDing%2C+Qichen%3BWeng%2C+Hao%3BDing%2C+Qian%3BMu%2C+Jiasheng%3BShu%2C+Yijun%3BBao%2C+Runfa%3BCao%2C+Yang%3BChen%2C+Peizhan%3BLiu%2C+Tianyu%3BJiang%2C+Lin%3BHu%2C+Yunping%3BDong%2C+Ping%3BGu%2C+Jun%3BLu%2C+Wei%3BShi%2C+Weibin%3BLu%2C+Jianhua%3BGong%2C+Wei%3BTang%2C+Zhaohui%3BZhang%2C+Yong%3BWang%2C+Xuefeng%3BChin%2C+Y+Eugene%3BWeng%2C+Xiaoling%3BZhang%2C+Hong%3BTang%2C+Wei%3BZheng%2C+Yonglan%3BHe%2C+Lin%3BWang%2C+Hui%3BLiu%2C+Yun%3BLiu%2C+Yingbin&rft.aulast=Li&rft.aufirst=Maolan&rft.date=2014-08-01&rft.volume=46&rft.issue=8&rft.spage=872&rft.isbn=&rft.btitle=&rft.title=Nature+genetics&rft.issn=1546-1718&rft_id=info:doi/10.1038%2Fng.3030
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-01-12
N1 - Date created - 2014-07-29
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Comment In:
Cancer Discov. 2014 Sep;4(9):OF12 [25185194]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1038/ng.3030
ER -
TY - JOUR
T1 - Inducible nitric oxide synthase is key to peroxynitrite-mediated, LPS-induced protein radical formation in murine microglial BV2 cells.
AN - 1549199269; 24746617
AB - Microglia are the resident immune cells in the brain. Microglial activation is characteristic of several inflammatory and neurodegenerative diseases including Alzheimer's disease, multiple sclerosis, and Parkinson's disease. Though lipopolysaccharide (LPS)-induced microglial activation in models of Parkinson's disease is well documented, the free radical-mediated protein radical formation and its underlying mechanism during LPS-induced microglial activation are not known. Here we have used immuno-spin trapping and RNA interference to investigate the role of inducible nitric oxide synthase (iNOS) in peroxynitrite-mediated protein radical formation in murine microglial BV2 cells treated with LPS. Treatment of BV2 cells with LPS resulted in morphological changes, induction of iNOS, and increased protein radical formation. Pretreatments with FeTPPS (a peroxynitrite decomposition catalyst), L-NAME (total NOS inhibitor), 1400W (iNOS inhibitor), and apocynin significantly attenuated LPS-induced protein radical formation and tyrosine nitration. Results obtained with coumarin-7-boronic acid, a highly specific probe for peroxynitrite detection, correlated with LPS-induced tyrosine nitration, which demonstrated involvement of peroxynitrite in protein radical formation. A similar degree of protection conferred by 1400W and L-NAME led us to conclude that only iNOS, and no other forms of NOS, is involved in LPS-induced peroxynitrite formation. Subsequently, siRNA for iNOS, the iNOS-specific inhibitor 1400W, the NF-κB inhibitor PDTC, and the p38 MAPK inhibitor SB202190 was used to inhibit iNOS directly or indirectly. Inhibition of iNOS precisely correlated with decreased protein radical formation in LPS-treated BV2 cells. The time course of protein radical formation also matched the time course of iNOS expression. Taken together, these results prove the role of iNOS in peroxynitrite-mediated protein radical formation in LPS-treated microglial BV2 cells.
Copyright © 2014 Elsevier Inc. All rights reserved.
JF - Free radical biology & medicine
AU - Kumar, Ashutosh
AU - Chen, Shih-Heng
AU - Kadiiska, Maria B
AU - Hong, Jau-Shyong
AU - Zielonka, Jacek
AU - Kalyanaraman, Balaraman
AU - Mason, Ronald P
AD - Free Radical Metabolism Group, Laboratory of Toxicology & Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. Electronic address: kumara10@niehs.nih.gov. ; Neuropharmacology Group, Laboratory of Toxicology & Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. ; Free Radical Metabolism Group, Laboratory of Toxicology & Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. ; Department of Biophysics and Free Radical Research Center, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 51
EP - 59
VL - 73
KW - 5,10,15,20-tetrakis(4-sulfonatophenyl)porphyrinato iron(III) chloride
KW - 0
KW - Acetophenones
KW - Amidines
KW - Antioxidants
KW - Benzylamines
KW - Boronic Acids
KW - Coumarins
KW - Enzyme Inhibitors
KW - Free Radicals
KW - Imidazoles
KW - Lipopolysaccharides
KW - Metalloporphyrins
KW - N-(3-(aminomethyl)benzyl)acetamidine
KW - NF-kappa B
KW - Pyridines
KW - RNA, Small Interfering
KW - Thiocarbamates
KW - prolinedithiocarbamate
KW - 135467-92-4
KW - Peroxynitrous Acid
KW - 14691-52-2
KW - Proline
KW - 9DLQ4CIU6V
KW - acetovanillone
KW - B6J7B9UDTR
KW - Nitric Oxide Synthase Type II
KW - EC 1.14.13.39
KW - p38 Mitogen-Activated Protein Kinases
KW - EC 2.7.11.24
KW - 4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole
KW - PVX798P8GI
KW - NG-Nitroarginine Methyl Ester
KW - V55S2QJN2X
KW - Index Medicus
KW - Nitrone adducts
KW - Parkinson disease
KW - Peroxynitrite
KW - Inducible nitric oxide synthase
KW - Free radicals
KW - Microglia
KW - Protein radical
KW - Lipopolysaccharide
KW - Boronic Acids -- pharmacology
KW - Benzylamines -- pharmacology
KW - Animals
KW - NG-Nitroarginine Methyl Ester -- pharmacology
KW - Imidazoles -- pharmacology
KW - Metalloporphyrins -- pharmacology
KW - Spin Trapping
KW - Coumarins -- pharmacology
KW - Antioxidants -- pharmacology
KW - Cell Line, Transformed
KW - RNA Interference
KW - Microglia -- metabolism
KW - NF-kappa B -- antagonists & inhibitors
KW - Proline -- pharmacology
KW - Acetophenones -- pharmacology
KW - Mice
KW - Amidines -- pharmacology
KW - p38 Mitogen-Activated Protein Kinases -- antagonists & inhibitors
KW - Microglia -- cytology
KW - Enzyme Inhibitors -- pharmacology
KW - Thiocarbamates -- pharmacology
KW - Pyridines -- pharmacology
KW - Proline -- analogs & derivatives
KW - Peroxynitrous Acid -- metabolism
KW - Nitric Oxide Synthase Type II -- antagonists & inhibitors
KW - Neurodegenerative Diseases -- metabolism
KW - Nitric Oxide Synthase Type II -- metabolism
KW - Nitric Oxide Synthase Type II -- genetics
KW - Free Radicals -- metabolism
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Free+radical+biology+%26+medicine&rft.atitle=Inducible+nitric+oxide+synthase+is+key+to+peroxynitrite-mediated%2C+LPS-induced+protein+radical+formation+in+murine+microglial+BV2+cells.&rft.au=Kumar%2C+Ashutosh%3BChen%2C+Shih-Heng%3BKadiiska%2C+Maria+B%3BHong%2C+Jau-Shyong%3BZielonka%2C+Jacek%3BKalyanaraman%2C+Balaraman%3BMason%2C+Ronald+P&rft.aulast=Kumar&rft.aufirst=Ashutosh&rft.date=2014-08-01&rft.volume=73&rft.issue=&rft.spage=51&rft.isbn=&rft.btitle=&rft.title=Free+radical+biology+%26+medicine&rft.issn=1873-4596&rft_id=info:doi/10.1016%2Fj.freeradbiomed.2014.04.014
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-05-11
N1 - Date created - 2014-07-26
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Int J Mol Med. 2013 May;31(5):1030-6 [23546639]
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Antioxid Redox Signal. 2006 Sep-Oct;8(9-10):1391-418 [16986999]
Neurobiol Dis. 2007 Feb;25(2):392-400 [17166727]
Brain Res Rev. 2007 Apr;54(1):205-18 [17500094]
Biochemistry. 2007 Jun 26;46(25):7536-48 [17530864]
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Neurosci Lett. 2010 Jun 14;477(1):6-10 [20399833]
Mov Disord. 2011 May;26(6):993-1002 [21626544]
J Biol Chem. 2012 Jan 27;287(5):2984-95 [22139901]
Arch Pharm Res. 2012 Mar;35(4):709-15 [22553064]
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Chem Res Toxicol. 2012 Sep 17;25(9):1793-9 [22731669]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.freeradbiomed.2014.04.014
ER -
TY - JOUR
T1 - LC-MS-based metabolomics: an update.
AN - 1548640885; 24710571
AB - Liquid chromatography-mass spectrometry (LC-MS)-based metabolomics can have a major impact in multiple research fields, especially when combined with other technologies, such as stable isotope tracers and genetically modified mice. This review highlights recent applications of metabolomic technology in the study of xenobiotic metabolism and toxicity, and the understanding of disease pathogenesis and therapeutics. Metabolomics has been employed to study metabolism of noscapine, an aryl hydrocarbon receptor antagonist, and to determine the mechanisms of liver toxicities of rifampicin and isoniazid, trichloroethylene, and gemfibrozil. Metabolomics-based insights into the pathogenesis of inflammatory bowel disease, alcohol-induced liver diseases, non-alcoholic steatohepatitis, and farnesoid X receptor signaling pathway-based therapeutic target discovery will also be discussed. Limitations in metabolomics technology such as sample preparation and lack of LC-MS databases and metabolite standards, need to be resolved in order to improve and broaden the application of metabolomic studies.
JF - Archives of toxicology
AU - Fang, Zhong-Ze
AU - Gonzalez, Frank J
AD - Laboratory of Metabolism, Center for Cancer Research, National Institutes of Health, Bethesda, MD, 20892, USA.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 1491
EP - 1502
VL - 88
IS - 8
KW - Pharmaceutical Preparations
KW - 0
KW - Xenobiotics
KW - Index Medicus
KW - Animals
KW - Pharmaceutical Preparations -- metabolism
KW - Disease -- etiology
KW - Pharmaceutical Preparations -- chemistry
KW - Biotransformation
KW - Xenobiotics -- metabolism
KW - Humans
KW - Xenobiotics -- toxicity
KW - Metabolomics -- methods
KW - Mass Spectrometry
KW - Chromatography, Liquid
KW - Metabolomics -- instrumentation
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+toxicology&rft.atitle=LC-MS-based+metabolomics%3A+an+update.&rft.au=Fang%2C+Zhong-Ze%3BGonzalez%2C+Frank+J&rft.aulast=Fang&rft.aufirst=Zhong-Ze&rft.date=2014-08-01&rft.volume=88&rft.issue=8&rft.spage=1491&rft.isbn=&rft.btitle=&rft.title=Archives+of+toxicology&rft.issn=1432-0738&rft_id=info:doi/10.1007%2Fs00204-014-1234-6
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-03-30
N1 - Date created - 2014-07-25
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1007/s00204-014-1234-6
ER -
TY - JOUR
T1 - Inactivation of Wnt signaling by a human antibody that recognizes the heparan sulfate chains of glypican-3 for liver cancer therapy.
AN - 1548194944; 24492943
AB - Wnt signaling is important for cancer pathogenesis and is often up-regulated in hepatocellular carcinoma (HCC). Heparan sulfate proteoglycans (HSPGs) function as coreceptors or modulators of Wnt activation. Glypican-3 (GPC3) is an HSPG that is highly expressed in HCC, where it can attract Wnt proteins to the cell surface and promote cell proliferation. Thus, GPC3 has emerged as a candidate therapeutic target in liver cancer. While monoclonal antibodies to GPC3 are currently being evaluated in preclinical and clinical studies, none have shown an effect on Wnt signaling. Here, we first document the expression of Wnt3a, multiple Wnt receptors, and GPC3 in several HCC cell lines, and demonstrate that GPC3 enhanced the activity of Wnt3a/β-catenin signaling in these cells. Then we report the identification of HS20, a human monoclonal antibody against GPC3, which preferentially recognized the heparan sulfate chains of GPC3, both the sulfated and nonsulfated portions. HS20 disrupted the interaction of Wnt3a and GPC3 and blocked Wnt3a/β-catenin signaling. Moreover, HS20 inhibited Wnt3a-dependent cell proliferation in vitro and HCC xenograft growth in nude mice. In addition, HS20 had no detectable undesired toxicity in mice. Taken together, our results show that a monoclonal antibody primarily targeting the heparin sulfate chains of GPC3 inhibited Wnt/β-catenin signaling in HCC cells and had potent antitumor activity in vivo.
An antibody directed against the heparan sulfate of a proteoglycan shows efficacy in blocking Wnt signaling and HCC growth, suggesting a novel strategy for liver cancer therapy. Published 2014. This article is a U.S. Government work and is in the public domain in the USA.
JF - Hepatology (Baltimore, Md.)
AU - Gao, Wei
AU - Kim, Heungnam
AU - Feng, Mingqian
AU - Phung, Yen
AU - Xavier, Charles P
AU - Rubin, Jeffrey S
AU - Ho, Mitchell
AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 576
EP - 587
VL - 60
IS - 2
KW - Antibodies, Monoclonal
KW - 0
KW - CTNNB1 protein, human
KW - GPC3 protein, human
KW - Glypicans
KW - beta Catenin
KW - Heparitin Sulfate
KW - 9050-30-0
KW - Index Medicus
KW - Animals
KW - Hep G2 Cells
KW - Humans
KW - Xenograft Model Antitumor Assays
KW - Cell Surface Display Techniques
KW - Mice, Nude
KW - Mice
KW - beta Catenin -- immunology
KW - Mice, Inbred BALB C
KW - Female
KW - Heparitin Sulfate -- immunology
KW - Carcinoma, Hepatocellular -- drug therapy
KW - Liver Neoplasms -- drug therapy
KW - Wnt Signaling Pathway -- immunology
KW - Wnt Signaling Pathway -- drug effects
KW - Glypicans -- immunology
KW - Antibodies, Monoclonal -- pharmacology
KW - Carcinoma, Hepatocellular -- immunology
KW - Liver Neoplasms -- immunology
KW - Antibodies, Monoclonal -- immunology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Hepatology+%28Baltimore%2C+Md.%29&rft.atitle=Inactivation+of+Wnt+signaling+by+a+human+antibody+that+recognizes+the+heparan+sulfate+chains+of+glypican-3+for+liver+cancer+therapy.&rft.au=Gao%2C+Wei%3BKim%2C+Heungnam%3BFeng%2C+Mingqian%3BPhung%2C+Yen%3BXavier%2C+Charles+P%3BRubin%2C+Jeffrey+S%3BHo%2C+Mitchell&rft.aulast=Gao&rft.aufirst=Wei&rft.date=2014-08-01&rft.volume=60&rft.issue=2&rft.spage=576&rft.isbn=&rft.btitle=&rft.title=Hepatology+%28Baltimore%2C+Md.%29&rft.issn=1527-3350&rft_id=info:doi/10.1002%2Fhep.26996
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-09-22
N1 - Date created - 2014-07-23
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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Comment In:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1002/hep.26996
ER -
TY - JOUR
T1 - In vitro anti-proliferative and anti-angiogenic activities of thalidomide dithiocarbamate analogs.
AN - 1547832584; 24859059
AB - Inhibition of angiogenesis is currently perceived as a promising strategy in the treatment of cancer. The anti-angiogenicity of thalidomide has inspired a second wave of research on this teratogenic drug. The present study aimed to investigate the anti-proliferative and anti-angiogenic activities of two thalidomide dithiocarbamate analogs by studying their anti-proliferative effects on human umbilical vein endothelial cells (HUVECs) and MDA-MB-231 human breast cancer cell lines. Their action on the expression levels of IL-6, IL-8, TNF-α, VEGF165, and MMP-2 was also assessed. Furthermore, their effect on angiogenesis was evaluated through wound healing, migration, tube formation, and nitric oxide (NO) assays. Results illustrated that the proliferation of HUVECs and MDA-MB-231 cells was not significantly affected by thalidomide at 6.25-100μM. Thalidomide failed to block angiogenesis at similar concentrations. By contrast, thalidomide dithiocarbamate analogs exhibited significant anti-proliferative action on HUVECs and MDA-MB-231 cells without causing cytotoxicity and also showed powerful anti-angiogenicity in wound healing, migration, tube formation, and NO assays. Thalidomide analogs 1 and 2 demonstrated more potent activity to suppress expression levels of IL-6, IL-8, TNF-α, VEGF165, and MMP-2 than thalidomide. Analog 1 consistently, showed the highest potency and efficacy in all the assays. Taken together, our results support further development and evaluation of novel thalidomide analogs as anti-tumor and anti-angiogenic agents.
Copyright © 2014. Published by Elsevier B.V.
JF - International immunopharmacology
AU - El-Aarag, Bishoy Y A
AU - Kasai, Tomonari
AU - Zahran, Magdy A H
AU - Zakhary, Nadia I
AU - Shigehiro, Tsukasa
AU - Sekhar, Sreeja C
AU - Agwa, Hussein S
AU - Mizutani, Akifumi
AU - Murakami, Hiroshi
AU - Kakuta, Hiroki
AU - Seno, Masaharu
AD - Chemistry Department, Faculty of Science, Menofia University, Egypt; Division of Chemistry and Biotechnology, Graduate School of Natural Science and Technology, Okayama University, Okayama 7008530, Japan. ; Division of Chemistry and Biotechnology, Graduate School of Natural Science and Technology, Okayama University, Okayama 7008530, Japan. Electronic address: t-kasai@cc.okayama-u.ac.jp. ; Chemistry Department, Faculty of Science, Menofia University, Egypt. ; Cancer Biology Department, National Cancer Institute, Cairo University, Egypt. ; Division of Chemistry and Biotechnology, Graduate School of Natural Science and Technology, Okayama University, Okayama 7008530, Japan. ; Division of Pharmaceutical Sciences, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama 7008530, Japan.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 283
EP - 292
VL - 21
IS - 2
KW - Angiogenesis Inhibitors
KW - 0
KW - Interleukin-6
KW - Interleukin-8
KW - Thiocarbamates
KW - Tumor Necrosis Factor-alpha
KW - VEGFA protein, human
KW - Vascular Endothelial Growth Factor A
KW - Nitric Oxide
KW - 31C4KY9ESH
KW - Thalidomide
KW - 4Z8R6ORS6L
KW - Matrix Metalloproteinase 2
KW - EC 3.4.24.24
KW - Index Medicus
KW - VEGF
KW - Angiogenesis
KW - Thalidomide dithiocarbamate analogs
KW - Migration
KW - NO
KW - Breast Neoplasms -- drug therapy
KW - Humans
KW - Interleukin-6 -- metabolism
KW - Breast Neoplasms -- metabolism
KW - Nitric Oxide -- metabolism
KW - Cell Line, Tumor
KW - Human Umbilical Vein Endothelial Cells
KW - Matrix Metalloproteinase 2 -- metabolism
KW - Interleukin-8 -- metabolism
KW - Tumor Necrosis Factor-alpha -- metabolism
KW - Cell Line
KW - Female
KW - Vascular Endothelial Growth Factor A -- metabolism
KW - Cell Proliferation -- drug effects
KW - Angiogenesis Inhibitors -- pharmacology
KW - Neovascularization, Pathologic -- drug therapy
KW - Neovascularization, Pathologic -- metabolism
KW - Thiocarbamates -- pharmacology
KW - Thalidomide -- pharmacology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+immunopharmacology&rft.atitle=In+vitro+anti-proliferative+and+anti-angiogenic+activities+of+thalidomide+dithiocarbamate+analogs.&rft.au=El-Aarag%2C+Bishoy+Y+A%3BKasai%2C+Tomonari%3BZahran%2C+Magdy+A+H%3BZakhary%2C+Nadia+I%3BShigehiro%2C+Tsukasa%3BSekhar%2C+Sreeja+C%3BAgwa%2C+Hussein+S%3BMizutani%2C+Akifumi%3BMurakami%2C+Hiroshi%3BKakuta%2C+Hiroki%3BSeno%2C+Masaharu&rft.aulast=El-Aarag&rft.aufirst=Bishoy+Y&rft.date=2014-08-01&rft.volume=21&rft.issue=2&rft.spage=283&rft.isbn=&rft.btitle=&rft.title=International+immunopharmacology&rft.issn=1878-1705&rft_id=info:doi/10.1016%2Fj.intimp.2014.05.007
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-04-09
N1 - Date created - 2014-07-22
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.intimp.2014.05.007
ER -
TY - JOUR
T1 - Morphine and codeine concentrations in human urine following controlled poppy seeds administration of known opiate content.
AN - 1547543220; 24887324
AB - Opiates are an important component for drug testing due to their high abuse potential. Proper urine opiate interpretation includes ruling out poppy seed ingestion; however, detailed elimination studies after controlled poppy seed administration with known morphine and codeine doses are not available. Therefore, we investigated urine opiate pharmacokinetics after controlled oral administration of uncooked poppy seeds with known morphine and codeine content. Participants were administered two 45 g oral poppy seed doses 8 h apart, each containing 15.7 mg morphine and 3mg codeine. Urine was collected ad libitum up to 32 h after the first dose. Specimens were analyzed with the Roche Opiates II immunoassay at 2000 and 300 μg/L cutoffs, and the ThermoFisher CEDIA(®) heroin metabolite (6-acetylmorphine, 6-AM) and Lin-Zhi 6-AM immunoassays with 10 μg/L cutoffs to determine if poppy seed ingestion could produce positive results in these heroin marker assays. In addition, all specimens were quantified for morphine and codeine by GC/MS. Participants (N=22) provided 391 urine specimens over 32 h following dosing; 26.6% and 83.4% were positive for morphine at 2000 and 300 μg/L GC/MS cutoffs, respectively. For the 19 subjects who completed the study, morphine concentrations ranged from <300 to 7522 μg/L with a median peak concentration of 5239 μg/L. The median first morphine-positive urine sample at 2000 μg/L cutoff concentration occurred at 6.6 h (1.2-12.1), with the last positive from 2.6 to 18 h after the second dose. No specimens were positive for codeine at a cutoff concentration of 2000 μg/L, but 20.2% exceeded 300 μg/L, with peak concentrations of 658 μg/L (284-1540). The Roche Opiates II immunoassay had efficiencies greater than 96% for the 2000 and 300 μg/L cutoffs. The CEDIA 6-AM immunoassay had a specificity of 91%, while the Lin-Zhi assay had no false positive results. These data provide valuable information for interpreting urine opiate results.
Copyright © 2014. Published by Elsevier Ireland Ltd.
JF - Forensic science international
AU - Smith, Michael L
AU - Nichols, Daniel C
AU - Underwood, Paula
AU - Fuller, Zachary
AU - Moser, Matthew A
AU - LoDico, Charles
AU - Gorelick, David A
AU - Newmeyer, Matthew N
AU - Concheiro, Marta
AU - Huestis, Marilyn A
AD - U.S. Army Forensic Toxicology Drug Testing Laboratory, Fort Meade, MD, USA. ; Division of Workplace Programs, Substance Abuse Mental Health Services Administration, Department of Health and Human Services, Rockville, MD, USA. ; Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD, USA; Currently at Department of Psychiatry, University of Maryland School of Medicine, Baltimore, MD, USA. ; Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD, USA; Program in Toxicology, University of Maryland Baltimore, Baltimore, MD, USA. ; Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD, USA. ; Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD, USA. Electronic address: mhuestis@intra.nida.nih.gov.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 87
EP - 90
VL - 241
KW - Analgesics, Opioid
KW - 0
KW - Morphine
KW - 76I7G6D29C
KW - Codeine
KW - Q830PW7520
KW - Index Medicus
KW - Poppy seeds
KW - Urine
KW - Controlled dose
KW - Humans
KW - Gas Chromatography-Mass Spectrometry
KW - Male
KW - Female
KW - Immunoassay
KW - Seeds
KW - Morphine -- urine
KW - Papaver
KW - Codeine -- urine
KW - Analgesics, Opioid -- urine
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Forensic+science+international&rft.atitle=Morphine+and+codeine+concentrations+in+human+urine+following+controlled+poppy+seeds+administration+of+known+opiate+content.&rft.au=Smith%2C+Michael+L%3BNichols%2C+Daniel+C%3BUnderwood%2C+Paula%3BFuller%2C+Zachary%3BMoser%2C+Matthew+A%3BLoDico%2C+Charles%3BGorelick%2C+David+A%3BNewmeyer%2C+Matthew+N%3BConcheiro%2C+Marta%3BHuestis%2C+Marilyn+A&rft.aulast=Smith&rft.aufirst=Michael&rft.date=2014-08-01&rft.volume=241&rft.issue=&rft.spage=87&rft.isbn=&rft.btitle=&rft.title=Forensic+science+international&rft.issn=1872-6283&rft_id=info:doi/10.1016%2Fj.forsciint.2014.04.042
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-10-21
N1 - Date created - 2014-07-19
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Drug Test Anal. 2014 Mar;6(3):194-201 [24339374]
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Forensic Sci Int. 1998 Jul 6;95(1):1-10 [9718666]
Clin Chem. 1997 Jun;43(6 Pt 1):1029-32 [9191557]
Planta Med. 1996 Dec;62(6):544-7 [9000887]
J Anal Toxicol. 1991 Jul-Aug;15(4):161-6 [1943064]
J Anal Toxicol. 1991 Mar-Apr;15(2):49-53 [2051744]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.forsciint.2014.04.042
ER -
TY - JOUR
T1 - Impact of neoadjuvant single or dual HER2 inhibition and chemotherapy backbone upon pathological complete response in operable and locally advanced breast cancer: Sensitivity analysis of randomized trials.
AN - 1546219126; 24877987
AB - The role of the dual HER2 inhibition, and the best chemotherapy backbone for neoadjuvant chemotherapy still represent an issue for clinical practice. A literature-based meta-analysis exploring single versus dual HER2 inhibition in terms of pathological complete response (pCR, breast plus axilla) rate and testing the interaction according to the chemotherapy (anthracyclines-taxanes or taxanes) was conducted. In addition, an event-based pooled analysis by extracting activity and safety events and deriving 95% confidence intervals (CI) was accomplished. Fourteen trials (4149 patients) were identified, with 6 trials (1820 patients) included in the meta-analysis and 31 arms (14 trials, 3580 patients) in the event-based pooled analysis. The dual HER2 inhibition significantly improves pCR rate, in the range of 16-19%, regardless of the chemotherapy backbone (relative risk 1.37, 95% CI 1.23-1.53, p<0.0001); pCR was significantly higher in the hormonal receptor negative population, regardless of the HER2 inhibition and type of chemotherapy. pCR and the rate of breast conserving surgery was higher when anthracyclines were added to taxanes, regardless of the HER2 inhibition. Severe neutropenia was higher with the addition of anthracyclines to taxanes, with an absolute difference of 19.7%, despite no differences in febrile neutropenia. While no significant differences according to the HER2 inhibition were found in terms of cardiotoxicity, a slightly difference for grade 3-4 (1.2%) against the addition of anthracyclines was calculated. The dual HER2 inhibition for the neoadjuvant treatment of HER2-positive breast cancer significantly increases pCR; the combination of anthracyclines, taxanes and anti-Her2 agents should be currently considered the standard of care.
Copyright © 2014 Elsevier Ltd. All rights reserved.
JF - Cancer treatment reviews
AU - Bria, Emilio
AU - Carbognin, Luisa
AU - Furlanetto, Jenny
AU - Pilotto, Sara
AU - Bonomi, Maria
AU - Guarneri, Valentina
AU - Vicentini, Cecilia
AU - Brunelli, Matteo
AU - Nortilli, Rolando
AU - Pellini, Francesca
AU - Sperduti, Isabella
AU - Giannarelli, Diana
AU - Pollini, Giovanni Paolo
AU - Conte, Pierfranco
AU - Tortora, Giampaolo
AD - Medical Oncology, Azienda Ospedaliera Universitaria Integrata, University of Verona, Verona, Italy. Electronic address: emiliobria@yahoo.it. ; Medical Oncology, Azienda Ospedaliera Universitaria Integrata, University of Verona, Verona, Italy. Electronic address: luisa.carbognin@gmail.com. ; Medical Oncology, Azienda Ospedaliera Universitaria Integrata, University of Verona, Verona, Italy. Electronic address: jenny.furlanetto@hotmail.it. ; Medical Oncology, Azienda Ospedaliera Universitaria Integrata, University of Verona, Verona, Italy. Electronic address: sara.pilotto.85@alice.it. ; Medical Oncology, Azienda Ospedaliera Universitaria Integrata, University of Verona, Verona, Italy. Electronic address: mari.bonomi0429@gmail.com. ; Medical Oncology, Istituto Oncologico Veneto IRCCS, University of Padova, Padova, Italy. Electronic address: valentina.guarneri@unipd.it. ; Medical Oncology, Azienda Ospedaliera Universitaria Integrata, University of Verona, Verona, Italy. Electronic address: cecivice@gmail.com. ; Department of Pathology and Diagnostic, Azienda Ospedaliera Universitaria Integrata, University of Verona, Verona, Italy. Electronic address: matteo.brunelli@univr.it. ; Medical Oncology, Azienda Ospedaliera Universitaria Integrata, University of Verona, Verona, Italy. Electronic address: rolando.nortilli@ospedaleuniverona.it. ; Chirurgia 'A', Department of Surgery and Oncology, Azienda Ospedaliera Universitaria Integrata, University of Verona, Verona, Italy. Electronic address: francesca.pellini@ospedaleuniverona.it. ; Biostatistics, Regina Elena National Cancer Institute, Roma, Italy. Electronic address: isperduti@yahoo.it. ; Biostatistics, Regina Elena National Cancer Institute, Roma, Italy. Electronic address: giannarelli@ifo.it. ; Chirurgia 'A', Department of Surgery and Oncology, Azienda Ospedaliera Universitaria Integrata, University of Verona, Verona, Italy. Electronic address: giovanni.pollini@ospedaleuniverona.it. ; Medical Oncology, Istituto Oncologico Veneto IRCCS, University of Padova, Padova, Italy. Electronic address: pierfranco.conte@unipd.it. ; Medical Oncology, Azienda Ospedaliera Universitaria Integrata, University of Verona, Verona, Italy. Electronic address: giampaolo.tortora@univr.it.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 847
EP - 856
VL - 40
IS - 7
KW - Anthracyclines
KW - 0
KW - Protein Kinase Inhibitors
KW - Taxoids
KW - ERBB2 protein, human
KW - EC 2.7.10.1
KW - Receptor, ErbB-2
KW - Index Medicus
KW - Neoadjuvant
KW - Meta-analysis
KW - Trastuzumab
KW - Breast cancer
KW - HER2-positive
KW - Randomized Controlled Trials as Topic
KW - Protein Kinase Inhibitors -- therapeutic use
KW - Humans
KW - Protein Kinase Inhibitors -- administration & dosage
KW - Neoadjuvant Therapy
KW - Anthracyclines -- administration & dosage
KW - Female
KW - Taxoids -- administration & dosage
KW - Breast Neoplasms -- pathology
KW - Receptor, ErbB-2 -- antagonists & inhibitors
KW - Breast Neoplasms -- therapy
KW - Breast Neoplasms -- enzymology
KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+treatment+reviews&rft.atitle=Impact+of+neoadjuvant+single+or+dual+HER2+inhibition+and+chemotherapy+backbone+upon+pathological+complete+response+in+operable+and+locally+advanced+breast+cancer%3A+Sensitivity+analysis+of+randomized+trials.&rft.au=Bria%2C+Emilio%3BCarbognin%2C+Luisa%3BFurlanetto%2C+Jenny%3BPilotto%2C+Sara%3BBonomi%2C+Maria%3BGuarneri%2C+Valentina%3BVicentini%2C+Cecilia%3BBrunelli%2C+Matteo%3BNortilli%2C+Rolando%3BPellini%2C+Francesca%3BSperduti%2C+Isabella%3BGiannarelli%2C+Diana%3BPollini%2C+Giovanni+Paolo%3BConte%2C+Pierfranco%3BTortora%2C+Giampaolo&rft.aulast=Bria&rft.aufirst=Emilio&rft.date=2014-08-01&rft.volume=40&rft.issue=7&rft.spage=847&rft.isbn=&rft.btitle=&rft.title=Cancer+treatment+reviews&rft.issn=1532-1967&rft_id=info:doi/10.1016%2Fj.ctrv.2014.05.001
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-08-05
N1 - Date created - 2014-06-10
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.ctrv.2014.05.001
ER -
TY - JOUR
T1 - Analytic and clinical performance of cobas HPV testing in anal specimens from HIV-positive men who have sex with men.
AN - 1546214580; 24899025
AB - Anal human papillomavirus (HPV) infections are common, and the incidence of anal cancer is high in HIV-infected men who have sex with men (MSM). To evaluate the performance of HPV assays in anal samples, we compared the cobas HPV test (cobas) to the Roche Linear Array HPV genotyping assay (LA) and cytology in HIV-infected MSM. Cytology and cobas and LA HPV testing were conducted for 342 subjects. We calculated agreement between the HPV assays and the clinical performance of HPV testing and HPV genotyping alone and in combination with anal cytology. We observed high agreement between cobas and LA, with cobas more likely than LA to show positive results for HPV16, HPV18, and other carcinogenic types. Specimens testing positive in cobas but not in LA were more likely to be positive for other markers of HPV-related disease compared to those testing negative in both assays, suggesting that at least some of these were true positives for HPV. cobas and LA showed high sensitivities but low specificities for the detection of anal intraepithelial neoplasia grade 2/3 (AIN2/3) in this population (100% sensitivity and 26% specificity for cobas versus 98.4% sensitivity and 28.9% specificity for LA). A combination of anal cytology and HPV genotyping provided the highest accuracy for detecting anal precancer. A higher HPV load was associated with a higher risk of AIN2/3 with HPV16 (P(trend) < 0.001), HPV18 (P(trend) = 0.07), and other carcinogenic types (P(trend) < 0.001). We demonstrate that cobas can be used for HPV detection in anal cytology specimens. Additional tests are necessary to identify men at the highest risk of anal cancer among those infected with high-risk HPV.
Copyright © 2014, American Society for Microbiology. All Rights Reserved.
JF - Journal of clinical microbiology
AU - Wentzensen, Nicolas
AU - Follansbee, Stephen
AU - Borgonovo, Sylvia
AU - Tokugawa, Diane
AU - Sahasrabuddhe, Vikrant V
AU - Chen, Jie
AU - Lorey, Thomas S
AU - Gage, Julia C
AU - Fetterman, Barbara
AU - Boyle, Sean
AU - Sadorra, Mark
AU - Tang, Scott Dahai
AU - Darragh, Teresa M
AU - Castle, Philip E
AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA wentzenn@mail.nih.gov. ; Kaiser Permanente Medical Center, San Francisco, California, USA. ; Kaiser Permanente TPMG Regional Laboratory, Berkeley, California, USA. ; Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA. ; Roche Molecular Systems, Pleasanton, California, USA. ; University of California, San Francisco, California, USA. ; Global Cancer Initiative, Chestertown, Maryland, USA.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 2892
EP - 2897
VL - 52
IS - 8
KW - Index Medicus
KW - Sensitivity and Specificity
KW - Young Adult
KW - Humans
KW - Adult
KW - Middle Aged
KW - Adolescent
KW - Cytological Techniques -- methods
KW - Male
KW - Homosexuality, Male
KW - Papillomavirus Infections -- diagnosis
KW - Papillomaviridae -- classification
KW - Anus Diseases -- diagnosis
KW - Papillomaviridae -- isolation & purification
KW - Papillomavirus Infections -- virology
KW - Papillomaviridae -- genetics
KW - Anus Diseases -- virology
KW - Genotyping Techniques -- methods
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-05-20
N1 - Date created - 2014-07-18
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Cancer Discov. 2013 Feb;3(2):148-57 [23299199]
J Infect Dis. 2013 Feb 1;207(3):392-401 [23162133]
J Infect Dis. 2013 Dec 1;208(11):1768-75 [23908478]
Int J Cancer. 2015 Jan 1;136(1):98-107 [24817381]
JAMA. 2002 Apr 24;287(16):2114-9 [11966386]
Int J Cancer. 2007 Dec 15;121(12):2787-93 [17722112]
Int J Cancer. 2009 Feb 1;124(3):516-20 [18973271]
Int J Cancer. 2009 Apr 1;124(7):1626-36 [19115209]
BMJ. 2009;339:b2569 [19638649]
J Natl Cancer Inst. 2009 Aug 19;101(16):1120-30 [19648510]
Am J Clin Pathol. 2011 Mar;135(3):468-75 [21350104]
Lancet Oncol. 2011 Sep;12(9):880-90 [21865084]
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J Clin Microbiol. 2012 Jan;50(1):61-5 [22075592]
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AIDS. 2012 Nov 13;26(17):2185-92 [23018436]
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Cancer Cytopathol. 2013 Feb;121(2):72-8 [22811048]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1128/JCM.03517-13
ER -
TY - JOUR
T1 - Risk of neurobehavioral disinhibition in prenatal methamphetamine-exposed young children with positive hair toxicology results.
AN - 1545420583; 24518561
AB - The objective was to evaluate the effects of prenatal methamphetamine exposure (PME) and postnatal drug exposures identified by child hair analysis on neurobehavioral disinhibition at 6.5 years of age.
Mother-infant pairs were enrolled in the Infant Development, Environment, and Lifestyle (IDEAL) Study in Los Angeles, Honolulu, Tulsa, and Des Moines. PME was determined by maternal self-report and/or positive meconium results. At the 6.5-year follow-up visit, hair was collected and analyzed for methamphetamine, tobacco, cocaine, and cannabinoid markers. Child behavioral and executive function test scores were aggregated to evaluate child neurobehavioral disinhibition. Hierarchical linear regression models assessed the impact of PME, postnatal substances, and combined PME with postnatal drug exposures on the child's neurobehavioral disinhibition aggregate score. Past year caregiver substance use was compared with child hair results. A total of 264 children were evaluated. Significantly more PME children (n = 133) had hair positive for methamphetamine/amphetamine (27.1% versus 8.4%) and nicotine/cotinine (38.3% versus 25.2%) than children without PME (n = 131). Overall, no significant differences in analyte hair concentrations were noted between groups. Significant differences in behavioral and executive function were observed between children with and without PME. No independent effects of postnatal methamphetamine or tobacco exposure, identified by positive hair test, were noted and no additional neurobehavioral disinhibition was observed in PME children with postnatal drug exposures, as compared with PME children without postnatal exposure.
Child hair testing offered a noninvasive means to evaluate postnatal environmental drug exposure, although no effects from postnatal drug exposure alone were seen. PME, alone and in combination with postnatal drug exposures, was associated with behavioral and executive function deficits at 6.5 years.
JF - Therapeutic drug monitoring
AU - Himes, Sarah K
AU - LaGasse, Linda L
AU - Derauf, Chris
AU - Newman, Elana
AU - Smith, Lynne M
AU - Arria, Amelia M
AU - Della Grotta, Sheri A
AU - Dansereau, Lynne M
AU - Abar, Beau
AU - Neal, Charles R
AU - Lester, Barry M
AU - Huestis, Marilyn A
AD - *Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland; †Department of Pediatrics, Brown Center for the Study of Children at Risk, Warren Alpert Medical School of Brown University, Women and Infants Hospital of Rhode Island, Providence, RI; ‡Division of Community Pediatric and Adolescent Medicine, Mayo Clinic, Rochester, Minnesota; §Department of Psychology, The University of Tulsa, Tulsa, Oklahoma; ¶Department of Pediatrics, LABioMed Institute at Harbor-UCLA Medical Center, David Geffen School of Medicine at UCLA, Torrance, California; ‖Department of Family Science, Center on Young Adult Health and Development, University of Maryland School of Public Health, College Park, Maryland; **Department of Emergency Medicine and Psychiatry, University of Rochester Medical Center, Rochester, New York; and ††Department of Pediatrics, John A. Burns School of Medicine, University of Hawaii, Honolulu, Hawaii.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 535
EP - 543
VL - 36
IS - 4
KW - Methamphetamine
KW - 44RAL3456C
KW - Nicotine
KW - 6M3C89ZY6R
KW - Cocaine
KW - I5Y540LHVR
KW - Index Medicus
KW - Risk
KW - Tobacco -- chemistry
KW - Mothers
KW - Humans
KW - Case-Control Studies
KW - Cocaine -- chemistry
KW - Child Development -- drug effects
KW - Child
KW - Female
KW - Pregnancy
KW - Nicotine -- chemistry
KW - Hair -- chemistry
KW - Methamphetamine -- chemistry
KW - Prenatal Exposure Delayed Effects -- diagnosis
KW - Amphetamine-Related Disorders -- diagnosis
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-03-02
N1 - Date created - 2014-07-15
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Pediatrics. 2002 May;109(5):815-25 [11986441]
Psychol Addict Behav. 2013 Sep;27(3):662-73 [23067308]
Am J Psychiatry. 2003 Jun;160(6):1078-85 [12777265]
Anal Chem. 2004 Aug 1;76(15):4358-63 [15283573]
Forensic Sci Int. 1997 Jan 17;84(1-3):123-8 [9042716]
J Abnorm Child Psychol. 1998 Aug;26(4):257-68 [9700518]
Drug Metab Dispos. 2005 Feb;33(2):258-61 [15528319]
Matern Child Health J. 2006 May;10(3):293-302 [16395620]
Ther Drug Monit. 2006 Jun;28(3):442-6 [16778731]
Am J Drug Alcohol Abuse. 2007;33(2):281-9 [17497551]
Forensic Sci Int. 2007 Jul 4;169(2-3):129-36 [16963215]
J Dev Behav Pediatr. 2007 Jun;28(3):219-24 [17565289]
Arch Dis Child Fetal Neonatal Ed. 2007 Sep;92(5):F351-5 [17077112]
Obstet Gynecol. 2008 Feb;111(2 Pt 1):341-7 [18238971]
Obstet Gynecol. 2009 Jun;113(6):1285-91 [19461424]
J Dev Behav Pediatr. 2009 Jun;30(3):185-92 [19525715]
J Burn Care Res. 2009 Jul-Aug;30(4):587-92 [19506505]
J Chromatogr B Analyt Technol Biomed Life Sci. 2009 Nov 1;877(29):3701-6 [19783234]
Ther Drug Monit. 2009 Dec;31(6):769-75 [19935364]
Forensic Sci Int. 2010 Mar 20;196(1-3):38-42 [20056364]
Annu Rev Public Health. 2010;31:385-98 [20070191]
J Addict Dis. 2010 Apr;29(2):259-76 [20407981]
Clin Chem. 2010 May;56(5):856-60 [20185623] Neurotoxicol Teratol. 2011 Jan-Feb;33(1):166-75 [20615464]
Neurotoxicol Teratol. 2011 Jan-Feb;33(1):176-84 [21256431]
J Forensic Leg Med. 2011 Apr;18(3):110-4 [21420647]
Dev Psychopathol. 2011 Aug;23(3):777-88 [21756431]
Pediatrics. 2012 Apr;129(4):681-8 [22430455]
Anal Chim Acta. 2012 May 13;726:35-43 [22541011]
Ther Drug Monit. 2012 Jun;34(3):337-44 [22495425]
Forensic Sci Int. 2012 Jun 10;219(1-3):179-82 [22300795]
J Pediatr. 2012 Sep;161(3):452-9 [22424953]
Child Psychiatry Hum Dev. 2012 Dec;43(6):943-57 [22552952]
Drug Alcohol Depend. 2012 Nov 1;126(1-2):80-6 [22608010]
J Dev Behav Pediatr. 2013 Jan;34(1):31-7 [23275056]
J Subst Abuse Treat. 2013 May-Jun;44(5):548-56 [23313146]
Pediatr Emerg Care. 2002 Aug;18(4):327-32 [12187145]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1097/FTD.0000000000000049
ER -
TY - JOUR
T1 - MicroRNA expression profiling of thymic epithelial tumors.
AN - 1545416547; 24863004
AB - Thymic epithelial tumors (TET) are the most frequent human primary mediastinal tumors in adults. A deep biological characterization of the processes at the basis of the transformed phenotype could strongly improve our understanding of the morphological and clinical heterogeneity of these diseases. MicroRNAs (miRNAs) are non-coding RNAs involved in post-transcriptional regulation and their altered expression accounts for the pathogenesis of several tumors.
The aim of this study was to identify the miRNAs that are differentially expressed in tumor vs normal thymic tissues or among the different tumor histotypes and that could impact on the biology of TET. microRNAs expression profiling was performed by microarray analysis of formalin-fixed paraffin embedded (FFPE) tissue from 54 thymic tumor samples and 12 normal counterparts, derived from two patient cohorts.
We identified groups of miRNAs differentially expressed between: (i) TET and normal thymic tissues, (ii) thymomas and thymic carcinomas, (iii) histotype groups. Moreover, we identified putative molecular pathways targeted by these differentially expressed miRNAs that could be involved in thymic carcinogenesis and in the maintenance and spreading of this tumor. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.
JF - Lung cancer (Amsterdam, Netherlands)
AU - Ganci, Federica
AU - Vico, Carmen
AU - Korita, Etleva
AU - Sacconi, Andrea
AU - Gallo, Enzo
AU - Mori, Federica
AU - Cambria, Annamaria
AU - Russo, Emanuele
AU - Anile, Marco
AU - Vitolo, Domenico
AU - Pescarmona, Edoardo
AU - Blandino, Rosario
AU - Facciolo, Francesco
AU - Venuta, Federico
AU - Blandino, Giovanni
AU - Marino, Mirella
AU - Fazi, Francesco
AD - Translational Oncogenomics Unit, "Regina Elena" National Cancer Institute, Rome, Italy. ; Department of Anatomical, Histological, Forensic & Orthopaedic Sciences, Section of Histology & Medical Embryology, Sapienza University of Rome, Rome, Italy. ; Department of Pathology, "Regina Elena" National Cancer Institute, Rome, Italy. ; Molecular Chemoprevention Unit, "Regina Elena" National Cancer Institute, Rome, Italy. ; Department of Oncology, Division of Pathology, S. Vincenzo Hospital, Taormina, Italy. ; Department of Thoracic Surgery, Azienda Policlinico Umberto I, Sapienza University of Rome, Rome, Italy; Fondazione Eleonora Lorillard Spencer Cenci, Italy. ; Department of Pathology, Azienda Policlinico Umberto I, "Sapienza" University of Rome, Rome, Italy. ; Department of Oncology, Division of Oncological Surgery S. Vincenzo Hospital, Taormina, Italy. ; Thoracic Surgery, "Regina Elena" National Cancer Institute, Rome, Italy. ; Department of Pathology, "Regina Elena" National Cancer Institute, Rome, Italy. Electronic address: marino@ifo.it. ; Department of Anatomical, Histological, Forensic & Orthopaedic Sciences, Section of Histology & Medical Embryology, Sapienza University of Rome, Rome, Italy. Electronic address: francesco.fazi@uniroma1.it.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 197
EP - 204
VL - 85
IS - 2
KW - MicroRNAs
KW - 0
KW - Receptor, Epidermal Growth Factor
KW - EC 2.7.10.1
KW - Index Medicus
KW - EGFR
KW - microRNAs
KW - miR-145
KW - Thymic epithelial tumors
KW - Receptor, Epidermal Growth Factor -- genetics
KW - Humans
KW - Thymus Gland -- metabolism
KW - Cluster Analysis
KW - Gene Expression Regulation, Neoplastic
KW - Gene Expression Profiling
KW - Neoplasms, Glandular and Epithelial -- genetics
KW - MicroRNAs -- genetics
KW - Thymus Neoplasms -- genetics
KW - Thymus Neoplasms -- pathology
KW - Neoplasms, Glandular and Epithelial -- pathology
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-07-09
N1 - Date created - 2014-07-15
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.lungcan.2014.04.008
ER -
TY - JOUR
T1 - Reversible cerebellar ataxia due to ovarian teratoma.
AN - 1545414798; 24726236
AB - Cerebellar dysfunction is a classic paraneoplastic syndrome associated with various types of cancer, including gynecological and breast tumors, small-cell lung cancer, thymoma, and Hodgkin's lymphoma. We present a 22-year-old woman with acute cerebellar ataxia that subsided upon removal of an ovarian teratoma. This patient may represent a new category of immune-mediated cerebellar ataxia that is reversible with removal of an underlying tumor.
Published by Elsevier Ltd.
JF - Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
AU - Park, Jung E
AU - Liang, Tsao-Wei
AD - Human Motor Control Section, Medical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 10 Center Drive Room 7D42, Bethesda, MD 20892, USA. Electronic address: junge.park@nih.gov. ; The Parkinson's Disease and Movement Disorders Program, Department of Neurology, Thomas Jefferson University, Philadelphia, PA, USA.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 1467
EP - 1469
VL - 21
IS - 8
KW - Index Medicus
KW - Ovarian teratoma
KW - Paraneoplastic
KW - Ataxia
KW - Oscillopsia
KW - Nystagmus
KW - Young Adult
KW - Humans
KW - Treatment Outcome
KW - Recovery of Function
KW - Follow-Up Studies
KW - Paraneoplastic Syndromes, Nervous System
KW - Female
KW - Teratoma -- complications
KW - Cerebellar Ataxia -- etiology
KW - Teratoma -- pathology
KW - Ovarian Neoplasms -- pathology
KW - Ovarian Neoplasms -- complications
KW - Ovarian Neoplasms -- surgery
KW - Teratoma -- surgery
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+neuroscience+%3A+official+journal+of+the+Neurosurgical+Society+of+Australasia&rft.atitle=Reversible+cerebellar+ataxia+due+to+ovarian+teratoma.&rft.au=Park%2C+Jung+E%3BLiang%2C+Tsao-Wei&rft.aulast=Park&rft.aufirst=Jung&rft.date=2014-08-01&rft.volume=21&rft.issue=8&rft.spage=1467&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+neuroscience+%3A+official+journal+of+the+Neurosurgical+Society+of+Australasia&rft.issn=1532-2653&rft_id=info:doi/10.1016%2Fj.jocn.2013.12.019
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-03-04
N1 - Date created - 2014-07-15
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.jocn.2013.12.019
ER -
TY - JOUR
T1 - A phase II trial of the Src-kinase inhibitor saracatinib after four cycles of chemotherapy for patients with extensive stage small cell lung cancer: NCCTG trial N-0621.
AN - 1545414555; 24957683
AB - To assess the efficacy and the Src-kinase inhibitor saracatinib (AZD-0530) after four cycles of platinum-based chemotherapy for extensive stage small cell lung cancer (SCLC).
Patients with at least stable disease received saracatinib at a dose of 175 mg/day by mouth until disease progression, unacceptable toxicity, or patient refusal. The primary endpoint was the 12-week progression-free survival (PFS) rate from initiation of saracatinib treatment. Planned interim analysis in first 20 patients, where 13 or more patients alive and progression-free at 12-weeks would allow continued enrollment to 40 total patients. All 23 evaluable patients received platinum based standard chemotherapy. Median age was 58 years (range: 48-82). 96% of patients had a performance status of 0/1. Median of two cycles given (range: 1-34). All 23 (100%) patients have ended treatment, most for disease progression (19/23). The 12-week PFS rate was 26% (6/23; 95% CI: 10-48%). From start of standard chemotherapy, median PFS was 4.7 months (95% CI: 4.5-5.1) and median OS was 11.2 months (95% CI: 9.9-13.8). Eight (35%) and three (13%) patients experienced at least one grade 3/4 or grade 4 AE, respectively. Commonly occurring grade 3/4 adverse events were thrombocytopenia (13%), fatigue (9%), nausea (9%), and vomiting (9%).
Saracatinib at a dose of 175 mg/day by mouth is well tolerated. However, the PFS rate observed at the pre-planned interim analysis did not meet the criteria for additional enrollment. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.
JF - Lung cancer (Amsterdam, Netherlands)
AU - Molina, Julian R
AU - Foster, Nathan R
AU - Reungwetwattana, Thanyanan
AU - Nelson, Garth D
AU - Grainger, Andrew V
AU - Steen, Preston D
AU - Stella, Philip J
AU - Marks, Randolph
AU - Wright, John
AU - Adjei, Alex A
AD - Division of Medical Oncology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, United States. Electronic address: molina.julian@mayo.edu. ; Division of Biomedical Statistics and Informatics, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, United States. ; Division of Medical Oncology, Department of Internal Medicine, Ramathibodi Hospital, Bangkok, Thailand. ; Columbus Oncology & Hematology, Inc., 810 Jasonway Avenue, Suite A, Columbus, OH 43214l, United States. ; MeritCare Hospital CCOP, 820 4(th) Street North, Fargo, ND 58102, United States. ; St. Joseph Mercy Cancer Center, 5301 McAuley Drive, Suite C-139, Ypsilanti, MI 48197, United States. ; Division of Medical Oncology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, United States. ; CTEP Program, National Cancer Institute, Executive Plaza North, Suite 7115A, Rockville, MD 20852-7426, United States. ; Roswell Park Cancer Institute, Elm and Carlton Street, Buffalo, NY 14263, United States.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 245
EP - 250
VL - 85
IS - 2
KW - Antineoplastic Agents
KW - 0
KW - Benzodioxoles
KW - Protein Kinase Inhibitors
KW - Quinazolines
KW - saracatinib
KW - 9KD24QGH76
KW - src-Family Kinases
KW - EC 2.7.10.2
KW - Index Medicus
KW - Small cell lung cancer
KW - Extensive stage
KW - C-Src
KW - Maintenance
KW - Saracatinib
KW - Neoplasm Staging
KW - Humans
KW - Disease Progression
KW - Aged
KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects
KW - src-Family Kinases -- antagonists & inhibitors
KW - Aged, 80 and over
KW - Treatment Outcome
KW - Follow-Up Studies
KW - Middle Aged
KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use
KW - Retreatment
KW - Female
KW - Male
KW - Benzodioxoles -- therapeutic use
KW - Antineoplastic Agents -- administration & dosage
KW - Small Cell Lung Carcinoma -- mortality
KW - Small Cell Lung Carcinoma -- drug therapy
KW - Lung Neoplasms -- drug therapy
KW - Protein Kinase Inhibitors -- administration & dosage
KW - Antineoplastic Agents -- adverse effects
KW - Quinazolines -- administration & dosage
KW - Protein Kinase Inhibitors -- therapeutic use
KW - Small Cell Lung Carcinoma -- pathology
KW - Benzodioxoles -- administration & dosage
KW - Protein Kinase Inhibitors -- adverse effects
KW - Quinazolines -- therapeutic use
KW - Benzodioxoles -- adverse effects
KW - Lung Neoplasms -- mortality
KW - Quinazolines -- adverse effects
KW - Antineoplastic Agents -- therapeutic use
KW - Lung Neoplasms -- pathology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Lung+cancer+%28Amsterdam%2C+Netherlands%29&rft.atitle=A+phase+II+trial+of+the+Src-kinase+inhibitor+saracatinib+after+four+cycles+of+chemotherapy+for+patients+with+extensive+stage+small+cell+lung+cancer%3A+NCCTG+trial+N-0621.&rft.au=Molina%2C+Julian+R%3BFoster%2C+Nathan+R%3BReungwetwattana%2C+Thanyanan%3BNelson%2C+Garth+D%3BGrainger%2C+Andrew+V%3BSteen%2C+Preston+D%3BStella%2C+Philip+J%3BMarks%2C+Randolph%3BWright%2C+John%3BAdjei%2C+Alex+A&rft.aulast=Molina&rft.aufirst=Julian&rft.date=2014-08-01&rft.volume=85&rft.issue=2&rft.spage=245&rft.isbn=&rft.btitle=&rft.title=Lung+cancer+%28Amsterdam%2C+Netherlands%29&rft.issn=1872-8332&rft_id=info:doi/10.1016%2Fj.lungcan.2014.03.004
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-07-09
N1 - Date created - 2014-07-15
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.lungcan.2014.03.004
ER -
TY - JOUR
T1 - Seroprevalence of 8 oncogenic human papillomavirus genotypes and acquired immunity against reinfection.
AN - 1544739307; 24569064
AB - Natural human papillomavirus (HPV) antibody titers have shown protection against subsequent HPV infection, but previous studies were restricted to few HPV genotypes. We examined the association of naturally occurring antibodies against 8 carcinogenic HPV types with subsequent infections.
A total of 2302 women enrolled in the Atypical Squamous Cells of Undetermined Significance/Low-Grade Squamous Intraepithelial Lesion Triage Study provided blood samples at baseline. Serum samples were tested for antibodies against 8 carcinogenic HPV genotypes (16, 18, 31, 33, 35, 45, 52, and 58) using a multiplex serology assay. We analyzed the relationship between HPV antibodies and HPV infection during 2 years of follow-up among women negative for the specific HPV type at baseline. Baseline seroprevalence for HPV16 L1 was associated with decreased risk of DNA positivity for HPV16 (odds ratio, 0.39 [95% confidence interval, .18-.86]) at ≥2 follow-up visits. We observed similar but nonsignificant decreased risks for HPV18 and 31. These findings were restricted to women reporting a new sex partner during follow-up. There was no association between baseline seroprevalence and detection of precancer during follow-up. Seroprevalence conferred protection against subsequent HPV infection for HPV16 and indicated possible protection for 2 other genotypes, suggesting that this effect is common to several HPV genotypes.
Published by Oxford University Press on behalf of the Infectious Diseases Society of America 2014. This work is written by (a) US Government employee(s) and is in the public domain in the US.
JF - The Journal of infectious diseases
AU - Wilson, Lauren
AU - Pawlita, Michael
AU - Castle, Phillip E
AU - Waterboer, Tim
AU - Sahasrabuddhe, Vikrant
AU - Gravitt, Patti E
AU - Schiffman, Mark
AU - Wentzensen, Nicolas
AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health (NIH), Bethesda Epidemiology Branch, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, North Carolina. ; German Cancer Research Center, Heidelberg, Germany. ; Global Cancer Initiative, Chestertown. ; Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health (NIH), Bethesda. ; Department of Epidemiology Department of Molecular Microbiology and Immunology, Johns Hopkins University, Baltimore, Maryland.
Y1 - 2014/08/01/
PY - 2014
DA - 2014 Aug 01
SP - 448
EP - 455
VL - 210
IS - 3
KW - Abridged Index Medicus
KW - Index Medicus
KW - serology
KW - natural immunity
KW - Human papillomavirus
KW - Genotype
KW - Odds Ratio
KW - Adaptive Immunity
KW - Humans
KW - Seroepidemiologic Studies
KW - Cervical Intraepithelial Neoplasia -- virology
KW - Female
KW - Papillomavirus Infections -- epidemiology
KW - Papillomaviridae -- classification
KW - Papillomavirus Infections -- blood
KW - Papillomaviridae -- genetics
KW - Oncogenic Viruses
KW - Papillomaviridae -- immunology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+infectious+diseases&rft.atitle=Seroprevalence+of+8+oncogenic+human+papillomavirus+genotypes+and+acquired+immunity+against+reinfection.&rft.au=Wilson%2C+Lauren%3BPawlita%2C+Michael%3BCastle%2C+Phillip+E%3BWaterboer%2C+Tim%3BSahasrabuddhe%2C+Vikrant%3BGravitt%2C+Patti+E%3BSchiffman%2C+Mark%3BWentzensen%2C+Nicolas&rft.aulast=Wilson&rft.aufirst=Lauren&rft.date=2014-08-01&rft.volume=210&rft.issue=3&rft.spage=448&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+infectious+diseases&rft.issn=1537-6613&rft_id=info:doi/10.1093%2Finfdis%2Fjiu104
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-08-25
N1 - Date created - 2014-07-11
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/infdis/jiu104
ER -
TY - JOUR
T1 - Mechanism and synergism in epithelial fluid and electrolyte secretion.
AN - 1544737734; 24240699
AB - A central function of epithelia is the control of the volume and electrolyte composition of bodily fluids through vectorial transport of electrolytes and the obligatory H2O. In exocrine glands, fluid and electrolyte secretion is carried out by both acinar and duct cells, with the portion of fluid secreted by each cell type varying among glands. All acinar cells secrete isotonic, plasma-like fluid, while the duct determines the final electrolyte composition of the fluid by absorbing most of the Cl(-) and secreting HCO3 (-). The key transporters mediating acinar fluid and electrolyte secretion are the basolateral Na(+)/K(+) /2Cl(-) cotransporter, the luminal Ca(2+)-activated Cl(-) channel ANO1 and basolateral and luminal Ca(2+)-activated K(+) channels. Ductal fluid and HCO3 (-) secretion are mediated by the basolateral membrane Na(+)-HCO3 (-) cotransporter NBCe1-B and the luminal membrane Cl(-)/HCO3 (-) exchanger slc26a6 and the Cl(-) channel CFTR. The function of the transporters is regulated by multiple inputs, which in the duct include major regulation by the WNK/SPAK pathway that inhibit secretion and the IRBIT/PP1 pathway that antagonize the effects of the WNK/SPAK pathway to both stimulate and coordinate the secretion. The function of these regulatory pathways in secretory glands acinar cells is yet to be examined. An important concept in biology is synergism among signaling pathways to generate the final physiological response that ensures regulation with high fidelity and guards against cell toxicity. While synergism is observed in all epithelial functions, the molecular mechanism mediating the synergism is not known. Recent work reveals a central role for IRBIT as a third messenger that integrates and synergizes the function of the Ca(2+) and cAMP signaling pathways in activation of epithelial fluid and electrolyte secretion. These concepts are discussed in this review using secretion by the pancreatic and salivary gland ducts as model systems.
JF - Pflugers Archiv : European journal of physiology
AU - Hong, Jeong Hee
AU - Park, Seonghee
AU - Shcheynikov, Nikolay
AU - Muallem, Shmuel
AD - Epithelial Signaling and Transport Section, Molecular Physiology and Therapeutics Branch, National Institute of Dental and Craniofacial Research, National Institute of Health, Bethesda, MD, 20892, USA.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 1487
EP - 1499
VL - 466
IS - 8
KW - Electrolytes
KW - 0
KW - Index Medicus
KW - Animals
KW - Pancreatic Ducts -- secretion
KW - Humans
KW - Salivary Ducts -- secretion
KW - Water-Electrolyte Balance -- physiology
KW - Signal Transduction -- physiology
KW - Epithelium -- secretion
KW - Body Fluids -- metabolism
KW - Electrolytes -- metabolism
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pflugers+Archiv+%3A+European+journal+of+physiology&rft.atitle=Mechanism+and+synergism+in+epithelial+fluid+and+electrolyte+secretion.&rft.au=Hong%2C+Jeong+Hee%3BPark%2C+Seonghee%3BShcheynikov%2C+Nikolay%3BMuallem%2C+Shmuel&rft.aulast=Hong&rft.aufirst=Jeong&rft.date=2014-08-01&rft.volume=466&rft.issue=8&rft.spage=1487&rft.isbn=&rft.btitle=&rft.title=Pflugers+Archiv+%3A+European+journal+of+physiology&rft.issn=1432-2013&rft_id=info:doi/10.1007%2Fs00424-013-1390-1
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-02-23
N1 - Date created - 2014-07-11
N1 - Date revised - 2017-01-13
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1007/s00424-013-1390-1
ER -
TY - JOUR
T1 - A mutation in the extracellular domain of the α7 nAChR reduces calcium permeability.
AN - 1544736798; 24177919
AB - The α7 neuronal nicotinic acetylcholine receptor (nAChR) displays the highest calcium permeability among the different subtypes of nAChRs expressed in the mammalian brain and can impact cellular events including neurotransmitter release, second messenger cascades, cell survival, and apoptosis. The selectivity for cations in nAChRs is thought to be achieved in part by anionic residues which are located on either side of the channel mouth and increase relative cationic concentration. Mutagenesis studies have improved our understanding of the role of the second transmembrane domain and the intracellular loop of the channel in ion selectivity. However, little is known about the influence that the extracellular domain (ECD) plays in ion permeation. In the α7 nAChR, it has been found that the ECD contains a ring of ten aspartates (two per subunit) that is believed to face the lumen of the pore and could attract cations for permeation. Using mutagenesis and a combination of electrophysiology and imaging techniques, we tested the possible involvement of these aspartate residues in the calcium permeability of the rat α7 nAChR. We found that one of these residues (the aspartate at position 44) appears to be essential since mutating it to alanine resulted in a decrease in amplitude for both whole cell and single-channel responses and in the complete disappearance of detectable calcium changes in most cells, which indicates that the ECD of the α7 nAChR plays a key role in calcium permeation.
JF - Pflugers Archiv : European journal of physiology
AU - Colón-Sáez, José O
AU - Yakel, Jerrel L
AD - Laboratory of Neurobiology, National Institute of Environmental Health Science, National Institutes of Health, Department of Health and Human Services, PO Box 12233, Research Triangle Park, NC, 27709, USA.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 1571
EP - 1579
VL - 466
IS - 8
KW - Protein Subunits
KW - 0
KW - alpha7 Nicotinic Acetylcholine Receptor
KW - Calcium
KW - SY7Q814VUP
KW - Index Medicus
KW - Rats
KW - Animals
KW - Protein Structure, Tertiary -- genetics
KW - Patch-Clamp Techniques
KW - Extracellular Space -- metabolism
KW - Cells, Cultured
KW - Calcium -- metabolism
KW - Protein Subunits -- genetics
KW - Neurons -- metabolism
KW - alpha7 Nicotinic Acetylcholine Receptor -- metabolism
KW - alpha7 Nicotinic Acetylcholine Receptor -- genetics
KW - Protein Subunits -- metabolism
KW - Mutation
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1544736798?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pflugers+Archiv+%3A+European+journal+of+physiology&rft.atitle=A+mutation+in+the+extracellular+domain+of+the+%CE%B17+nAChR+reduces+calcium+permeability.&rft.au=Col%C3%B3n-S%C3%A1ez%2C+Jos%C3%A9+O%3BYakel%2C+Jerrel+L&rft.aulast=Col%C3%B3n-S%C3%A1ez&rft.aufirst=Jos%C3%A9&rft.date=2014-08-01&rft.volume=466&rft.issue=8&rft.spage=1571&rft.isbn=&rft.btitle=&rft.title=Pflugers+Archiv+%3A+European+journal+of+physiology&rft.issn=1432-2013&rft_id=info:doi/10.1007%2Fs00424-013-1385-y
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-02-23
N1 - Date created - 2014-07-11
N1 - Date revised - 2017-01-13
N1 - SuppNotes - Cited By:
Proc Natl Acad Sci U S A. 2000 Mar 28;97(7):3643-8 [10716716]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1007/s00424-013-1385-y
ER -
TY - JOUR
T1 - Disposition of fragrance ingredient [14C]1-(1,2,3,4,5,6,7,8-octahydro-2,3,8,8-tetramethyl-2-naphthalenyl)ethanone in male Fisher rats following oral administration and dermal application.
AN - 1544322611; 24533629
AB - 1. Disposition of 1-(1,2,3,4,5,6,7,8-octahydro-2,3,8,8-tetramethyl-2-naphthalenyl)ethanone (β-OTNE), a fragrance ingredient in variety of consumer products, was investigated following a single oral (20 mg/kg) or a dermal (55 or 550 mg/kg) dose of [(14)C]β-OTNE to male Fisher rats. 2. Following oral administration, 28% and 39% of the dose was recovered in urine and feces, respectively, 48 h following administration. About 73% of a 20 mg/kg dose was excreted in bile within 48 h post-administration supporting significant oral absorption of [(14)C]β-OTNE. 3. Following dermal application to a covered site, absorption of [(14)C]β-OTNE 96 h following application was low (ca. 14%) and dose-independent. When the dose site was uncovered, the absorption increased to ca. 33% (55 mg/kg) and ca. 72% (550 mg/kg). 4. [(14)C]β-OTNE was distributed to tissues following both routes of exposure with the highest radioactive equivalents found in bladder, liver, kidney, adipose and pancreas. 5. Elimination of [(14)C]β-OTNE equivalents in blood and tissues was slow following both oral and dermal application suggesting potential for accumulation following multiple exposure.
JF - Xenobiotica; the fate of foreign compounds in biological systems
AU - Waidyanatha, Suramya
AU - Ryan, Kristen
AD - Division of National Toxicology Program, National Institute of Environmental Health Sciences , Research Triangle Park, NC , USA.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 749
EP - 756
VL - 44
IS - 8
KW - Carbon Radioisotopes
KW - 0
KW - Naphthalenes
KW - Perfume
KW - 1-(1,2,3,4,5,6,7,8-octahydro-2,3,8,8-tetramethyl-2-naphthalenyl)ethanone
KW - 1GD7ODM28Y
KW - Index Medicus
KW - oral absorption
KW - dermal absorption
KW - enterohepatic recirculation
KW - biliary excretion
KW - 1-(1,2,3,4,5,6,7,8-Octahydro-2,3,8,8-tetramethyl-2-naphthalenyl)ethanone
KW - fragrance ingredient
KW - Administration, Oral
KW - Animals
KW - Rats, Inbred F344
KW - Administration, Cutaneous
KW - Isomerism
KW - Tissue Distribution -- drug effects
KW - Radioactivity
KW - Time Factors
KW - Male
KW - Naphthalenes -- blood
KW - Perfume -- analysis
KW - Naphthalenes -- administration & dosage
KW - Naphthalenes -- pharmacokinetics
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Xenobiotica%3B+the+fate+of+foreign+compounds+in+biological+systems&rft.atitle=Disposition+of+fragrance+ingredient+%5B14C%5D1-%281%2C2%2C3%2C4%2C5%2C6%2C7%2C8-octahydro-2%2C3%2C8%2C8-tetramethyl-2-naphthalenyl%29ethanone+in+male+Fisher+rats+following+oral+administration+and+dermal+application.&rft.au=Waidyanatha%2C+Suramya%3BRyan%2C+Kristen&rft.aulast=Waidyanatha&rft.aufirst=Suramya&rft.date=2014-08-01&rft.volume=44&rft.issue=8&rft.spage=749&rft.isbn=&rft.btitle=&rft.title=Xenobiotica%3B+the+fate+of+foreign+compounds+in+biological+systems&rft.issn=1366-5928&rft_id=info:doi/10.3109%2F00498254.2014.888489
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-03-02
N1 - Date created - 2014-07-09
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.3109/00498254.2014.888489
ER -
TY - JOUR
T1 - Poisoning of mitochondrial topoisomerase I by lamellarin D.
AN - 1542650962; 24890608
AB - Lamellarin D (Lam-D) is a hexacyclic pyrole alkaloid isolated from marine invertebrates, whose biologic properties have been attributed to mitochondrial targeting. Mitochondria contain their own DNA (mtDNA), and the only specific mitochondrial topoisomerase in vertebrates is mitochondrial topoisomerase I (Top1mt). Here, we show that Top1mt is a direct mitochondrial target of Lam-D. In vitro Lam-D traps Top1mt and induces Top1mt cleavage complexes (Top1mtcc). Using single-molecule analyses, we also show that Lam-D slows down supercoil relaxation of Top1mt and strongly inhibits Top1mt religation in contrast to the inefficacy of camptothecin on Top1mt. In living cells, we show that Lam-D accumulates rapidly inside mitochondria, induces cellular Top1mtcc, and leads to mtDNA damage. This study provides evidence that Top1mt is a direct mitochondrial target of Lam-D and suggests that developing Top1mt inhibitors represents a novel strategy for targeting mitochondrial DNA. U.S. Government work not protected by U.S. copyright.
JF - Molecular pharmacology
AU - Khiati, Salim
AU - Seol, Yeonee
AU - Agama, Keli
AU - Dalla Rosa, Ilaria
AU - Agrawal, Surbhi
AU - Fesen, Katherine
AU - Zhang, Hongliang
AU - Neuman, Keir C
AU - Pommier, Yves
AD - Developmental Therapeutics Branch and Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute (S.K., K.A., I.D.R., S.A., K.F., H.Z., Y.P.) and Laboratory of Molecular Biophysics, National Heart, Lung, and Blood Institute (Y.S., K.C.N.), National Institutes of Health, Bethesda, Maryland. ; Developmental Therapeutics Branch and Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute (S.K., K.A., I.D.R., S.A., K.F., H.Z., Y.P.) and Laboratory of Molecular Biophysics, National Heart, Lung, and Blood Institute (Y.S., K.C.N.), National Institutes of Health, Bethesda, Maryland pommier@nih.gov.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 193
EP - 199
VL - 86
IS - 2
KW - Coumarins
KW - 0
KW - DNA, Mitochondrial
KW - Heterocyclic Compounds, 4 or More Rings
KW - Isoquinolines
KW - lamellarin D
KW - DNA Topoisomerases, Type I
KW - EC 5.99.1.2
KW - Index Medicus
KW - Humans
KW - DNA, Mitochondrial -- metabolism
KW - Cell Line, Tumor
KW - DNA, Mitochondrial -- genetics
KW - Isoquinolines -- pharmacology
KW - Coumarins -- pharmacology
KW - Mitochondria -- drug effects
KW - Heterocyclic Compounds, 4 or More Rings -- pharmacology
KW - Mitochondria -- metabolism
KW - DNA Topoisomerases, Type I -- genetics
KW - Mitochondria -- genetics
KW - DNA Topoisomerases, Type I -- metabolism
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+pharmacology&rft.atitle=Poisoning+of+mitochondrial+topoisomerase+I+by+lamellarin+D.&rft.au=Khiati%2C+Salim%3BSeol%2C+Yeonee%3BAgama%2C+Keli%3BDalla+Rosa%2C+Ilaria%3BAgrawal%2C+Surbhi%3BFesen%2C+Katherine%3BZhang%2C+Hongliang%3BNeuman%2C+Keir+C%3BPommier%2C+Yves&rft.aulast=Khiati&rft.aufirst=Salim&rft.date=2014-08-01&rft.volume=86&rft.issue=2&rft.spage=193&rft.isbn=&rft.btitle=&rft.title=Molecular+pharmacology&rft.issn=1521-0111&rft_id=info:doi/10.1124%2Fmol.114.092833
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-08-15
N1 - Date created - 2014-07-02
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Oncogene. 1999 Nov 18;18(48):6641-6 [10597269]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1124/mol.114.092833
ER -
TY - JOUR
T1 - Regulation of human CYP2C9 expression by electrophilic stress involves activator protein 1 activation and DNA looping.
AN - 1541378763; 24830941
AB - Cytochrome P450 (CYP)2C9 and CYP2C19 are important human enzymes that metabolize therapeutic drugs, environmental chemicals, and physiologically important endogenous compounds. Initial studies using primary human hepatocytes showed induction of both the CYP2C9 and CYP2C19 genes by tert-butylhydroquinone (tBHQ). As a pro-oxidant, tBHQ regulates the expression of cytoprotective genes by activation of redox-sensing transcription factors, such as the nuclear factor E2-related factor 2 (Nrf2) and members of the activator protein 1 (AP-1) family of proteins. The promoter region of CYP2C9 contains two putative AP-1 sites (TGAGTCA) at positions -2201 and -1930, which are also highly conserved in CYP2C19. The CYP2C9 promoter is activated by ectopic expression of cFos and JunD, whereas Nrf2 had no effect. Using specific kinase inhibitors for mitogen-activated protein kinase, we showed that extracellular signal-regulated kinase and Jun N-terminal kinase are essential for tBHQ-induced expression of CYP2C9. Electrophoretic mobility shift assays demonstrate that cFos distinctly interacts with the distal AP-1 site and JunD with the proximal site. Because cFos regulates target genes as heterodimers with Jun proteins, we hypothesized that DNA looping might be required to bring the distal and proximal AP-1 sites together to activate the CYP2C9 promoter. Chromosome conformation capture analyses confirmed the formation of a DNA loop in the CYP2C9 promoter, possibly allowing interaction between cFos at the distal site and JunD at the proximal site to activate CYP2C9 transcription in response to electrophiles. These results indicate that oxidative stress generated by exposure to electrophilic xenobiotics and metabolites induces the expression of CYP2C9 and CYP2C19 in human hepatocytes.
U.S. Government work not protected by U.S. copyright.
JF - Molecular pharmacology
AU - Makia, Ngome L
AU - Surapureddi, Sailesh
AU - Monostory, Katalin
AU - Prough, Russell A
AU - Goldstein, Joyce A
AD - Human Metabolism Group, Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina (N.L.M., S.S., J.A.G.); Department of Biochemistry and Molecular Biology, University of Louisville School of Medicine, Louisville, Kentucky (R.A.P.); and Research Centre for Natural Sciences, Hungarian Academy of Science, Budapest, Hungary (K.M.). ; Human Metabolism Group, Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina (N.L.M., S.S., J.A.G.); Department of Biochemistry and Molecular Biology, University of Louisville School of Medicine, Louisville, Kentucky (R.A.P.); and Research Centre for Natural Sciences, Hungarian Academy of Science, Budapest, Hungary (K.M.) goldste1@niehs.nih.gov.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 125
EP - 137
VL - 86
IS - 2
KW - Proto-Oncogene Proteins c-fos
KW - 0
KW - Proto-Oncogene Proteins c-jun
KW - Transcription Factor AP-1
KW - Xenobiotics
KW - DNA
KW - 9007-49-2
KW - CYP2C9 protein, human
KW - EC 1.14.13.-
KW - Cytochrome P-450 CYP2C9
KW - Aryl Hydrocarbon Hydroxylases
KW - EC 1.14.14.1
KW - CYP2C19 protein, human
KW - Cytochrome P-450 CYP2C19
KW - Extracellular Signal-Regulated MAP Kinases
KW - EC 2.7.11.24
KW - Index Medicus
KW - Hep G2 Cells
KW - Xenobiotics -- metabolism
KW - Humans
KW - Transcription, Genetic -- genetics
KW - Liver -- metabolism
KW - Promoter Regions, Genetic -- genetics
KW - Oxidative Stress -- genetics
KW - Cell Line, Tumor
KW - Binding Sites -- genetics
KW - Hepatocytes -- metabolism
KW - Aryl Hydrocarbon Hydroxylases -- metabolism
KW - Proto-Oncogene Proteins c-fos -- metabolism
KW - Transcription Factor AP-1 -- metabolism
KW - Proto-Oncogene Proteins c-fos -- genetics
KW - DNA -- genetics
KW - Proto-Oncogene Proteins c-jun -- genetics
KW - Proto-Oncogene Proteins c-jun -- metabolism
KW - Extracellular Signal-Regulated MAP Kinases -- metabolism
KW - Aryl Hydrocarbon Hydroxylases -- genetics
KW - Transcription Factor AP-1 -- genetics
KW - Extracellular Signal-Regulated MAP Kinases -- genetics
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541378763?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+pharmacology&rft.atitle=Regulation+of+human+CYP2C9+expression+by+electrophilic+stress+involves+activator+protein+1+activation+and+DNA+looping.&rft.au=Makia%2C+Ngome+L%3BSurapureddi%2C+Sailesh%3BMonostory%2C+Katalin%3BPrough%2C+Russell+A%3BGoldstein%2C+Joyce+A&rft.aulast=Makia&rft.aufirst=Ngome&rft.date=2014-08-01&rft.volume=86&rft.issue=2&rft.spage=125&rft.isbn=&rft.btitle=&rft.title=Molecular+pharmacology&rft.issn=1521-0111&rft_id=info:doi/10.1124%2Fmol.114.092585
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-08-15
N1 - Date created - 2014-06-27
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1124/mol.114.092585
ER -
TY - JOUR
T1 - CMT-associated mutations in glycyl- and tyrosyl-tRNA synthetases exhibit similar pattern of toxicity and share common genetic modifiers in Drosophila.
AN - 1539472304; 24807208
AB - Aminoacyl-tRNA synthetases are ubiquitously expressed proteins that charge tRNAs with their cognate amino acids. By ensuring the fidelity of protein synthesis, these enzymes are essential for the viability of every cell. Yet, mutations in six tRNA synthetases specifically affect the peripheral nerves and cause Charcot-Marie-Tooth (CMT) disease. The CMT-causing mutations in tyrosyl- and glycyl-tRNA synthetases (YARS and GARS, respectively) alter the activity of the proteins in a range of ways (some mutations do not impact charging function, while others abrogate it), making a loss of function in tRNA charging unlikely to be the cause of disease pathology. It is currently unknown which cellular mechanisms are triggered by the mutant enzymes and how this leads to neurodegeneration. Here, by expressing two pathogenic mutations (G240R, P234KY) in Drosophila, we generated a model for GARS-associated neuropathy. We observed compromised viability, and behavioral, electrophysiological and morphological impairment in flies expressing the cytoplasmic isoform of mutant GARS. Their features recapitulated several hallmarks of CMT pathophysiology and were similar to the phenotypes identified in our previously described Drosophila model of YARS-associated neuropathy. Furthermore, CG8316 and CG15599 - genes identified in a retinal degeneration screen to modify mutant YARS, also modified the mutant GARS phenotypes. Our study presents genetic evidence for common mutant-specific interactions between two CMT-associated aminoacyl-tRNA synthetases, lending support for a shared mechanism responsible for the synthetase-induced peripheral neuropathies. Copyright © 2014 Elsevier Inc. All rights reserved.
JF - Neurobiology of disease
AU - Ermanoska, Biljana
AU - Motley, William W
AU - Leitão-Gonçalves, Ricardo
AU - Asselbergh, Bob
AU - Lee, LaTasha H
AU - De Rijk, Peter
AU - Sleegers, Kristel
AU - Ooms, Tinne
AU - Godenschwege, Tanja A
AU - Timmerman, Vincent
AU - Fischbeck, Kenneth H
AU - Jordanova, Albena
AD - Molecular Neurogenomics Group, Department of Molecular Genetics, VIB, University of Antwerp, Antwerp 2610, Belgium; Neurogenetics Laboratory, Institute Born-Bunge, University of Antwerp, Antwerp 2610, Belgium. ; Neurogenetics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA; Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. ; Molecular Neurogenomics Group, Department of Molecular Genetics, VIB, University of Antwerp, Antwerp 2610, Belgium; Neurogenetics Laboratory, Institute Born-Bunge, University of Antwerp, Antwerp 2610, Belgium; Peripheral Neuropathy Group, Department of Molecular Genetics, VIB, University of Antwerp, Antwerp 2610, Belgium. ; Neurogenetics Laboratory, Institute Born-Bunge, University of Antwerp, Antwerp 2610, Belgium; Centralized Service Facility, Department of Molecular Genetics, VIB, University of Antwerp, Antwerp 2610, Belgium. ; Department of Biological Sciences, Florida Atlantic University, Jupiter, FL 33458, USA. ; Applied Molecular Genomics Unit, Department of Molecular Genetics, VIB, University of Antwerp, Antwerp 2610, Belgium. ; Neurogenetics Laboratory, Institute Born-Bunge, University of Antwerp, Antwerp 2610, Belgium; Neurodegenerative Brain Diseases Group, Department of Molecular Genetics, VIB, University of Antwerp, Antwerp 2610, Belgium. ; Neurogenetics Laboratory, Institute Born-Bunge, University of Antwerp, Antwerp 2610, Belgium; Peripheral Neuropathy Group, Department of Molecular Genetics, VIB, University of Antwerp, Antwerp 2610, Belgium. ; Neurogenetics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA. ; Molecular Neurogenomics Group, Department of Molecular Genetics, VIB, University of Antwerp, Antwerp 2610, Belgium; Neurogenetics Laboratory, Institute Born-Bunge, University of Antwerp, Antwerp 2610, Belgium. Electronic address: albena.jordanova@molgen.vib-ua.be.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 180
EP - 189
VL - 68
KW - Dextrans
KW - 0
KW - Drosophila Proteins
KW - Fluoro-Ruby
KW - Rhodamines
KW - Tyrosine-tRNA Ligase
KW - EC 6.1.1.1
KW - Glycine-tRNA Ligase
KW - EC 6.1.1.14
KW - Index Medicus
KW - Aminoacyl-tRNA synthetase
KW - Charcot–Marie–Tooth disease
KW - Drosophila
KW - Animals
KW - Retina -- ultrastructure
KW - Retinal Degeneration -- diagnosis
KW - Humans
KW - Membrane Potentials -- physiology
KW - Disease Models, Animal
KW - Animals, Genetically Modified
KW - Neurons -- pathology
KW - Nerve Fibers -- physiology
KW - Membrane Potentials -- genetics
KW - Wings, Animal -- pathology
KW - Wings, Animal -- ultrastructure
KW - Neurons -- physiology
KW - Drosophila Proteins -- genetics
KW - Retina -- pathology
KW - Retinal Degeneration -- etiology
KW - Drosophila Proteins -- metabolism
KW - Female
KW - Male
KW - Retinal Degeneration -- genetics
KW - Charcot-Marie-Tooth Disease -- pathology
KW - Tyrosine-tRNA Ligase -- genetics
KW - Peripheral Nervous System Diseases -- etiology
KW - Peripheral Nervous System Diseases -- genetics
KW - Charcot-Marie-Tooth Disease -- complications
KW - Mutation -- genetics
KW - Glycine-tRNA Ligase -- genetics
KW - Charcot-Marie-Tooth Disease -- genetics
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurobiology+of+disease&rft.atitle=CMT-associated+mutations+in+glycyl-+and+tyrosyl-tRNA+synthetases+exhibit+similar+pattern+of+toxicity+and+share+common+genetic+modifiers+in+Drosophila.&rft.au=Ermanoska%2C+Biljana%3BMotley%2C+William+W%3BLeit%C3%A3o-Gon%C3%A7alves%2C+Ricardo%3BAsselbergh%2C+Bob%3BLee%2C+LaTasha+H%3BDe+Rijk%2C+Peter%3BSleegers%2C+Kristel%3BOoms%2C+Tinne%3BGodenschwege%2C+Tanja+A%3BTimmerman%2C+Vincent%3BFischbeck%2C+Kenneth+H%3BJordanova%2C+Albena&rft.aulast=Ermanoska&rft.aufirst=Biljana&rft.date=2014-08-01&rft.volume=68&rft.issue=&rft.spage=180&rft.isbn=&rft.btitle=&rft.title=Neurobiology+of+disease&rft.issn=1095-953X&rft_id=info:doi/10.1016%2Fj.nbd.2014.04.020
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-05-11
N1 - Date created - 2014-06-20
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Lancet Neurol. 2009 Jul;8(7):654-67 [19539237]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.nbd.2014.04.020
ER -
TY - JOUR
T1 - Correlation of plasma viral loads and presence of Chikungunya IgM antibodies with cytokine/chemokine levels during acute Chikungunya virus infection
AN - 1534838879; 20079634
AB - Chikungunya (CHIKV) is an emerging arboviral infection of public health concern in India contributing to widespread morbidity. The precise molecular events occurring early in the infection have not been well understood. Cytokines/chemokines are suspected to play a key role in its pathogenesis. Very few studies have correlated the plasma levels of cytokines/chemokines with diagnostic markers such as viral loads and presence of CHIKV IgM antibodies. Understanding these dynamics in the early phase of CHIKV infection is likely to provide an insight into the evolution of the immune response, identify biomarkers for assessing severity, and for development of newer therapeutic strategies. This study was therefore undertaken to estimate the levels of various cytokines/chemokines in plasma samples of patients infected with CHIKV and correlate to viral load and CHIKV IgM antibodies. Cytokine/chemokine levels and viral loads in plasma were measured using cytometric bead array and TaqMan real time PCR assay, respectively. The findings revealed that acute phase of CHIKV infection is characterized by predominant inflammatory responses mediated by IL-6, IL-8, IP-10, MCP-1, and MIG (P<0.003). Plasma levels of IL-6 (r=0.53, P<0.05) and MCP-1 (r=0.83, P<0.05) emerged as reliable biomarkers of high viral loads in Chikungunya patients. Further, presence of elevated levels of MCP-1 and MIG during the chronic phase of the disease suggests that these chemokines may contribute to perpetuation of symptoms. Hence, these chemokines might serve as targets for the development of treatment to ameliorate the symptoms during the acute phase and prevent the development of chronic manifestations.
JF - Journal of Medical Virology
AU - Reddy, Vijayalakshmi
AU - Mani, Reeta Subramaniam
AU - Desai, Anita
AU - Ravi, Vasanthapuram
AD - Department of Neurovirology, National Institute of Mental Health and Neurosciences, Bangalore, Karnataka, India.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 1393
EP - 1401
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 86
IS - 8
SN - 0146-6615, 0146-6615
KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Immunology Abstracts; Virology & AIDS Abstracts
KW - Interleukin 6
KW - Virology
KW - Symptoms
KW - Chemokines
KW - Nucleotide sequence
KW - Disease control
KW - Biomarkers
KW - Defence mechanisms
KW - Morbidity
KW - Interleukin 8
KW - India
KW - Public health
KW - IP-10 protein
KW - Cytokines
KW - Polymerase chain reaction
KW - Chikungunya virus
KW - Monocyte chemoattractant protein 1
KW - biomarkers
KW - Inflammation
KW - Plasma levels
KW - Antibodies
KW - Viral diseases
KW - Immune response
KW - Evolution
KW - Immunoglobulin M
KW - V 22350:Immunology
KW - Q1 08484:Species interactions: parasites and diseases
KW - F 06910:Microorganisms & Parasites
KW - Q5 08524:Public health, medicines, dangerous organisms
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Medical+Virology&rft.atitle=Correlation+of+plasma+viral+loads+and+presence+of+Chikungunya+IgM+antibodies+with+cytokine%2Fchemokine+levels+during+acute+Chikungunya+virus+infection&rft.au=Reddy%2C+Vijayalakshmi%3BMani%2C+Reeta+Subramaniam%3BDesai%2C+Anita%3BRavi%2C+Vasanthapuram&rft.aulast=Reddy&rft.aufirst=Vijayalakshmi&rft.date=2014-08-01&rft.volume=86&rft.issue=8&rft.spage=1393&rft.isbn=&rft.btitle=&rft.title=Journal+of+Medical+Virology&rft.issn=01466615&rft_id=info:doi/10.1002%2Fjmv.23875
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-01
N1 - Last updated - 2016-10-12
N1 - SubjectsTermNotLitGenreText - Virology; Symptoms; Antibodies; Viral diseases; Nucleotide sequence; Disease control; Biomarkers; Defence mechanisms; Public health; Interleukin 6; Chemokines; Monocyte chemoattractant protein 1; biomarkers; Interleukin 8; Morbidity; Inflammation; Plasma levels; IP-10 protein; Polymerase chain reaction; Cytokines; Immune response; Immunoglobulin M; Evolution; Chikungunya virus; India
DO - http://dx.doi.org/10.1002/jmv.23875
ER -
TY - JOUR
T1 - PCR-based assay to detect sheeppox virus in ocular, nasal, and rectal swabs from infected Moroccan sheep.
AN - 1529846215; 24698762
AB - Sheeppox is now enzootic in Morocco. The development of a reliable method for rapid diagnosis of the disease is a central part of any control strategy. The aim of this study is to determine the diagnostic value of a variety of clinical samples such as ovine nasal, ocular or rectal swabs for the detection of sheeppox virus (SPPV) by qualitative conventional polymerase chain reaction (PCR), using a single pair of primers targeting the inverted terminal repeats of the SPPV InS-1 strain, a virulent field isolate. Swab and blood samples were collected from forty animals naturally infected with SPPV who had clinical signs of sheeppox. All animals tested PCR-positive for SPPV. Positive results were obtained infrequently with blood samples, whereas swab samples from at least two sites (nasal, ocular, rectal) were positive per evaluated animal. These results indicate that swab samples are suitable for quantitative molecular SPPV diagnosis. PCR product sequences obtained from all types of sheep samples proved to be identical to the corresponding regions of sheeppox virus strain Romania 65. Copyright © 2014. Published by Elsevier B.V.
JF - Journal of virological methods
AU - Zro, K
AU - Azelmat, S
AU - Bendouro, Y
AU - Kuhn, J H
AU - El Fahime, E
AU - Ennaji, M M
AD - Laboratory of Virology, Microbiology and Quality/Ecotoxicology and Biodiversity, Hassan II University Mohammedia-Casablanca, Faculty of Science and Technology Mohammedia, BP 146 Mohammedia 20650, Morocco; Regional Laboratory of Analysis and Research of Oujda, National Office for the Safety of Food Products, 60 000 Oujda, Morocco. ; Military Hospital of Instruction Mohammed V, Rabat 14 000, Morocco. ; Regional Laboratory of Analysis and Research of Oujda, National Office for the Safety of Food Products, 60 000 Oujda, Morocco. ; Integrated Research Facility at Fort Detrick, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 8200 Research Plaza, Fort Detrick, Frederick, MD, United States. ; Functional Genomics Platform Scientific Research Technical Support Unit - Biology - National Center of Scientific and Technical Research, Rabat 14 000, Morocco. ; Laboratory of Virology, Microbiology and Quality/Ecotoxicology and Biodiversity, Hassan II University Mohammedia-Casablanca, Faculty of Science and Technology Mohammedia, BP 146 Mohammedia 20650, Morocco. Electronic address: m.ennaji@yahoo.fr.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 38
EP - 43
VL - 204
KW - DNA Primers
KW - 0
KW - DNA, Viral
KW - Index Medicus
KW - Capripoxvirus
KW - Sheeppox virus
KW - Poxvirus
KW - Poxviridae
KW - PCR
KW - Genotype
KW - Rectum -- virology
KW - Eye -- virology
KW - Animals
KW - Morocco
KW - DNA Primers -- genetics
KW - Sheep
KW - Nasal Mucosa -- virology
KW - DNA, Viral -- genetics
KW - Blood -- virology
KW - Capripoxvirus -- isolation & purification
KW - Capripoxvirus -- genetics
KW - Veterinary Medicine -- methods
KW - Polymerase Chain Reaction -- methods
KW - Sheep Diseases -- diagnosis
KW - Capripoxvirus -- classification
KW - Poxviridae Infections -- diagnosis
KW - Poxviridae Infections -- virology
KW - Molecular Diagnostic Techniques -- methods
KW - Sheep Diseases -- virology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virological+methods&rft.atitle=PCR-based+assay+to+detect+sheeppox+virus+in+ocular%2C+nasal%2C+and+rectal+swabs+from+infected+Moroccan+sheep.&rft.au=Zro%2C+K%3BAzelmat%2C+S%3BBendouro%2C+Y%3BKuhn%2C+J+H%3BEl+Fahime%2C+E%3BEnnaji%2C+M+M&rft.aulast=Zro&rft.aufirst=K&rft.date=2014-08-01&rft.volume=204&rft.issue=&rft.spage=38&rft.isbn=&rft.btitle=&rft.title=Journal+of+virological+methods&rft.issn=1879-0984&rft_id=info:doi/10.1016%2Fj.jviromet.2014.03.019
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-01-05
N1 - Date created - 2014-05-26
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.jviromet.2014.03.019
ER -
TY - JOUR
T1 - Fenretinide induces ubiquitin-dependent proteasomal degradation of stearoyl-CoA desaturase in human retinal pigment epithelial cells.
AN - 1518817344; 24357007
AB - Stearoyl-CoA desaturase (SCD, SCD1), an endoplasmic reticulum (ER) resident protein and a rate-limiting enzyme in monounsaturated fatty acid biosynthesis, regulates cellular functions by controlling the ratio of saturated to monounsaturated fatty acids. Increase in SCD expression is strongly implicated in the proliferation and survival of cancer cells, whereas its decrease is known to impair proliferation, induce apoptosis, and restore insulin sensitivity. We examined whether fenretinide, (N-(4-hydroxyphenyl)retinamide, 4HPR), which induces apoptosis in cancer cells and recently shown to improve insulin sensitivity, can modulate the expression of SCD. We observed that fenretinide decreased SCD protein and enzymatic activity in the ARPE-19 human retinal pigment epithelial cell line. Increased expression of BiP/GRP78, ATF4, and GADD153 implicated ER stress. Tunicamycin and thapsigargin, compounds known to induce ER stress, also decreased the SCD protein. This decrease was completely blocked by the proteasome inhibitor MG132. In addition, PYR41, an inhibitor of ubiquitin activating enzyme E1, blocked the fenretinide-mediated decrease in SCD. Immunoprecipitation analysis using anti-ubiquitin and anti-SCD antibodies and the blocking of SCD loss by PYR41 inhibition of ubiquitination further corroborate that fenretinide mediates the degradation of SCD in human RPE cells via the ubiquitin-proteasome dependent pathway. Therefore, the effect of fenretinide on SCD should be considered in its potential therapeutic role against cancer, type-2 diabetes, and retinal diseases. © 2013 Wiley Periodicals, Inc.
JF - Journal of cellular physiology
AU - Samuel, William
AU - Kutty, R Krishnan
AU - Duncan, Todd
AU - Vijayasarathy, Camasamudram
AU - Kuo, Bryan C
AU - Chapa, Krysten M
AU - Redmond, T Michael
AD - Laboratory of Retinal Cell and Molecular Biology, National Eye Institute, National Institutes of Health, Bethesda, Maryland.
Y1 - 2014/08//
PY - 2014
DA - August 2014
SP - 1028
EP - 1038
VL - 229
IS - 8
KW - Antineoplastic Agents
KW - 0
KW - Ubiquitin
KW - Fenretinide
KW - 187EJ7QEXL
KW - Stearoyl-CoA Desaturase
KW - EC 1.14.19.1
KW - Index Medicus
KW - Gene Expression Regulation, Enzymologic -- drug effects
KW - Humans
KW - Apoptosis -- physiology
KW - Apoptosis -- drug effects
KW - Stress, Physiological -- drug effects
KW - Antineoplastic Agents -- pharmacology
KW - Cell Line
KW - Endoplasmic Reticulum -- drug effects
KW - Stearoyl-CoA Desaturase -- metabolism
KW - Ubiquitin -- metabolism
KW - Epithelial Cells -- enzymology
KW - Epithelial Cells -- drug effects
KW - Retinal Pigment Epithelium -- cytology
KW - Fenretinide -- pharmacology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+cellular+physiology&rft.atitle=Fenretinide+induces+ubiquitin-dependent+proteasomal+degradation+of+stearoyl-CoA+desaturase+in+human+retinal+pigment+epithelial+cells.&rft.au=Samuel%2C+William%3BKutty%2C+R+Krishnan%3BDuncan%2C+Todd%3BVijayasarathy%2C+Camasamudram%3BKuo%2C+Bryan+C%3BChapa%2C+Krysten+M%3BRedmond%2C+T+Michael&rft.aulast=Samuel&rft.aufirst=William&rft.date=2014-08-01&rft.volume=229&rft.issue=8&rft.spage=1028&rft.isbn=&rft.btitle=&rft.title=Journal+of+cellular+physiology&rft.issn=1097-4652&rft_id=info:doi/10.1002%2Fjcp.24527
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-07-21
N1 - Date created - 2014-04-23
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1002/jcp.24527
ER -
TY - CPAPER
T1 - Diversity of Anti-Cancer Activity among a Subset of the USDA Apple Germplasm Core Collection
T2 - 2014 Annual Conference of the American Society for Horticultural Science (ASHS 2014)
AN - 1541353518; 6288750
JF - 2014 Annual Conference of the American Society for Horticultural Science (ASHS 2014)
AU - Thompson, Matthew
AU - Stushnoff, Cecil
Y1 - 2014/07/28/
PY - 2014
DA - 2014 Jul 28
KW - Germplasm
KW - Species diversity
KW - Malus
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541353518?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Conference+of+the+American+Society+for+Horticultural+Science+%28ASHS+2014%29&rft.atitle=Diversity+of+Anti-Cancer+Activity+among+a+Subset+of+the+USDA+Apple+Germplasm+Core+Collection&rft.au=Thompson%2C+Matthew%3BStushnoff%2C+Cecil&rft.aulast=Thompson&rft.aufirst=Matthew&rft.date=2014-07-28&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Conference+of+the+American+Society+for+Horticultural+Science+%28ASHS+2014%29&rft.issn=&rft_id=info:doi/
L2 - http://ashs.confex.com/ashs/2014/webprogram/start.html
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-27
N1 - Last updated - 2014-06-30
ER -
TY - CPAPER
T1 - Selecting pharmacological interventions through rapid screening motifs and proper cell models
T2 - 2014 American Dairy Science Association- American Society of Animal Science and and the Canadian Society of Animal Science Annual Meeting (JAM 2014)
AN - 1548625018; 6289697
JF - 2014 American Dairy Science Association- American Society of Animal Science and and the Canadian Society of Animal Science Annual Meeting (JAM 2014)
AU - Zudaire, E
Y1 - 2014/07/20/
PY - 2014
DA - 2014 Jul 20
KW - Screening
KW - Intervention
KW - Cell culture
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1548625018?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Dairy+Science+Association-+American+Society+of+Animal+Science+and+and+the+Canadian+Society+of+Animal+Science+Annual+Meeting+%28JAM+2014%29&rft.atitle=Selecting+pharmacological+interventions+through+rapid+screening+motifs+and+proper+cell+models&rft.au=Zudaire%2C+E&rft.aulast=Zudaire&rft.aufirst=E&rft.date=2014-07-20&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Dairy+Science+Association-+American+Society+of+Animal+Science+and+and+the+Canadian+Society+of+Animal+Science+Annual+Meeting+%28JAM+2014%29&rft.issn=&rft_id=info:doi/
L2 - https://www.asas.org/docs/default-source/jam2014/jam_program_june4.pdf?sfvrsn=0
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-30
N1 - Last updated - 2014-07-28
ER -
TY - JOUR
T1 - A cell-penetrating antibody fragment against HIV-1 Rev has high antiviral activity: characterization of the paratope.
AN - 1549630918; 24878961
AB - The HIV-1 protein Rev oligomerizes on viral transcripts and directs their nuclear export. Previously, a Fab against Rev generated by phage display was used to crystallize and solve the structure of the Rev oligomerization domain. Here we have investigated the capability of this Fab to block Rev oligomerization and inhibit HIV-1 replication. The Fab itself did not have antiviral activity, but when a Tat-derived cell-penetrating peptide was appended, the resulting molecule (FabRev1-Tat) was strongly inhibitory of three different CCR5-tropic HIV-1 isolates (IC50 = 0.09-0.44 μg/ml), as assessed by suppression of reverse transcriptase activity in infected peripheral blood mononuclear cells, and had low cell toxicity (TC50 > 100 μg/ml). FabRev1-Tat was taken up by both peripheral blood mononuclear and HEK293T cells, appearing in both the cytoplasm and nucleus, as shown by immunofluorescence confocal laser scanning microscopy. Computational alanine scanning was used to identify key residues in the complementarity-determining regions to guide mutagenesis experiments. Residues in the light chain CDR3 (LCDR3) were assessed to be important. Residues in LCDR3 were mutated, and LCDR3-Tyr(92) was found to be critical for binding to Rev, as judged by surface plasmon resonance and electron microscopy. Peptides corresponding to all six CDR regions were synthesized and tested for Rev binding. None of the linear peptides had significant affinity for Rev, but four of the amide-cyclic forms did. Especially cyclic-LCDR3 (LGGYPAASYRTA) had high affinity for Rev and was able to effectively depolymerize Rev filaments, as shown by both surface plasmon resonance and electron microscopy.
© 2014 by The American Society for Biochemistry and Molecular Biology, Inc.
JF - The Journal of biological chemistry
AU - Zhuang, Xiaolei
AU - Stahl, Stephen J
AU - Watts, Norman R
AU - DiMattia, Michael A
AU - Steven, Alasdair C
AU - Wingfield, Paul T
AD - From the Protein Expression Laboratory and. ; the Laboratory of Structural Biology Research, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland 20892. ; From the Protein Expression Laboratory and pelpw@helix.nih.gov.
Y1 - 2014/07/18/
PY - 2014
DA - 2014 Jul 18
SP - 20222
EP - 20233
VL - 289
IS - 29
KW - Anti-HIV Agents
KW - 0
KW - Cell-Penetrating Peptides
KW - Complementarity Determining Regions
KW - Immunoglobulin Fab Fragments
KW - rev Gene Products, Human Immunodeficiency Virus
KW - rev protein, Human Immunodeficiency Virus-1
KW - Index Medicus
KW - Monoclonal Antibody
KW - AIDS
KW - Phage Display
KW - Cyclic Peptide
KW - Cell-penetrating peptide (CPP)
KW - Models, Molecular
KW - HEK293 Cells
KW - Humans
KW - Protein Multimerization -- drug effects
KW - Amino Acid Sequence
KW - Protein Binding
KW - Mutagenesis, Site-Directed
KW - Microscopy, Electron, Transmission
KW - Protein Engineering
KW - Virus Replication -- drug effects
KW - Binding Sites, Antibody -- genetics
KW - Kinetics
KW - Molecular Sequence Data
KW - Binding Sites, Antibody -- immunology
KW - Virus Replication -- immunology
KW - Anti-HIV Agents -- chemistry
KW - Cell-Penetrating Peptides -- immunology
KW - HIV-1 -- immunology
KW - Cell-Penetrating Peptides -- genetics
KW - Anti-HIV Agents -- immunology
KW - rev Gene Products, Human Immunodeficiency Virus -- metabolism
KW - rev Gene Products, Human Immunodeficiency Virus -- genetics
KW - Immunoglobulin Fab Fragments -- genetics
KW - Anti-HIV Agents -- pharmacology
KW - rev Gene Products, Human Immunodeficiency Virus -- antagonists & inhibitors
KW - Immunoglobulin Fab Fragments -- immunology
KW - HIV-1 -- physiology
KW - Cell-Penetrating Peptides -- pharmacology
KW - HIV-1 -- drug effects
KW - Immunoglobulin Fab Fragments -- pharmacology
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1549630918?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=A+cell-penetrating+antibody+fragment+against+HIV-1+Rev+has+high+antiviral+activity%3A+characterization+of+the+paratope.&rft.au=Zhuang%2C+Xiaolei%3BStahl%2C+Stephen+J%3BWatts%2C+Norman+R%3BDiMattia%2C+Michael+A%3BSteven%2C+Alasdair+C%3BWingfield%2C+Paul+T&rft.aulast=Zhuang&rft.aufirst=Xiaolei&rft.date=2014-07-18&rft.volume=289&rft.issue=29&rft.spage=20222&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M114.581090
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-10-06
N1 - Date created - 2014-07-29
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1074/jbc.M114.581090
ER -
TY - JOUR
T1 - The nuclear receptor peroxisome proliferator-activated receptor-β/δ (PPARβ/δ) promotes oncogene-induced cellular senescence through repression of endoplasmic reticulum stress.
AN - 1549630858; 24898257
AB - Endoplasmic reticulum (ER) stress and ER stress-associated unfolded protein response (UPR) can promote cancer cell survival, but it remains unclear whether they can influence oncogene-induced senescence. The present study examined the role of ER stress in senescence using oncogene-dependent models. Increased ER stress attenuated senescence in part by up-regulating phosphorylated protein kinase B (p-AKT) and decreasing phosphorylated extracellular signal-regulated kinase (p-ERK). A positive feed forward loop between p-AKT, ER stress, and UPR was discovered whereby a transient increase of ER stress caused reduced senescence and promotion of tumorigenesis. Decreased ER stress was further correlated with increased senescence in both mouse and human tumors. Interestingly, H-RAS-expressing Pparβ/δ null cells and tumors having increased cell proliferation exhibited enhanced ER stress, decreased cellular senescence, and/or enhanced tumorigenicity. Collectively, these results demonstrate a new role for ER stress and UPR that attenuates H-RAS-induced senescence and suggest that PPARβ/δ can repress this oncogene-induced ER stress to promote senescence in accordance with its role as a tumor modifier that suppresses carcinogenesis.
© 2014 by The American Society for Biochemistry and Molecular Biology, Inc.
JF - The Journal of biological chemistry
AU - Zhu, Bokai
AU - Ferry, Christina H
AU - Markell, Lauren K
AU - Blazanin, Nicholas
AU - Glick, Adam B
AU - Gonzalez, Frank J
AU - Peters, Jeffrey M
AD - From the Department of Veterinary and Biomedical Sciences and The Center for Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, Pennsylvania 16802 and. ; the Laboratory of Metabolism, NCI, National Institutes of Health, Bethesda, Maryland 20892. ; From the Department of Veterinary and Biomedical Sciences and The Center for Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, Pennsylvania 16802 and jmp21@psu.edu.
Y1 - 2014/07/18/
PY - 2014
DA - 2014 Jul 18
SP - 20102
EP - 20119
VL - 289
IS - 29
KW - ATF4 protein, human
KW - 0
KW - Atf4 protein, mouse
KW - DNA-Binding Proteins
KW - Heat-Shock Proteins
KW - PPAR delta
KW - PPAR-beta
KW - RNA, Small Interfering
KW - Regulatory Factor X Transcription Factors
KW - Transcription Factors
KW - molecular chaperone GRP78
KW - Activating Transcription Factor 4
KW - 145891-90-3
KW - TOR Serine-Threonine Kinases
KW - EC 2.7.1.1
KW - mTOR protein, mouse
KW - Proto-Oncogene Proteins c-akt
KW - EC 2.7.11.1
KW - Index Medicus
KW - Cancer Therapy
KW - Keratinocyte
KW - Oncogene-induced Endoplasmic Reticulum Stress
KW - H-RAS-induced Senescence
KW - Tumor Suppressor Gene
KW - Peroxisome Proliferator-activated Receptor β/δ
KW - Cancer Biology
KW - Cancer
KW - Animals
KW - TOR Serine-Threonine Kinases -- metabolism
KW - Humans
KW - DNA-Binding Proteins -- genetics
KW - Gene Expression
KW - Models, Biological
KW - Skin Neoplasms -- genetics
KW - Genes, p53
KW - Keratinocytes -- cytology
KW - Keratinocytes -- metabolism
KW - Colonic Neoplasms -- pathology
KW - Adenoma -- pathology
KW - Signal Transduction
KW - Cell Transformation, Neoplastic -- genetics
KW - Proto-Oncogene Proteins c-akt -- metabolism
KW - Colonic Neoplasms -- genetics
KW - Activating Transcription Factor 4 -- genetics
KW - Cell Transformation, Neoplastic -- metabolism
KW - Skin Neoplasms -- pathology
KW - Mice
KW - RNA, Small Interfering -- genetics
KW - Transcription Factors -- genetics
KW - Skin Neoplasms -- metabolism
KW - Adenoma -- metabolism
KW - Gene Knockdown Techniques
KW - Cells, Cultured
KW - Unfolded Protein Response
KW - Colonic Neoplasms -- metabolism
KW - Adenoma -- genetics
KW - Heat-Shock Proteins -- genetics
KW - Genes, ras
KW - PPAR-beta -- metabolism
KW - PPAR delta -- deficiency
KW - PPAR delta -- genetics
KW - PPAR-beta -- genetics
KW - Endoplasmic Reticulum Stress
KW - Cell Aging -- physiology
KW - PPAR-beta -- deficiency
KW - PPAR delta -- metabolism
KW - Cell Aging -- genetics
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1549630858?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=The+nuclear+receptor+peroxisome+proliferator-activated+receptor-%CE%B2%2F%CE%B4+%28PPAR%CE%B2%2F%CE%B4%29+promotes+oncogene-induced+cellular+senescence+through+repression+of+endoplasmic+reticulum+stress.&rft.au=Zhu%2C+Bokai%3BFerry%2C+Christina+H%3BMarkell%2C+Lauren+K%3BBlazanin%2C+Nicholas%3BGlick%2C+Adam+B%3BGonzalez%2C+Frank+J%3BPeters%2C+Jeffrey+M&rft.aulast=Zhu&rft.aufirst=Bokai&rft.date=2014-07-18&rft.volume=289&rft.issue=29&rft.spage=20102&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M114.551069
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-10-06
N1 - Date created - 2014-07-29
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Mol Cancer Res. 2007 Dec;5(12):1263-75 [18171984]
Trends Mol Med. 2007 Oct;13(10):433-42 [17905659]
Oncogene. 2008 May 1;27(20):2801-9 [18193093]
Cell. 2008 Jun 13;133(6):1019-31 [18555778]
Toxicology. 2008 Dec 5;254(1-2):112-7 [18950674]
Carcinogenesis. 2008 Dec;29(12):2406-14 [18799709]
Oncogene. 2009 Jun 18;28(24):2324-36 [19421146]
Nat Protoc. 2009;4(12):1798-806 [20010931]
Toxicol Sci. 2010 Jan;113(1):27-36 [19748995]
Mol Pharmacol. 2010 Sep;78(3):419-30 [20516370]
Cancer Res. 2010 Nov 1;70(21):8526-36 [20959475]
Mol Cancer Ther. 2010 Dec;9(12):3267-77 [21159610]
Biochem J. 2011 Mar 1;434(2):181-8 [21309747]
Mol Cell. 2011 Apr 8;42(1):36-49 [21474066]
Cell Signal. 2011 Dec;23(12):2039-50 [21843636]
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Gastroenterology. 2000 Oct;119(4):929-42 [11040180]
Cancer Res. 2003 Jul 1;63(13):3447-52 [12839923]
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Nature. 1981 Sep 3;293(5827):72-4 [6791032]
Cancer Res. 1988 Jan 1;48(1):165-9 [3121168]
Cancer Res. 1992 Jun 1;52(11):3145-56 [1375535]
Methods Enzymol. 1995;254:3-20 [8531694]
Cancer Res. 1996 Sep 1;56(17):3895-7 [8752154]
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Cancer Cell. 2006 Dec;10(6):459-72 [17157787]
Cancer Cell. 2007 Apr;11(4):349-60 [17418411]
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Biochem Biophys Res Commun. 2007 Aug 3;359(3):643-8 [17560946]
Cell. 2007 Jun 29;129(7):1261-74 [17604717]
Annu Rev Pathol. 2008;3:399-425 [18039139]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1074/jbc.M114.551069
ER -
TY - JOUR
T1 - Super-suppression of mitochondrial reactive oxygen species signaling impairs compensatory autophagy in primary mitophagic cardiomyopathy.
AN - 1546213634; 24874428
AB - Mitochondrial reactive oxygen species (ROS) are implicated in aging, chronic degenerative neurological syndromes, and myopathies. On the basis of free radical hypothesis, dietary, pharmacological, and genetic ROS suppression has been tested to minimize tissue damage, with remarkable therapeutic efficacy. The effects of mitochondrial-specific ROS suppression in primary mitophagic dysfunction are unknown.
An in vivo dose-ranging analysis of ROS suppression in an experimental cardiomyopathy provoked by defective mitochondrial clearance. Mice lacking mitofusin 2 (Mfn2) in hearts have impaired parkin-mediated mitophagy leading to accumulation of damaged ROS-producing organelles and progressive heart failure. As expected, cardiomyocyte-directed expression of mitochondrial-targeted catalase at modest levels normalized mitochondrial ROS production and prevented mitochondrial depolarization, respiratory impairment, and structural degeneration in Mfn2 null hearts. In contrast, catalase expression at higher levels that supersuppressed mitochondrial ROS failed to improve either mitochondrial fitness or cardiomyopathy, revealing that ROS toxicity is not the primary mechanism for cardiac degeneration. Lack of benefit from supersuppressing ROS was associated with failure to invoke secondary autophagic pathways of mitochondrial quality control, revealing a role for ROS signaling in mitochondrial clearance. Mitochondrial permeability transition pore function was normal, and genetic inhibition of mitochondrial permeability transition pore function did not alter mitochondrial or cardiac degeneration, in Mfn2 null hearts.
Local mitochondrial ROS (1) contribute to mitochondrial degeneration and (2) activate mitochondrial quality control mechanisms. A therapeutic window for mitochondrial ROS suppression should minimize the former while retaining the latter, which we achieved by expressing lower levels of catalase. © 2014 American Heart Association, Inc.
JF - Circulation research
AU - Song, Moshi
AU - Chen, Yun
AU - Gong, Guohua
AU - Murphy, Elizabeth
AU - Rabinovitch, Peter S
AU - Dorn, Gerald W
AD - From the Department of Internal Medicine, Center for Pharmacogenomics, Washington University School of Medicine, St. Louis, MO (M.S., G.G., G.W.D.); National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD (E.M.); and Department of Pathology, University of Washington, Seattle (P.S.R.). ; From the Department of Internal Medicine, Center for Pharmacogenomics, Washington University School of Medicine, St. Louis, MO (M.S., G.G., G.W.D.); National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD (E.M.); and Department of Pathology, University of Washington, Seattle (P.S.R.). gdorn@dom.wustl.edu.
Y1 - 2014/07/18/
PY - 2014
DA - 2014 Jul 18
SP - 348
EP - 353
VL - 115
IS - 3
KW - Mitochondrial Membrane Transport Proteins
KW - 0
KW - Myh6 protein, mouse
KW - Oxidants
KW - Reactive Oxygen Species
KW - mitochondrial permeability transition pore
KW - Hydrogen Peroxide
KW - BBX060AN9V
KW - GTP Phosphohydrolases
KW - EC 3.6.1.-
KW - Mfn2 protein, mouse
KW - Myosin Heavy Chains
KW - EC 3.6.4.1
KW - Cyclophilins
KW - EC 5.2.1.-
KW - cyclophilin D
KW - EC 5.2.1.8
KW - Index Medicus
KW - mitochondria
KW - mitochondrial degradation
KW - cardiomyopathies
KW - mitofusin 1
KW - catalase
KW - Mitochondrial Membrane Transport Proteins -- metabolism
KW - Animals
KW - Myosin Heavy Chains -- genetics
KW - Cyclophilins -- genetics
KW - Hydrogen Peroxide -- metabolism
KW - Humans
KW - Oxidants -- metabolism
KW - Myocardium -- metabolism
KW - Male
KW - Female
KW - Mitochondrial Membranes -- metabolism
KW - Mice, Knockout
KW - Signal Transduction -- physiology
KW - Reactive Oxygen Species -- metabolism
KW - Cardiomyopathies -- metabolism
KW - GTP Phosphohydrolases -- genetics
KW - Cardiomyopathies -- pathology
KW - Mitochondria, Heart -- metabolism
KW - Autophagy -- physiology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Circulation+research&rft.atitle=Super-suppression+of+mitochondrial+reactive+oxygen+species+signaling+impairs+compensatory+autophagy+in+primary+mitophagic+cardiomyopathy.&rft.au=Song%2C+Moshi%3BChen%2C+Yun%3BGong%2C+Guohua%3BMurphy%2C+Elizabeth%3BRabinovitch%2C+Peter+S%3BDorn%2C+Gerald+W&rft.aulast=Song&rft.aufirst=Moshi&rft.date=2014-07-18&rft.volume=115&rft.issue=3&rft.spage=348&rft.isbn=&rft.btitle=&rft.title=Circulation+research&rft.issn=1524-4571&rft_id=info:doi/10.1161%2FCIRCRESAHA.115.304384
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-09-16
N1 - Date created - 2014-07-18
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
J Cell Biol. 2010 Apr 19;189(2):211-21 [20404107]
Circulation. 2009 Jun 2;119(21):2789-97 [19451351]
Proc Natl Acad Sci U S A. 2010 May 18;107(20):9035-42 [20418503]
Circ Res. 2010 Jun 11;106(11):1681-91 [20413785]
Trends Biochem Sci. 2011 Jan;36(1):30-8 [20728362]
Mol Cell Biol. 2011 Mar;31(6):1309-28 [21245373]
Circ Res. 2011 Apr 1;108(7):837-46 [21311045]
Circ Res. 2012 Sep 14;111(7):863-75 [22777004]
J Biol Chem. 2013 Jan 18;288(3):1979-90 [23204527]
Science. 2013 Apr 26;340(6131):471-5 [23620051]
PLoS Biol. 2010 Jan;8(1):e1000298 [20126261]
Nature. 2003 Jun 12;423(6941):769-73 [12802338]
Int J Biochem Cell Biol. 2004 Dec;36(12):2463-72 [15325585]
Nature. 2005 Mar 31;434(7033):658-62 [15800627]
Science. 2005 Jun 24;308(5730):1909-11 [15879174]
Circ Res. 2006 Mar 31;98(6):837-45 [16514068]
J Clin Invest. 2009 Jan;119(1):203-12 [19065046]
Mol Cell. 2009 May 15;34(3):259-69 [19450525]
Comment In:
Circ Res. 2014 Jul 18;115(3):329-31 [25035131]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1161/CIRCRESAHA.115.304384
ER -
TY - JOUR
T1 - Genetic instability in lymphoblastoid cell lines expressing biallelic and monoallelic variants in the human MUTYH gene.
AN - 1539466318; 24569162
AB - The MUTYH DNA glycosylase counteracts mutagenesis by removing adenine misincorporated opposite DNA 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG). Biallelic germline mutations in MUTYH cause the autosomal recessive MUTYH-associated polyposis (MAP). The impact on genetic instability of the p.Tyr179Cys and p.Arg245His MUTYH variants was evaluated in lymphoblastoid cell lines (LCLs) derived from MAP patients and their relatives in comparison to wild-type LCLs. No difference in MUTYH expression was identified between wild type and LCLs with the p.Tyr179Cys, while the p.Arg245His mutation was associated with an unstable MUTYH protein. LCLs homozygous for the p.Tyr179Cys or the p.Arg245His variant contained increased DNA 8-oxodG levels and exhibited a mutator phenotype at the PIG-A gene. The extent of the increased spontaneous mutation frequency was 3-fold (range 1.6- to 4.6-fold) in four independent LCLs carrying the p.Tyr179Cys variant, while a larger increase (6-fold) was observed in two p.Arg245His LCLs. A similar hypermutability and S-phase delay following treatment with KBrO3 was observed in LCLs homozygous for either variant. When genetic instability was investigated in monoallelic p.Arg245His carriers, mutant frequencies showed an increase which is intermediate between wild-type and homozygous cells, whereas the mutator effect in heterozygous p.Tyr179Cys LCLs was similar to that in homozygotes. These findings indicate that the type of MUTYH mutation can affect the extent of genome instability associated with MUTYH inactivation. In addition, the mild spontaneous mutator phenotype observed in monoallelic carriers highlights the biological importance of this gene in the protection of the genome against endogenous DNA damage. © The Author 2014. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.
JF - Human molecular genetics
AU - Grasso, Francesca
AU - Giacomini, Elisa
AU - Sanchez, Massimo
AU - Degan, Paolo
AU - Gismondi, Viviana
AU - Mazzei, Filomena
AU - Varesco, Liliana
AU - Viel, Alessandra
AU - Bignami, Margherita
AD - Department of Environment and Primary Prevention and. ; Experimental Oncology 1, CRO Aviano National Cancer Institute, Aviano, Italy. ; Department of Cell Biology and Neuroscience, Istituto Superiore di Sanità, Rome, Italy. ; Department of Translational Oncology and. ; Unit of Hereditary Cancer, IRCCS AOU San Martino-IST, Genoa, Italy. ; Department of Environment and Primary Prevention and margherita.bignami@iss.it.
Y1 - 2014/07/15/
PY - 2014
DA - 2014 Jul 15
SP - 3843
EP - 3852
VL - 23
IS - 14
KW - Bromates
KW - 0
KW - Membrane Proteins
KW - phosphatidylinositol glycan-class A protein
KW - potassium bromate
KW - 04MB35W6ZA
KW - 8-oxo-7-hydrodeoxyguanosine
KW - 88847-89-6
KW - DNA Glycosylases
KW - EC 3.2.2.-
KW - mutY adenine glycosylase
KW - Deoxyguanosine
KW - G9481N71RO
KW - Index Medicus
KW - Young Adult
KW - Genetic Variation
KW - Polymorphism, Single Nucleotide
KW - Protein Stability
KW - Humans
KW - Membrane Proteins -- metabolism
KW - Membrane Proteins -- genetics
KW - Adult
KW - Bromates -- pharmacology
KW - Middle Aged
KW - Deoxyguanosine -- analysis
KW - Cell Cycle -- drug effects
KW - Cell Line
KW - Male
KW - Deoxyguanosine -- analogs & derivatives
KW - Adenomatous Polyposis Coli -- genetics
KW - Genomic Instability
KW - DNA Glycosylases -- metabolism
KW - DNA Glycosylases -- genetics
KW - Adenomatous Polyposis Coli -- blood
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Human+molecular+genetics&rft.atitle=Genetic+instability+in+lymphoblastoid+cell+lines+expressing+biallelic+and+monoallelic+variants+in+the+human+MUTYH+gene.&rft.au=Grasso%2C+Francesca%3BGiacomini%2C+Elisa%3BSanchez%2C+Massimo%3BDegan%2C+Paolo%3BGismondi%2C+Viviana%3BMazzei%2C+Filomena%3BVaresco%2C+Liliana%3BViel%2C+Alessandra%3BBignami%2C+Margherita&rft.aulast=Grasso&rft.aufirst=Francesca&rft.date=2014-07-15&rft.volume=23&rft.issue=14&rft.spage=3843&rft.isbn=&rft.btitle=&rft.title=Human+molecular+genetics&rft.issn=1460-2083&rft_id=info:doi/10.1093%2Fhmg%2Fddu097
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-02-09
N1 - Date created - 2014-06-21
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/hmg/ddu097
ER -
TY - JOUR
T1 - The design and discovery of water soluble 4-substituted-2,6-dimethylfuro[2,3-d]pyrimidines as multitargeted receptor tyrosine kinase inhibitors and microtubule targeting antitumor agents.
AN - 1536685001; 24890652
AB - The design, synthesis and biological evaluations of fourteen 4-substituted 2,6-dimethylfuro[2,3-d]pyrimidines are reported. Four compounds (11-13, 15) inhibit vascular endothelial growth factor receptor-2 (VEGFR-2), platelet-derived growth factor receptor β (PDGFR-β), and target tubulin leading to cytotoxicity. Compound 11 has nanomolar potency, comparable to sunitinib and semaxinib, against tumor cell lines overexpressing VEGFR-2 and PDGFR-β. Further, 11 binds at the colchicine site on tubulin, depolymerizes cellular microtubules and inhibits purified tubulin assembly and overcomes both βIII-tubulin and P-glycoprotein-mediated drug resistance, and initiates mitotic arrest leading to apoptosis. In vivo, its HCl salt, 21, reduced tumor size and vascularity in xenograft and allograft murine models and was superior to docetaxel and sunitinib, without overt toxicity. Thus 21 affords potential combination chemotherapy in a single agent. Copyright © 2014 Elsevier Ltd. All rights reserved.
JF - Bioorganic & medicinal chemistry
AU - Zhang, Xin
AU - Raghavan, Sudhir
AU - Ihnat, Michael
AU - Thorpe, Jessica E
AU - Disch, Bryan C
AU - Bastian, Anja
AU - Bailey-Downs, Lora C
AU - Dybdal-Hargreaves, Nicholas F
AU - Rohena, Cristina C
AU - Hamel, Ernest
AU - Mooberry, Susan L
AU - Gangjee, Aleem
AD - Division of Medicinal Chemistry, Graduate School of Pharmaceutical Sciences, Duquesne University, 600 Forbes Avenue, Pittsburgh, PA 15282, United States. ; College of Pharmacy, University of Oklahoma Health Science Center, 1110 North Stonewall, Oklahoma City, OK 73117, United States. ; Department of Pharmacology, Cancer Therapy & Research Center, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229, United States. ; Screening Technologies Branch, Developmental Therapeutics Program, Division of Cancer Treatment and Diagnosis, Frederick National Laboratory for Cancer Research, National Institutes of Health, 1050 Boyles Street, Frederick, MD 21702, United States. ; Division of Medicinal Chemistry, Graduate School of Pharmaceutical Sciences, Duquesne University, 600 Forbes Avenue, Pittsburgh, PA 15282, United States. Electronic address: gangjee@duq.edu.
Y1 - 2014/07/15/
PY - 2014
DA - 2014 Jul 15
SP - 3753
EP - 3772
VL - 22
IS - 14
KW - Aniline Compounds
KW - 0
KW - Antineoplastic Agents
KW - N-(4-methoxyphenyl)-N,2,6-trimethylfuro(2,3-d)pyrimidin-4-amine
KW - Protein Kinase Inhibitors
KW - Pyrimidines
KW - Water
KW - 059QF0KO0R
KW - Receptor Protein-Tyrosine Kinases
KW - EC 2.7.10.1
KW - Index Medicus
KW - Microtubule targeting agents
KW - Anticancer agents
KW - Single agent combination chemotherapy
KW - Tyrosine kinase inhibitors
KW - Cell Proliferation -- drug effects
KW - Drug Screening Assays, Antitumor
KW - Animals
KW - Solubility
KW - HeLa Cells
KW - Dose-Response Relationship, Drug
KW - Humans
KW - Mice, Nude
KW - Mice
KW - Cell Line, Tumor
KW - Mice, Inbred BALB C
KW - Female
KW - Structure-Activity Relationship
KW - Pyrimidines -- chemistry
KW - Drug Discovery
KW - Aniline Compounds -- pharmacology
KW - Protein Kinase Inhibitors -- pharmacology
KW - Water -- chemistry
KW - Pyrimidines -- pharmacology
KW - Receptor Protein-Tyrosine Kinases -- antagonists & inhibitors
KW - Microtubules -- drug effects
KW - Receptor Protein-Tyrosine Kinases -- metabolism
KW - Neoplasms, Experimental -- pathology
KW - Aniline Compounds -- chemistry
KW - Pyrimidines -- chemical synthesis
KW - Apoptosis -- drug effects
KW - Antineoplastic Agents -- chemical synthesis
KW - Protein Kinase Inhibitors -- chemistry
KW - Protein Kinase Inhibitors -- chemical synthesis
KW - Neoplasms, Experimental -- drug therapy
KW - Antineoplastic Agents -- chemistry
KW - Antineoplastic Agents -- pharmacology
KW - Aniline Compounds -- chemical synthesis
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Bioorganic+%26+medicinal+chemistry&rft.atitle=The+design+and+discovery+of+water+soluble+4-substituted-2%2C6-dimethylfuro%5B2%2C3-d%5Dpyrimidines+as+multitargeted+receptor+tyrosine+kinase+inhibitors+and+microtubule+targeting+antitumor+agents.&rft.au=Zhang%2C+Xin%3BRaghavan%2C+Sudhir%3BIhnat%2C+Michael%3BThorpe%2C+Jessica+E%3BDisch%2C+Bryan+C%3BBastian%2C+Anja%3BBailey-Downs%2C+Lora+C%3BDybdal-Hargreaves%2C+Nicholas+F%3BRohena%2C+Cristina+C%3BHamel%2C+Ernest%3BMooberry%2C+Susan+L%3BGangjee%2C+Aleem&rft.aulast=Zhang&rft.aufirst=Xin&rft.date=2014-07-15&rft.volume=22&rft.issue=14&rft.spage=3753&rft.isbn=&rft.btitle=&rft.title=Bioorganic+%26+medicinal+chemistry&rft.issn=1464-3391&rft_id=info:doi/10.1016%2Fj.bmc.2014.04.049
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-12-28
N1 - Date created - 2014-06-16
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Oncologist. 2010;15(12):1253-61 [21147873]
Oncology. 2010;79(1-2):129-35 [21088439]
Mini Rev Med Chem. 2011 Jan;11(1):18-31 [21034401]
Acta Crystallogr D Biol Crystallogr. 2011 Apr;67(Pt 4):386-94 [21460457]
Invest New Drugs. 2011 Jun;29(3):499-505 [20094773]
Nature. 2011 May 19;473(7347):398-402 [21460836]
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Bioorg Med Chem. 2005 Sep 15;13(18):5475-91 [16039863]
Nature. 2005 Dec 15;438(7070):967-74 [16355214]
Cancer Treat Rev. 2006 May;32(3):166-79 [16527420]
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Cancer Res. 2008 Nov 1;68(21):8881-8 [18974132]
Mol Cancer Ther. 2008 Dec;7(12):3670-84 [19074844]
Bioorg Med Chem. 2009 Oct 15;17(20):7324-36 [19748785]
J Med Chem. 2010 Jan 14;53(1):325-34 [19894742]
Br J Cancer. 2010 Jan 19;102(2):316-24 [20029418]
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Lancet Oncol. 2010 Jul;11(7):619-26 [20570559]
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Oncologist. 2003;8(5):411-24 [14530494]
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Lung. 2003;181(5):267-73 [14705770]
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Nature. 2004 Mar 11;428(6979):198-202 [15014504]
Cancer Res. 1992 Jul 15;52(14):3892-900 [1617665]
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Breast. 2012 Aug;21(4):507-13 [22336056]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.bmc.2014.04.049
ER -
TY - JOUR
T1 - The chemical uncoupler 2,4-dinitrophenol (DNP) protects against diet-induced obesity and improves energy homeostasis in mice at thermoneutrality.
AN - 1549631531; 24872412
AB - The chemical uncoupler 2,4-dinitrophenol (DNP) was an effective and widely used weight loss drug in the early 1930s. However, the physiology of DNP has not been studied in detail because toxicity, including hyperthermia and death, reduced interest in the clinical use of chemical uncouplers. To investigate DNP action, mice fed a high fat diet and housed at 30 °C (to minimize facultative thermogenesis) were treated with 800 mg/liter DNP in drinking water. DNP treatment increased energy expenditure by ∼ 17%, but did not change food intake. DNP-treated mice weighed 26% less than controls after 2 months of treatment due to decreased fat mass, without a change in lean mass. DNP improved glucose tolerance and reduced hepatic steatosis without observed toxicity. DNP treatment also reduced circulating T3 and T4 levels, Ucp1 expression, and brown adipose tissue activity, demonstrating that DNP-mediated heat generation substituted for brown adipose tissue thermogenesis. At 22 °C, a typical vivarium temperature that is below thermoneutrality, DNP treatment had no effect on body weight, adiposity, or glucose homeostasis. Thus, environmental temperature should be considered when assessing an anti-obesity drug in mice, particularly agents acting on energy expenditure. Furthermore, the beneficial effects of DNP suggest that chemical uncouplers deserve further investigation for the treatment of obesity and its comorbidities.
© 2014 by The American Society for Biochemistry and Molecular Biology, Inc.
JF - The Journal of biological chemistry
AU - Goldgof, Margalit
AU - Xiao, Cuiying
AU - Chanturiya, Tatyana
AU - Jou, William
AU - Gavrilova, Oksana
AU - Reitman, Marc L
AD - From the Diabetes, Endocrinology, and Obesity Branch and. ; the Mouse Metabolism Core, NIDDK, National Institutes of Health, Bethesda, Maryland 20892. ; From the Diabetes, Endocrinology, and Obesity Branch and marc.reitman@nih.gov.
Y1 - 2014/07/11/
PY - 2014
DA - 2014 Jul 11
SP - 19341
EP - 19350
VL - 289
IS - 28
KW - Ion Channels
KW - 0
KW - Mitochondrial Proteins
KW - Ucp1 protein, mouse
KW - Uncoupling Agents
KW - Uncoupling Protein 1
KW - 2,4-Dinitrophenol
KW - Q13SKS21MN
KW - Index Medicus
KW - Obesity
KW - Drug Development
KW - CL316243
KW - Thermoregulation
KW - Uncoupling Protein
KW - Thermoneutrality
KW - Brown Adipose Tissue
KW - Energy Metabolism
KW - Adipocyte
KW - Eating -- drug effects
KW - Mitochondrial Proteins -- biosynthesis
KW - Animals
KW - Adipose Tissue, Brown -- metabolism
KW - Ion Channels -- biosynthesis
KW - Mice
KW - Gene Expression Regulation -- drug effects
KW - Adipose Tissue, Brown -- pathology
KW - Obesity -- drug therapy
KW - Body Temperature Regulation -- drug effects
KW - Obesity -- pathology
KW - Obesity -- metabolism
KW - Adiposity -- drug effects
KW - Energy Metabolism -- drug effects
KW - 2,4-Dinitrophenol -- pharmacology
KW - Uncoupling Agents -- pharmacology
KW - Obesity -- chemically induced
KW - Diet -- adverse effects
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1549631531?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=The+chemical+uncoupler+2%2C4-dinitrophenol+%28DNP%29+protects+against+diet-induced+obesity+and+improves+energy+homeostasis+in+mice+at+thermoneutrality.&rft.au=Goldgof%2C+Margalit%3BXiao%2C+Cuiying%3BChanturiya%2C+Tatyana%3BJou%2C+William%3BGavrilova%2C+Oksana%3BReitman%2C+Marc+L&rft.aulast=Goldgof&rft.aufirst=Margalit&rft.date=2014-07-11&rft.volume=289&rft.issue=28&rft.spage=19341&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M114.568204
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-09-29
N1 - Date created - 2014-07-29
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1074/jbc.M114.568204
ER -
TY - JOUR
T1 - Tyrosine 308 is necessary for ligand-directed Gs protein-biased signaling of β2-adrenoceptor.
AN - 1549631147; 24831005
AB - Interaction of a given G protein-coupled receptor to multiple different G proteins is a widespread phenomenon. For instance, β2-adrenoceptor (β2-AR) couples dually to Gs and Gi proteins. Previous studies have shown that cAMP-dependent protein kinase (PKA)-mediated phosphorylation of β2-AR causes a switch in receptor coupling from Gs to Gi. More recent studies have demonstrated that phosphorylation of β2-AR by G protein-coupled receptor kinases, particularly GRK2, markedly enhances the Gi coupling. We have previously shown that although most β2-AR agonists cause both Gs and Gi activation, (R,R')-fenoterol preferentially activates β2-AR-Gs signaling. However, the structural basis for this functional selectivity remains elusive. Here, using docking simulation and site-directed mutagenesis, we defined Tyr-308 as the key amino acid residue on β2-AR essential for Gs-biased signaling. Following stimulation with a β2-AR-Gs-biased agonist (R,R')-4'-aminofenoterol, the Gi disruptor pertussis toxin produced no effects on the receptor-mediated ERK phosphorylation in HEK293 cells nor on the contractile response in cardiomyocytes expressing the wild-type β2-AR. Interestingly, Y308F substitution on β2-AR enabled (R,R')-4'-aminofenoterol to activate Gi and to produce these responses in a pertussis toxin-sensitive manner without altering β2-AR phosphorylation by PKA or G protein-coupled receptor kinases. These results indicate that, in addition to the phosphorylation status, the intrinsic structural feature of β2-AR plays a crucial role in the receptor coupling selectivity to G proteins. We conclude that specific interactions between the ligand and the Tyr-308 residue of β2-AR stabilize receptor conformations favoring the receptor-Gs protein coupling and subsequently result in Gs-biased agonism.
© 2014 by The American Society for Biochemistry and Molecular Biology, Inc.
JF - The Journal of biological chemistry
AU - Woo, Anthony Yiu-Ho
AU - Jozwiak, Krzysztof
AU - Toll, Lawrence
AU - Tanga, Mary J
AU - Kozocas, Joseph A
AU - Jimenez, Lucita
AU - Huang, Ying
AU - Song, Ying
AU - Plazinska, Anita
AU - Pajak, Karolina
AU - Paul, Rajib K
AU - Bernier, Michel
AU - Wainer, Irving W
AU - Xiao, Rui-Ping
AD - From the Key Laboratory of Chemical Genomics, School of Chemical Biology and Biotechnology, Peking University Shenzhen Graduate School, Shenzhen 518055, China, the Institute of Molecular Medicine, Centers for Life Sciences, Peking University, Beijing 100871, China, the Laboratory of Cardiovascular Science and yiuhowoo@pkusz.edu.cn. ; the Department of Chemistry, Medical University of Lublin, Lublin, Poland. ; the Torrey Pines Institute for Molecular Studies, Port St. Lucie, Florida 34987, and. ; SRI International, Menlo Park, California 94025. ; From the Key Laboratory of Chemical Genomics, School of Chemical Biology and Biotechnology, Peking University Shenzhen Graduate School, Shenzhen 518055, China, the Institute of Molecular Medicine, Centers for Life Sciences, Peking University, Beijing 100871, China. ; Laboratory of Clinical Investigation, NIA, National Institutes of Health, Baltimore, Maryland 21224. ; the Institute of Molecular Medicine, Centers for Life Sciences, Peking University, Beijing 100871, China, xiaor@pku.edu.cn.
Y1 - 2014/07/11/
PY - 2014
DA - 2014 Jul 11
SP - 19351
EP - 19363
VL - 289
IS - 28
KW - ADRB2 protein, human
KW - 0
KW - Adrenergic beta-2 Receptor Agonists
KW - Receptors, Adrenergic, beta-2
KW - Tyrosine
KW - 42HK56048U
KW - Extracellular Signal-Regulated MAP Kinases
KW - EC 2.7.11.24
KW - Index Medicus
KW - Site-directed Mutagenesis
KW - Molecular Pharmacology
KW - Cardiomyocyte Contraction
KW - Adrenergic Receptor
KW - Functional Selectivity
KW - Molecular Docking
KW - G Protein-coupled Receptor (GPCR)
KW - Signal Transduction
KW - Cardiovascular
KW - Animals
KW - HEK293 Cells
KW - Humans
KW - Mice
KW - Extracellular Signal-Regulated MAP Kinases -- metabolism
KW - Mutation, Missense
KW - Mice, Knockout
KW - Phosphorylation -- drug effects
KW - Rats
KW - Rats, Sprague-Dawley
KW - Adrenergic beta-2 Receptor Agonists -- pharmacology
KW - Protein Stability -- drug effects
KW - Phosphorylation -- physiology
KW - Tyrosine -- genetics
KW - Tyrosine -- metabolism
KW - Amino Acid Substitution
KW - Male
KW - Extracellular Signal-Regulated MAP Kinases -- genetics
KW - Myocytes, Cardiac -- cytology
KW - Signal Transduction -- physiology
KW - Signal Transduction -- drug effects
KW - Receptors, Adrenergic, beta-2 -- genetics
KW - Receptors, Adrenergic, beta-2 -- metabolism
KW - Myocytes, Cardiac -- metabolism
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1549631147?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Tyrosine+308+is+necessary+for+ligand-directed+Gs+protein-biased+signaling+of+%CE%B22-adrenoceptor.&rft.au=Woo%2C+Anthony+Yiu-Ho%3BJozwiak%2C+Krzysztof%3BToll%2C+Lawrence%3BTanga%2C+Mary+J%3BKozocas%2C+Joseph+A%3BJimenez%2C+Lucita%3BHuang%2C+Ying%3BSong%2C+Ying%3BPlazinska%2C+Anita%3BPajak%2C+Karolina%3BPaul%2C+Rajib+K%3BBernier%2C+Michel%3BWainer%2C+Irving+W%3BXiao%2C+Rui-Ping&rft.aulast=Woo&rft.aufirst=Anthony&rft.date=2014-07-11&rft.volume=289&rft.issue=28&rft.spage=19351&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M114.558882
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-09-29
N1 - Date created - 2014-07-29
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Circulation. 2003 Sep 30;108(13):1633-9 [12975249]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1074/jbc.M114.558882
ER -
TY - JOUR
T1 - Profiling of the Tox21 10K compound library for agonists and antagonists of the estrogen receptor alpha signaling pathway.
AN - 1544736661; 25012808
AB - The U.S. Tox21 program has screened a library of approximately 10,000 (10K) environmental chemicals and drugs in three independent runs for estrogen receptor alpha (ERα) agonist and antagonist activity using two types of ER reporter gene cell lines, one with an endogenous full length ERα (ER-luc; BG1 cell line) and the other with a transfected partial receptor consisting of the ligand binding domain (ER-bla; ERα β-lactamase cell line), in a quantitative high-throughput screening (qHTS) format. The ability of the two assays to correctly identify ERα agonists and antagonists was evaluated using a set of 39 reference compounds with known ERα activity. Although both assays demonstrated adequate (i.e. >80%) predictivity, the ER-luc assay was more sensitive and the ER-bla assay more specific. The qHTS assay results were compared with results from previously published ERα binding assay data and showed >80% consistency. Actives identified from both the ER-bla and ER-luc assays were analyzed for structure-activity relationships (SARs) revealing known and potentially novel ERα active structure classes. The results demonstrate the feasibility of qHTS to identify environmental chemicals with the potential to interact with the ERα signaling pathway and the two different assay formats improve the confidence in correctly identifying these chemicals.
JF - Scientific reports
AU - Huang, Ruili
AU - Sakamuru, Srilatha
AU - Martin, Matt T
AU - Reif, David M
AU - Judson, Richard S
AU - Houck, Keith A
AU - Casey, Warren
AU - Hsieh, Jui-Hua
AU - Shockley, Keith R
AU - Ceger, Patricia
AU - Fostel, Jennifer
AU - Witt, Kristine L
AU - Tong, Weida
AU - Rotroff, Daniel M
AU - Zhao, Tongan
AU - Shinn, Paul
AU - Simeonov, Anton
AU - Dix, David J
AU - Austin, Christopher P
AU - Kavlock, Robert J
AU - Tice, Raymond R
AU - Xia, Menghang
AD - NIH Chemical Genomics Center, National Center for Advancing Translational Sciences, National Institutes of Health, Rockville, MD 20850, USA. ; National Center for Computational Toxicology, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711, USA. ; Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA. ; ILS Inc., Research Triangle Park, NC 27709, USA. ; Division of Bioinformatics and Biostatistics, National Center for Toxicological Research, US Food and Drug Administration, Jefferson, AR 72079, USA.
Y1 - 2014/07/11/
PY - 2014
DA - 2014 Jul 11
SP - 5664
VL - 4
KW - Estrogen Receptor alpha
KW - 0
KW - Ligands
KW - Small Molecule Libraries
KW - Index Medicus
KW - Protein Binding -- drug effects
KW - Humans
KW - HEK293 Cells
KW - High-Throughput Screening Assays -- methods
KW - Genes, Reporter -- drug effects
KW - Cell Line
KW - Structure-Activity Relationship
KW - Small Molecule Libraries -- pharmacology
KW - Signal Transduction -- drug effects
KW - Estrogen Receptor alpha -- antagonists & inhibitors
KW - Estrogen Receptor alpha -- agonists
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1544736661?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Scientific+reports&rft.atitle=Profiling+of+the+Tox21+10K+compound+library+for+agonists+and+antagonists+of+the+estrogen+receptor+alpha+signaling+pathway.&rft.au=Huang%2C+Ruili%3BSakamuru%2C+Srilatha%3BMartin%2C+Matt+T%3BReif%2C+David+M%3BJudson%2C+Richard+S%3BHouck%2C+Keith+A%3BCasey%2C+Warren%3BHsieh%2C+Jui-Hua%3BShockley%2C+Keith+R%3BCeger%2C+Patricia%3BFostel%2C+Jennifer%3BWitt%2C+Kristine+L%3BTong%2C+Weida%3BRotroff%2C+Daniel+M%3BZhao%2C+Tongan%3BShinn%2C+Paul%3BSimeonov%2C+Anton%3BDix%2C+David+J%3BAustin%2C+Christopher+P%3BKavlock%2C+Robert+J%3BTice%2C+Raymond+R%3BXia%2C+Menghang&rft.aulast=Huang&rft.aufirst=Ruili&rft.date=2014-07-11&rft.volume=4&rft.issue=&rft.spage=5664&rft.isbn=&rft.btitle=&rft.title=Scientific+reports&rft.issn=2045-2322&rft_id=info:doi/10.1038%2Fsrep05664
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-10-28
N1 - Date created - 2014-07-11
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Toxicol Sci. 2000 Mar;54(1):138-53 [10746941]
Risk Anal. 2009 Apr;29(4):485-7; discussion 492-7 [19076321]
Toxicol Sci. 2000 Sep;57(1):54-60 [10966511]
Comb Chem High Throughput Screen. 2000 Oct;3(5):437-44 [11032959]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1038/srep05664
ER -
TY - JOUR
T1 - Pharmacophore modeling of nilotinib as an inhibitor of ATP-binding cassette drug transporters and BCR-ABL kinase using a three-dimensional quantitative structure-activity relationship approach.
AN - 1543682412; 24865254
AB - Nilotinib (Tasigna) is a tyrosine kinase inhibitor approved by the FDA to treat chronic phase chronic myeloid leukemia patients. It is also a transport substrate of the ATP-binding cassette (ABC) drug efflux transporters ABCB1 (P-glycoprotein, P-gp) and ABCG2 (BCRP), which may have an effect on the pharmacokinetics and toxicity of this drug. The goal of this study was to identify pharmacophoric features of nilotinib in order to potentially develop specific inhibitors of BCR-ABL kinase with minimal interactions with ABC drug transporters. Three-dimensional pharmacophore modeling and quantitative structure-activity relationship (QSAR) studies were carried out on a series of nilotinib analogues to identify chemical features that contribute to inhibitory activity of nilotinib against BCR-ABL kinase activity, P-gp, and ABCG2. Twenty-five derivatives of nilotinib were synthesized and were then tested to measure their activity to inhibit BCR-ABL kinase and to inhibit the function of ABC drug transporters. A set of in vitro experiments including kinase activity and cell-based transport assays and photolabeling of P-gp and ABCG2 with a transport substrate, [(125)I]-iodoarylazido-prazosin (IAAP), were carried out in isolated membranes to evaluate the potency of the derivatives to inhibit the function of ABC drug transporters and BCR-ABL kinase. Sixteen, fourteen, and ten compounds were selected as QSAR data sets, respectively, to generate PHASE v3.1 pharmacophore models for BCR-ABL kinase, ABCG2, and P-gp inhibitors. The IC50 values of these derivatives against P-gp, ABCG2, or BCR-ABL kinase were used to generate pharmacophore features required for optimal interactions with these targets. A seven-point pharmacophore (AADDRRR) for BCR-ABL kinase inhibitory activity, a six-point pharmacophore (ADHRRR) for ABCG2 inhibitory activity, and a seven-point pharmacophore (AADDRRR) for P-gp inhibitory activity were generated. The derived models clearly demonstrate high predictive power for test sets of BCR-ABL, ABCG2, and P-gp inhibitors. In aggregate, these results should aid in the development of specific inhibitors of BCR-ABL kinase that exhibit no or minimal interaction with ABC drug transporters.
JF - Molecular pharmaceutics
AU - Shukla, Suneet
AU - Kouanda, Abdul
AU - Silverton, Latoya
AU - Talele, Tanaji T
AU - Ambudkar, Suresh V
AD - Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, NIH , Bethesda, Maryland 20892, United States.
Y1 - 2014/07/07/
PY - 2014
DA - 2014 Jul 07
SP - 2313
EP - 2322
VL - 11
IS - 7
KW - 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide
KW - 0
KW - Antineoplastic Agents
KW - P-Glycoproteins
KW - Protein Kinase Inhibitors
KW - Pyrimidines
KW - Fusion Proteins, bcr-abl
KW - EC 2.7.10.2
KW - Index Medicus
KW - P-Glycoproteins -- chemistry
KW - Quantitative Structure-Activity Relationship
KW - Humans
KW - MCF-7 Cells
KW - Cell Line, Tumor
KW - Antineoplastic Agents -- chemistry
KW - Antineoplastic Agents -- pharmacology
KW - Pyrimidines -- chemistry
KW - Protein Kinase Inhibitors -- pharmacokinetics
KW - Pyrimidines -- pharmacology
KW - Protein Kinase Inhibitors -- chemistry
KW - Fusion Proteins, bcr-abl -- antagonists & inhibitors
KW - ATP-Binding Cassette Transporters -- antagonists & inhibitors
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2016-05-04
N1 - Date created - 2014-07-07
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1021/mp400762h
ER -
TY - JOUR
T1 - Cu(I)-mediated allosteric switching in a copper-sensing operon repressor (CsoR).
AN - 1549631628; 24831014
AB - The copper-sensing operon repressor (CsoR) is representative of a major Cu(I)-sensing family of bacterial metalloregulatory proteins that has evolved to prevent cytoplasmic copper toxicity. It is unknown how Cu(I) binding to tetrameric CsoRs mediates transcriptional derepression of copper resistance genes. A phylogenetic analysis of 227 DUF156 protein members, including biochemically or structurally characterized CsoR/RcnR repressors, reveals that Geobacillus thermodenitrificans (Gt) CsoR characterized here is representative of CsoRs from pathogenic bacilli Listeria monocytogenes and Bacillus anthracis. The 2.56 Å structure of Cu(I)-bound Gt CsoR reveals that Cu(I) binding induces a kink in the α2-helix between two conserved copper-ligating residues and folds an N-terminal tail (residues 12-19) over the Cu(I) binding site. NMR studies of Gt CsoR reveal that this tail is flexible in the apo-state with these dynamics quenched upon Cu(I) binding. Small angle x-ray scattering experiments on an N-terminally truncated Gt CsoR (Δ2-10) reveal that the Cu(I)-bound tetramer is hydrodynamically more compact than is the apo-state. The implications of these findings for the allosteric mechanisms of other CsoR/RcnR repressors are discussed.
© 2014 by The American Society for Biochemistry and Molecular Biology, Inc.
JF - The Journal of biological chemistry
AU - Chang, Feng-Ming James
AU - Coyne, H Jerome
AU - Cubillas, Ciro
AU - Vinuesa, Pablo
AU - Fang, Xianyang
AU - Ma, Zhen
AU - Ma, Dejian
AU - Helmann, John D
AU - García-de los Santos, Alejandro
AU - Wang, Yun-Xing
AU - Dann, Charles E
AU - Giedroc, David P
AD - From the Department of Chemistry, Indiana University, Bloomington, Indiana 47405-7102. ; the Programa de Ingeniería Genómica, Centro de Ciencias Genómicas, Universidad Nacional Autónoma de México, Apdo. Postal 565-A, Cuernavaca, Morelos, México, 04510. ; the Structural Biophysics Laboratory, Center for Cancer Research, NCI-National Institutes of Health, Frederick, Maryland 21702-1201, and. ; the Department of Microbiology, Cornell University, Ithaca, New York 14853-8101. ; From the Department of Chemistry, Indiana University, Bloomington, Indiana 47405-7102, giedroc@indiana.edu.
Y1 - 2014/07/04/
PY - 2014
DA - 2014 Jul 04
SP - 19204
EP - 19217
VL - 289
IS - 27
KW - Bacterial Proteins
KW - 0
KW - DNA, Bacterial
KW - Repressor Proteins
KW - Copper
KW - 789U1901C5
KW - Index Medicus
KW - X-ray Crystallography
KW - Metal Sensor Protein
KW - X-ray Scattering
KW - Metalloregulation
KW - Phylogenetics
KW - Transcription Repressor
KW - Phylogeny
KW - Gene Expression Regulation, Bacterial
KW - Bacillus anthracis -- genetics
KW - Allosteric Regulation -- drug effects
KW - Models, Molecular
KW - Transcription, Genetic
KW - DNA, Bacterial -- metabolism
KW - Geobacillus -- metabolism
KW - Protein Multimerization
KW - Protein Structure, Quaternary
KW - Bacterial Proteins -- genetics
KW - Bacterial Proteins -- chemistry
KW - Repressor Proteins -- metabolism
KW - Copper -- metabolism
KW - Bacterial Proteins -- metabolism
KW - Operon -- genetics
KW - Copper -- pharmacology
KW - Repressor Proteins -- chemistry
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-10-14
N1 - Date created - 2014-07-29
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1074/jbc.M114.556704
ER -
TY - JOUR
T1 - Efficacy of ex vivo activated and expanded natural killer cells and T lymphocytes for colorectal cancer patients.
AN - 1826605685; 24944796
AB - Immune cell-based therapies using natural killer (NK) cells and cytotoxic T cells are under constant scrutiny, with the aim to design an effective and reduced-toxicity therapy, which will benefit patients via improved quality of life and improved prognosis. Four patients with stage IV colon cancer were administered 1, 3, 5 and 6 effector cell intravenous infusions, respectively. Peripheral blood was collected from the patients and the ex vivo activation and expansion of NK and T cells was performed in Good Manufacturing Practice-certified clean rooms for ~12-15 days. Immunophenotypic analysis of the peripheral blood mononuclear cells (PBMCs) and expanded NK and T cells was conducted using flow cytometry and the patients were followed up. On average, 4.8×107 initial PBMCs and 2.7×109 total expanded cells were obtained. The intravenous infusions of the expanded cells were not accompanied by adverse reactions. Improved prognosis, reflected by a considerable decrease in the cancer markers, accompanied by an improved quality of life in the patients were observed. In conclusion, potential strategies are currently under development for the large-scale production of effectors cells; therefore, autologous immune enhancement therapy (AIET) may be considered as a viable approach to cancer treatment.
JF - Biomedical reports
AU - Subramani, Baskar
AU - Pullai, Chithra Ramanathan
AU - Krishnan, Kohila
AU - Sugadan, Sheela Devi
AU - Deng, Xuewen
AU - Hiroshi, Terunuma
AU - Ratnavelu, Kananathan
AD - Nichi-Asia Life Science, Sdn. Bhd., Petaling Jaya 47810, Malaysia. ; Biotherapy Institute of Japan, Tokyo 135-0051, Japan. ; Nilai Cancer Institute (NCI) Hospital, Nilai 71800, Malaysia.
Y1 - 2014/07//
PY - 2014
DA - July 2014
SP - 505
EP - 508
VL - 2
IS - 4
SN - 2049-9434, 2049-9434
KW - FOLFOX
KW - colorectal cancer
KW - autologous immune enhancement therapy
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biomedical+reports&rft.atitle=Efficacy+of+ex+vivo+activated+and+expanded+natural+killer+cells+and+T+lymphocytes+for+colorectal+cancer+patients.&rft.au=Subramani%2C+Baskar%3BPullai%2C+Chithra+Ramanathan%3BKrishnan%2C+Kohila%3BSugadan%2C+Sheela+Devi%3BDeng%2C+Xuewen%3BHiroshi%2C+Terunuma%3BRatnavelu%2C+Kananathan&rft.aulast=Subramani&rft.aufirst=Baskar&rft.date=2014-07-01&rft.volume=2&rft.issue=4&rft.spage=505&rft.isbn=&rft.btitle=&rft.title=Biomedical+reports&rft.issn=20499434&rft_id=info:doi/
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date created - 2014-06-19
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
ER -
TY - JOUR
T1 - Oncolytic Viruses Targeting Tumor Stem Cells
AN - 1808673543; PQ0003438638
AB - A workshop "Targeting Oncolytic Viruses to Tumor Stem Cells," organized by the Division of Cancer Biology, NCI, NIH, was held on September 6, 2013 in Rockville, MD. Seventeen invited experts presented an overview of their current research in this area and discussed the state of current research on the use of oncolytic viruses targeted to stem cells as a potential cancer therapy. The goal was to evaluate the evidence that this approach might increase the efficacy of oncolytic virus therapy and to identify gaps in knowledge that have retarded progress in this area. Cancer Res; 74(13); 3396-8. copyright 2014 AACR.
JF - Cancer Research
AU - Chiocca, EAntonio
AU - Blair, Donald
AU - Mufson, RAllan
AD - Department of Neurosurgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA and, mufsonr@mail.nih.gov
Y1 - 2014/07/01/
PY - 2014
DA - 2014 Jul 01
SP - 3396
EP - 3398
PB - American Association for Cancer Research, 615 Chestnut St., 17th Floor Philadelphia PA 19106-4404 United States
VL - 74
IS - 13
SN - 0008-5472, 0008-5472
KW - Biotechnology and Bioengineering Abstracts; Virology & AIDS Abstracts
KW - Stem cells
KW - Conferences
KW - Reviews
KW - Oncolysis
KW - Tumors
KW - Cancer
KW - W 30965:Miscellaneous, Reviews
KW - V 22370:Oncology
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808673543?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Research&rft.atitle=Oncolytic+Viruses+Targeting+Tumor+Stem+Cells&rft.au=Chiocca%2C+EAntonio%3BBlair%2C+Donald%3BMufson%2C+RAllan&rft.aulast=Chiocca&rft.aufirst=EAntonio&rft.date=2014-07-01&rft.volume=74&rft.issue=13&rft.spage=3396&rft.isbn=&rft.btitle=&rft.title=Cancer+Research&rft.issn=00085472&rft_id=info:doi/10.1158%2F0008-5472.CAN-14-0290
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2016-07-01
N1 - Last updated - 2016-09-01
N1 - SubjectsTermNotLitGenreText - Stem cells; Conferences; Reviews; Oncolysis; Tumors; Cancer
DO - http://dx.doi.org/10.1158/0008-5472.CAN-14-0290
ER -
TY - JOUR
T1 - In Vivo Fluorescence Lifetime Imaging for Monitoring the Efficacy of the Cancer Treatment
AN - 1808650030; PQ0003438901
AB - Purpose: Advances in tumor biology created a foundation for targeted therapy aimed at inactivation of specific molecular mechanisms responsible for cell malignancy. In this paper, we used in vivo fluorescence lifetime imaging with HER2-targeted fluorescent probes as an alternative imaging method to investigate the efficacy of targeted therapy with 17-DMAG (an HSP90 inhibitor) on tumors with high expression of HER2 receptors.Experimental Design: HER2-specific Affibody, conjugated to Alexafluor 750, was injected into nude mice bearing HER2-positive tumor xenograft. The fluorescence lifetime was measured before treatment and monitored after the probe injections at 12 hours after the last treatment dose, when the response to the 17-DMAG therapy was the most pronounced as well as a week after the last treatment when the tumors grew back almost to their pretreatment size.Results: Imaging results showed significant difference between the fluorescence lifetimes at the tumor and the contralateral site ( similar to 0.13 ns) in the control group (before treatment) and 7 days after the last treatment when the tumors grew back to their pretreatment dimensions. However, at the time frame that the treatment had its maximum effect (12 hours after the last treatment), the difference between the fluorescence lifetime at the tumor and contralateral site decreased to 0.03 ns.Conclusions: The results showed a good correlation between fluorescence lifetime and the efficacy of the treatment. These findings show that in vivo fluorescence lifetime imaging can be used as a promising molecular imaging tool for monitoring the treatment outcome in preclinical models and potentially in patients. Clin Cancer Res; 20(13); 3531-9. copyright 2014 AACR.
JF - Clinical Cancer Research
AU - Ardeshirpour, Yasaman
AU - Chernomordik, Victor
AU - Hassan, Moinuddin
AU - Zielinski, Rafal
AU - Capala, Jacek
AU - Gandjbakhche, Amir
AD - NIH/National Institute of Child Health and Human Development, Bethesda; , amir@helix.nih.gov
Y1 - 2014/07/01/
PY - 2014
DA - 2014 Jul 01
SP - 3531
EP - 3539
PB - American Association for Cancer Research, 615 Chestnut St., 17th Floor Philadelphia PA 19106-4404 United States
VL - 20
IS - 13
SN - 1078-0432, 1078-0432
KW - Biotechnology and Bioengineering Abstracts
KW - Hsp90 protein
KW - Molecular modelling
KW - Malignancy
KW - Fluorescence
KW - ErbB-2 protein
KW - Animal models
KW - Fluorescent indicators
KW - Tumors
KW - Xenografts
KW - imaging
KW - Cancer
KW - W 30915:Pharmaceuticals & Vaccines
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808650030?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+Cancer+Research&rft.atitle=In+Vivo+Fluorescence+Lifetime+Imaging+for+Monitoring+the+Efficacy+of+the+Cancer+Treatment&rft.au=Ardeshirpour%2C+Yasaman%3BChernomordik%2C+Victor%3BHassan%2C+Moinuddin%3BZielinski%2C+Rafal%3BCapala%2C+Jacek%3BGandjbakhche%2C+Amir&rft.aulast=Ardeshirpour&rft.aufirst=Yasaman&rft.date=2014-07-01&rft.volume=20&rft.issue=13&rft.spage=3531&rft.isbn=&rft.btitle=&rft.title=Clinical+Cancer+Research&rft.issn=10780432&rft_id=info:doi/10.1158%2F1078-0432.CCR-13-1826
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2016-07-01
N1 - Last updated - 2016-08-17
N1 - SubjectsTermNotLitGenreText - Hsp90 protein; Molecular modelling; Malignancy; ErbB-2 protein; Fluorescence; Animal models; Fluorescent indicators; Xenografts; Tumors; imaging; Cancer
DO - http://dx.doi.org/10.1158/1078-0432.CCR-13-1826
ER -
TY - JOUR
T1 - Experimental Effects of Injunctive Norms on Simulated Risky Driving Among Teenage Males
AN - 1732820916; PQ0002164767
AB - Objective: Teenage passengers affect teenage driving performance, possibly by social influence. To examine the effect of social norms on driving behavior, male teenagers were randomly assigned to drive in a simulator with a peer-aged confederate to whom participants were primed to attribute either risk-accepting or risk-averse social norms. It was hypothesized that teenage drivers would engage in more risky driving behavior in the presence of peer passengers than no passengers, and with a risk-accepting compared with a risk-averse passenger. Method: 66 male participants aged 16 to 18 years holding a provisional driver license were randomized to drive with a risk-accepting or risk-averse passenger in a simulator. Failure to Stop at a red light and percent Time in Red (light) were measured as primary risk-relevant outcomes of interest at 18 intersections, while driving once alone and once with their assigned passenger. Results: The effect of passenger presence on risky driving was moderated by passenger type for Failed to Stop in a generalized linear mixed model (OR = 1.84, 95% CI [1.19, 2.86], p < .001), and percent Time in Red in a mixed model (B = 7.71, 95% CI [1.54, 13.87], p < .05). Conclusions: Exposure of teenage males to a risk-accepting confederate peer increased teenage males' risky simulated driving behavior compared with exposure to a risk-averse confederate peer. These results indicate that variability in teenage risky driving could be partially explained by social norms.
JF - Health Psychology
AU - Simons-Morton, Bruce G
AU - Bingham, C Raymond
AU - Falk, Emily B
AU - Li, Kaigang
AU - Pradhan, Anuj K
AU - Ouimet, Marie Claude
AU - Almani, Farideh
AU - Shope, Jean T
AD - Eunice Kennedy Shriver National Institute of Child Health & Human Development, Bethesda, Maryland, Mortonb@mail.nih.gov
PY - 2014
SP - 616
EP - 627
PB - American Psychological Association, 750 First St., N.E. Washington DC 20002-4242 United States
VL - 33
IS - 7
SN - 0278-6133, 0278-6133
KW - Risk Abstracts
KW - social norms
KW - social influence
KW - risk behavior
KW - adolescents
KW - randomized trial
KW - Risk aversion
KW - Driving ability
KW - Behavior
KW - Males
KW - Risk taking
KW - Adolescents
KW - R2 23110:Psychological aspects
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1732820916?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Health+Psychology&rft.atitle=Experimental+Effects+of+Injunctive+Norms+on+Simulated+Risky+Driving+Among+Teenage+Males&rft.au=Simons-Morton%2C+Bruce+G%3BBingham%2C+C+Raymond%3BFalk%2C+Emily+B%3BLi%2C+Kaigang%3BPradhan%2C+Anuj+K%3BOuimet%2C+Marie+Claude%3BAlmani%2C+Farideh%3BShope%2C+Jean+T&rft.aulast=Simons-Morton&rft.aufirst=Bruce&rft.date=2014-07-01&rft.volume=33&rft.issue=7&rft.spage=616&rft.isbn=&rft.btitle=&rft.title=Health+Psychology&rft.issn=02786133&rft_id=info:doi/10.1037%2Fa0034837
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-11-01
N1 - Last updated - 2015-12-09
N1 - SubjectsTermNotLitGenreText - Risk aversion; Driving ability; Behavior; Males; Risk taking; Adolescents
DO - http://dx.doi.org/10.1037/a0034837
ER -
TY - JOUR
T1 - FutureTox II: Contemporary Concepts in Toxicology: "Pathways to Prediction: In Vitro and In Silico Models for Predictive Toxicology"
AN - 1683354759; PQ0001555045
AB - The Society of Toxicology (SOT) held a very successful FutureTox II Contemporary Concepts in Toxicology (CCT) Conference in Chapel Hill, North Carolina, on January 16th and 17th, 2014. There were over 291 attendees representing industry, government and academia; the sessions were also telecast to 9 locations, including Health Canada, US FDA/National Center for Toxicologic Research, the US EPA and the California EPA Office of Environmental Health Hazard Assessment. The conference also included more than 50 posters as well as several vendor exhibits. The theme of the meeting was Pathways to Prediction: In Vitro and In Silico Models for Predictive Toxicology.
JF - Toxicologic Pathology
AU - Elmore, Susan A
AU - Ryan, Anne M
AU - Wood, Charles E
AU - Crabbs, Torrie A
AU - Sills, Robert C
AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA, elmore@niehs.nih.gov
Y1 - 2014/07//
PY - 2014
DA - July 2014
SP - 940
EP - 942
PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom
VL - 42
IS - 5
SN - 0192-6233, 0192-6233
KW - Toxicology Abstracts
KW - Conferences
KW - Models
KW - X 24300:Methods
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1683354759?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+Pathology&rft.atitle=FutureTox+II%3A+Contemporary+Concepts+in+Toxicology%3A+%22Pathways+to+Prediction%3A+In+Vitro+and+In+Silico+Models+for+Predictive+Toxicology%22&rft.au=Elmore%2C+Susan+A%3BRyan%2C+Anne+M%3BWood%2C+Charles+E%3BCrabbs%2C+Torrie+A%3BSills%2C+Robert+C&rft.aulast=Elmore&rft.aufirst=Susan&rft.date=2014-07-01&rft.volume=42&rft.issue=5&rft.spage=940&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F0192623314537135
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-05-01
N1 - Number of references - 5
N1 - Last updated - 2016-08-03
N1 - SubjectsTermNotLitGenreText - Conferences; Models
DO - http://dx.doi.org/10.1177/0192623314537135
ER -
TY - JOUR
T1 - Spontaneous Mesotheliomas in F344/N Rats Are Characterized by Dysregulation of Cellular Growth and Immune Function Pathways
AN - 1683351728; PQ0001555032
AB - Aged male Fischer 344/N rats are prone to developing spontaneous peritoneal mesotheliomas that arise predominantly from the tunica vaginalis of the testes. A definitive cause for the predominance of this neoplasm in F344/N rats is unknown. Investigation of the molecular alterations that occur in spontaneous rat mesotheliomas may provide insight into their pathogenesis as well enable a better understanding regarding the mechanisms underlying chemically induced mesothelioma in rodents. Mesothelial cell function represents a complex interplay of pathways related to host defense mechanisms and maintenance of cellular homeostasis. Global gene expression profiles of spontaneous mesotheliomas from vehicle control male F344/N rats from 2-year National Toxicology Program carcinogenicity bioassays were analyzed to determine the molecular features of these tumors and elucidate tumor-specific gene expression profiles. The resulting gene expression pattern showed that spontaneous mesotheliomas are associated with upregulation of various growth factors, oncogenes, cytokines, pattern recognition response receptors, and pathogen-associated molecular patterns receptors, and the production of reactive oxygen and nitrogen species, as well as downregulation of apoptosis pathways. Alterations in these pathways in turn trigger molecular responses that stimulate cell proliferation and promote tumor survival and progression.
JF - Toxicologic Pathology
AU - Blackshear, Pamela E
AU - Pandiri, Arun R
AU - Ton, Thai-Vu T
AU - Clayton, Natasha P
AU - Shockley, Keith R
AU - Peddada, Shyamal D
AU - Gerrish, Kevin E
AU - Sills, Robert C
AU - Hoenerhoff, Mark J
AD - Integrated Laboratory Systems, Inc., Research Triangle Park, North Carolina, USA, hoenerhm@niehs.nih.gov
PY - 2014
SP - 863
EP - 876
PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom
VL - 42
IS - 5
SN - 0192-6233, 0192-6233
KW - Immunology Abstracts; Toxicology Abstracts
KW - mesothelioma
KW - F344/N rat
KW - National Toxicology Program
KW - microarray
KW - gene expression
KW - mesothelial cell
KW - Fred-PE cells
KW - Cell survival
KW - Testes
KW - Apoptosis
KW - Peritoneum
KW - Homeostasis
KW - Tumors
KW - Gene expression
KW - Oxygen
KW - Pattern recognition
KW - Oncogenes
KW - Carcinogenicity
KW - Cytokines
KW - Defense mechanisms
KW - Immune response
KW - Growth factors
KW - Cell proliferation
KW - Nitrogen
KW - X 24490:Other
KW - F 06950:Immunogenetics, MHC, HLA
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1683351728?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+Pathology&rft.atitle=Spontaneous+Mesotheliomas+in+F344%2FN+Rats+Are+Characterized+by+Dysregulation+of+Cellular+Growth+and+Immune+Function+Pathways&rft.au=Blackshear%2C+Pamela+E%3BPandiri%2C+Arun+R%3BTon%2C+Thai-Vu+T%3BClayton%2C+Natasha+P%3BShockley%2C+Keith+R%3BPeddada%2C+Shyamal+D%3BGerrish%2C+Kevin+E%3BSills%2C+Robert+C%3BHoenerhoff%2C+Mark+J&rft.aulast=Blackshear&rft.aufirst=Pamela&rft.date=2014-07-01&rft.volume=42&rft.issue=5&rft.spage=863&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F0192623313501894
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-05-01
N1 - Number of references - 80
N1 - Last updated - 2016-01-21
N1 - SubjectsTermNotLitGenreText - Testes; Cell survival; Apoptosis; Peritoneum; Tumors; Homeostasis; Gene expression; Pattern recognition; Oxygen; Oncogenes; Carcinogenicity; mesothelioma; Cytokines; Growth factors; Immune response; Defense mechanisms; Cell proliferation; Nitrogen
DO - http://dx.doi.org/10.1177/0192623313501894
ER -
TY - JOUR
T1 - Body size perception and weight control in youth: 9-year international trends from 24 countries
AN - 1680441575; 20507744
AB - Objectives: To examine 9-year trends and relationships regarding misperceptions of body size and dieting for weight loss among adolescents from 24 countries, and explore the influence of country-level overweight prevalence. Methods: Sociodemographic characteristics, body size perception and dieting for weight loss were assessed in the Health Behaviour in School-aged Children survey conducted in 24 countries cross-sectionally at three time points (2001/2002, 2005/2006 and 2009/2010). Logistic regression models examined change over time in overestimation of body size in non-overweight adolescents, underestimation of body size in overweight adolescents, dieting for weight loss in non-overweight and overweight adolescents and relationships between body size perception and dieting. Analyses were stratified by weight status and sex. Covariates included country-level overweight prevalence, family affluence and country level of development. Body mass index was only included in models examining dieting for weight loss. Results: Country-level overweight prevalence increased over time (11.6-14.7%). Compared with Time 1, overweight adolescents had greater odds of body size underestimation at Time 3 (odds ratio (OR)=1.68 for girls; OR=1.10 for boys), whereas non-overweight adolescents had lower odds of body size overestimation at Time 3 (OR=0.87 for girls; OR=0.89 for boys). Controlling for country-level overweight prevalence attenuated these relationships. Compared with Time 1, overweight and non-overweight boys were 10% more likely to diet at Time 3, whereas overweight and non-overweight girls were 19% and 16%, respectively, less likely to diet at Time 3. Controlling for country-level overweight prevalence did not impact trends in dieting for weight loss. Additionally, the association of self-perceived overweight with increased odds of dieting diminished over time. Conclusions: Body size perceptions among adolescents may have changed over time concurrent with shifts in country-level body weight. However, controlling for country-level overweight prevalence did not impact trends in dieting for weight loss, suggesting a potentially stronger impact of social comparison on weight-related perceptions than on behavior.
JF - International Journal of Obesity
AU - Quick, V
AU - Nansel, T R
AU - Liu, D
AU - Lipsky, L M
AU - Due, P
AU - Iannotti, R J
AD - Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development/NIH, Bethesda, MD, USA
Y1 - 2014/07//
PY - 2014
DA - Jul 2014
SP - 988
EP - 994
PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL - 38
IS - 7
SN - 0307-0565, 0307-0565
KW - Physical Education Index
KW - Anthropometry
KW - Obesity
KW - Weight control
KW - Perception
KW - Boys
KW - Adolescence
KW - Girls
KW - Diet (weight control)
KW - Trends
KW - PE 030:Exercise, Health & Physical Fitness
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1680441575?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aphysicaleducation&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Obesity&rft.atitle=Body+size+perception+and+weight+control+in+youth%3A+9-year+international+trends+from+24+countries&rft.au=Quick%2C+V%3BNansel%2C+T+R%3BLiu%2C+D%3BLipsky%2C+L+M%3BDue%2C+P%3BIannotti%2C+R+J&rft.aulast=Quick&rft.aufirst=V&rft.date=2014-07-01&rft.volume=38&rft.issue=7&rft.spage=988&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Obesity&rft.issn=03070565&rft_id=info:doi/10.1038%2Fijo.2014.62
LA - English
DB - Physical Education Index
N1 - Date revised - 2015-05-01
N1 - Last updated - 2015-06-12
N1 - SubjectsTermNotLitGenreText - Anthropometry; Obesity; Weight control; Boys; Perception; Girls; Adolescence; Diet (weight control); Trends
DO - http://dx.doi.org/10.1038/ijo.2014.62
ER -
TY - JOUR
T1 - Ultra-low Dose Interleukin-2 Promotes Immune-modulating Function of Regulatory T Cells and Natural Killer Cells in Healthy Volunteers
AN - 1673384558; PQ0001372915
AB - Low-dose interleukin-2 (IL-2) expands regulatory T cells (T sub(regs)) and natural killer (NK) cells after stem cell transplantation (SCT) and may reduce graft-versus-host disease (GVHD). We hypothesized that ultra-low dose (ULD) IL-2 could serve as an immune-modulating agent for stem cell donors to prevent GVHD following SCT. However, the safety, dose level, and immune signatures of ULD IL-2 in immune-competent healthy subjects remain unknown. Here, we have characterized the phenotype and function of T sub(regs) and NK cells as well as the gene expression and cytokine profiles of 21 healthy volunteers receiving 50,000 to 200,000 units/m super(2)/day IL-2 for 5 days. ULD IL-2 was well tolerated and induced a significant increase in the frequency of T sub(regs) with increased suppressive function. There was a marked expansion of CD56 super(bright) NK cells with enhanced interferon- gamma (IFN- gamma ) production. Serum cytokine profiling demonstrated increase of IFN- gamma induced protein 10 (IP-10). Gene expression analysis revealed significant changes in a highly restricted set of genes, including FOXP3, IL-2RA, and CISH. This is the first study to evaluate global immune-modulating function of ULD IL-2 in healthy subjects and to support the future studies administrating ULD IL-2 to stem cell donors.
JF - Molecular Therapy
AU - Ito, Sawa
AU - Bollard, Catherine M
AU - Carlsten, Mattias
AU - Melenhorst, Jan Joseph
AU - Biancotto, Angelique
AU - Wang, Ena
AU - Chen, Jinguo
AU - Kotliarov, Yuri
AU - Cheung, Foo
AU - Xie, Zhi
AD - Hematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA
Y1 - 2014/07//
PY - 2014
DA - Jul 2014
SP - 1388
EP - 1395
PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom
VL - 22
IS - 7
SN - 1525-0016, 1525-0016
KW - Immunology Abstracts; Biotechnology and Bioengineering Abstracts
KW - Gene expression
KW - gamma -Interferon
KW - Immunoregulation
KW - Interleukin 2
KW - IP-10 protein
KW - Foxp3 protein
KW - Natural killer cells
KW - Lymphocytes T
KW - Graft-versus-host reaction
KW - Immunomodulation
KW - Interleukin 2 receptors
KW - W 30940:Products
KW - F 06960:Molecular Immunology
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1673384558?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+Therapy&rft.atitle=Ultra-low+Dose+Interleukin-2+Promotes+Immune-modulating+Function+of+Regulatory+T+Cells+and+Natural+Killer+Cells+in+Healthy+Volunteers&rft.au=Ito%2C+Sawa%3BBollard%2C+Catherine+M%3BCarlsten%2C+Mattias%3BMelenhorst%2C+Jan+Joseph%3BBiancotto%2C+Angelique%3BWang%2C+Ena%3BChen%2C+Jinguo%3BKotliarov%2C+Yuri%3BCheung%2C+Foo%3BXie%2C+Zhi&rft.aulast=Ito&rft.aufirst=Sawa&rft.date=2014-07-01&rft.volume=22&rft.issue=7&rft.spage=1388&rft.isbn=&rft.btitle=&rft.title=Molecular+Therapy&rft.issn=15250016&rft_id=info:doi/10.1038%2Fmt.2014.50
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-04-01
N1 - Last updated - 2015-11-16
N1 - SubjectsTermNotLitGenreText - Gene expression; Immunoregulation; gamma -Interferon; IP-10 protein; Interleukin 2; Foxp3 protein; Lymphocytes T; Natural killer cells; Graft-versus-host reaction; Immunomodulation; Interleukin 2 receptors
DO - http://dx.doi.org/10.1038/mt.2014.50
ER -
TY - JOUR
T1 - Toxicity and carcinogenicity studies of Ginkgo biloba extract in rat and mouse: liver, thyroid, and nose are targets.
AN - 1672090815; 23960164
AB - Ginkgo biloba extract (GBE) is a popular herbal supplement that is used to improve circulation and brain function. In spite of widespread human exposure to relatively high doses over potentially long periods of time, there is a paucity of data from animal studies regarding the toxicity and carcinogenicity associated with GBE. In order to fill this knowledge gap, 3-month and 2-year toxicity and carcinogenicity studies with GBE administered by oral gavage to B6C3F1/N mice and F344/N rats were performed as part of the National Toxicology Program's Dietary Supplements and Herbal Medicines Initiative. The targets of GBE treatment were the liver, thyroid, and nose. These targets were consistent across exposure period, sex, and species, albeit with varying degrees of effect observed among studies. Key findings included a notably high incidence of hepatoblastomas in male and female mice and evidence of carcinogenic potential in the thyroid gland of both mice and rats. Various nonneoplastic lesions were observed beyond control levels in the liver, thyroid gland, and nose of rats and mice administered GBE. Although these results cannot be directly extrapolated to humans, the findings fill an important data gap in assessing risk associated with GBE use.
© 2014 by The Author(s).
JF - Toxicologic pathology
AU - Rider, Cynthia V
AU - Nyska, Abraham
AU - Cora, Michelle C
AU - Kissling, Grace E
AU - Smith, Cynthia
AU - Travlos, Gregory S
AU - Hejtmancik, Milton R
AU - Fomby, Laurene M
AU - Colleton, Curtis A
AU - Ryan, Michael J
AU - Kooistra, Linda
AU - Morrison, James P
AU - Chan, Po C
AD - National Institute of Environmental Health Sciences, Research Triangle Park, Durham, North Carolina, USA ridercv@niehs.nih.gov. ; Integrated Laboratory Systems Incorporated, Research Triangle Park, Durham, North Carolina, USA. ; National Institute of Environmental Health Sciences, Research Triangle Park, Durham, North Carolina, USA. ; Battelle, Columbus, Ohio, USA. ; Charles River Laboratories, Pathology Associates, Durham, North Carolina, USA.
Y1 - 2014/07//
PY - 2014
DA - July 2014
SP - 830
EP - 843
VL - 42
IS - 5
KW - Carcinogens
KW - 0
KW - Plant Extracts
KW - Index Medicus
KW - hepatocarcinogenicity
KW - thyroid tumors
KW - natural medicine
KW - nasal lesions
KW - herbal
KW - Rats
KW - Mice, Inbred Strains
KW - Animals
KW - Rats, Inbred F344
KW - Dose-Response Relationship, Drug
KW - Carcinogens -- toxicity
KW - Carcinogenicity Tests
KW - Mice
KW - Drug Evaluation, Preclinical
KW - Male
KW - Female
KW - Organ Size -- drug effects
KW - Liver -- pathology
KW - Thyroid Gland -- drug effects
KW - Ginkgo biloba -- toxicity
KW - Thyroid Gland -- pathology
KW - Liver -- drug effects
KW - Nose -- pathology
KW - Plant Extracts -- toxicity
KW - Plant Extracts -- chemistry
KW - Nose -- drug effects
KW - Ginkgo biloba -- chemistry
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+pathology&rft.atitle=Toxicity+and+carcinogenicity+studies+of+Ginkgo+biloba+extract+in+rat+and+mouse%3A+liver%2C+thyroid%2C+and+nose+are+targets.&rft.au=Rider%2C+Cynthia+V%3BNyska%2C+Abraham%3BCora%2C+Michelle+C%3BKissling%2C+Grace+E%3BSmith%2C+Cynthia%3BTravlos%2C+Gregory+S%3BHejtmancik%2C+Milton+R%3BFomby%2C+Laurene+M%3BColleton%2C+Curtis+A%3BRyan%2C+Michael+J%3BKooistra%2C+Linda%3BMorrison%2C+James+P%3BChan%2C+Po+C&rft.aulast=Rider&rft.aufirst=Cynthia&rft.date=2014-07-01&rft.volume=42&rft.issue=5&rft.spage=830&rft.isbn=&rft.btitle=&rft.title=Toxicologic+pathology&rft.issn=1533-1601&rft_id=info:doi/10.1177%2F0192623313501235
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-11-20
N1 - Date created - 2015-04-08
N1 - Date revised - 2017-01-13
N1 - SuppNotes - Cited By:
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Toxicol Pathol. 2002 Sep-Oct;30(5):580-91 [12371667]
Eur J Pharmacol. 2004 Jun 28;494(2-3):131-8 [15212966]
Toxicol Pathol. 2004 Jul-Aug;32(4):393-401 [15307212]
Biometrics. 1988 Jun;44(2):417-31 [3390507]
Fundam Appl Toxicol. 1989 May;12(4):731-7 [2744275]
Endocr Rev. 1991 May;12(2):135-50 [2070777]
Drug Metab Rev. 1993;25(1-2):173-205 [8449146]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1177/0192623313501235
ER -
TY - JOUR
T1 - The influence of age on serum concentrations of cardiac troponin I: results in rats, monkeys, and commercial sera.
AN - 1672090352; 24129761
AB - Cardiac troponins serve as serum biomarkers of myocardial injury. The current study examined the influence of age on serum concentrations of cardiac troponin I (cTnI). An ultrasensitive immunoassay was used to monitor cTnI concentrations in Sprague-Dawley (SD) rats and Erythrocebus patas monkeys of different ages. The mean cTnI concentrations were highest in 10-day-old rats compared to 25-, 40-, and 80-day-old SD rats. Cardiomyocyte remodeling was apparent in hearts from 10-day-old SD rats as evident by hypercellularity, irregularly shaped nuclei, and moderate numbers of myocytes undergoing mitosis and apoptosis. The mean concentration of cTnI in 5 newborn monkeys was considerably higher than that of three 1-year-old monkeys. Evidence of cardiomyocyte remodeling was also observed in these newborn hearts (loss of myofibrils and cytoplasmic vacuolation). Commercial animal serum samples were also analyzed. The concentrations of cTnI detected in fetal equine and porcine serum were considerably higher than that found in adult equine and porcine serum samples Likewise, fetal bovine serum had higher cTnI concentrations (>2,400 pg/ml) than did adult caprine and laprine samples (2.5-2.7 pg/ml). The present study found age-related differences in cTnI concentrations, with higher levels occurring at younger ages. This effect was consistent across several animal species.
© 2014 by The Author(s).
JF - Toxicologic pathology
AU - Herman, Eugene H
AU - Knapton, Alan
AU - Liu, Yongmin
AU - Lipshultz, Steven E
AU - Estis, Joel
AU - Todd, John
AU - Woodward, Ruth A
AU - Cochran, Thomas
AU - Zhang, Jun
AU - Poirier, Miriam C
AD - Food and Drug Administration, Division of Drug Safety Research, Silver Spring, Maryland, USA eugene.herman@fda.hhs.gov. ; Food and Drug Administration, Division of Drug Safety Research, Silver Spring, Maryland, USA. ; National Institutes of Health, National Cancer Institute, Carcinogen-DNA Interactions Section, Bethesda, Maryland, USA. ; Department of Pediatrics, Leonard M. Miller School of Medicine, Mailman Center for Child Development, University of Miami, Miami, Florida, USA. ; Singulex, Inc., Alameda, California, USA. ; Shared Animal Facility, NIH Animal Center, Dickerson, Maryland, USA.
Y1 - 2014/07//
PY - 2014
DA - July 2014
SP - 888
EP - 896
VL - 42
IS - 5
KW - Biomarkers
KW - 0
KW - Troponin I
KW - Index Medicus
KW - Sprague-Dawley rats
KW - patas monkeys
KW - cardiac troponin I
KW - young age.
KW - Swine
KW - Animals
KW - Horses
KW - Myocardium -- metabolism
KW - Rats
KW - Myofibrils -- metabolism
KW - Cattle
KW - Rats, Sprague-Dawley
KW - Heart Injuries -- blood
KW - Erythrocebus patas
KW - Female
KW - Male
KW - Immunoassay
KW - Age Factors
KW - Troponin I -- blood
KW - Biomarkers -- blood
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1672090352?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+pathology&rft.atitle=The+influence+of+age+on+serum+concentrations+of+cardiac+troponin+I%3A+results+in+rats%2C+monkeys%2C+and+commercial+sera.&rft.au=Herman%2C+Eugene+H%3BKnapton%2C+Alan%3BLiu%2C+Yongmin%3BLipshultz%2C+Steven+E%3BEstis%2C+Joel%3BTodd%2C+John%3BWoodward%2C+Ruth+A%3BCochran%2C+Thomas%3BZhang%2C+Jun%3BPoirier%2C+Miriam+C&rft.aulast=Herman&rft.aufirst=Eugene&rft.date=2014-07-01&rft.volume=42&rft.issue=5&rft.spage=888&rft.isbn=&rft.btitle=&rft.title=Toxicologic+pathology&rft.issn=1533-1601&rft_id=info:doi/10.1177%2F0192623313505154
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-11-20
N1 - Date created - 2015-04-08
N1 - Date revised - 2017-01-13
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1177/0192623313505154
ER -
TY - JOUR
T1 - Social support, self-efficacy for decision-making, and follow-up care use in long-term cancer survivors
AN - 1665162096
AB - Objective Cancer survivors play an important role in coordinating their follow-up care and making treatment-related decisions. Little is known about how modifiable factors such as social support are associated with active participation in follow-up care. This study tests associations between social support, cancer-related follow-up care use, and self-efficacy for participation in decision-making related to follow-up care (SEDM). We also identified sociodemographic and clinical factors associated with social support among long-term survivors. Methods The FOllow-up Care Use among Survivors study is a cross-sectional, population-based survey of breast, prostate, colon, and gynecologic cancer survivors ( n=1522) 4–14 years post-diagnosis. Multivariable regression models were used to test associations between perceived social support (tangible and emotional/informational support modeled separately), follow-up care use (past 2 years), and SEDM, as well as to identify factors associated with perceived support. Results Neither support type was associated with follow-up care use (all p>0.05), although marital status was uniquely, positively associated with follow-up care use ( p<0.05). Both tangible support (B for a standard deviation increase (SE)=9.75(3.15), p<0.05) and emotional/informational support (B(SE)=12.61(3.05), p<0.001) were modestly associated with SEDM. Being married, having adequate financial resources, history of recurrence, and better perceived health status were associated with higher perceived tangible and emotional support (all p<0.05). Conclusions While perceived social support may facilitate survivor efficacy for participation in decision-making during cancer follow-up care, other factors, including marital satisfaction, appear to influence follow-up care use. Marital status and social support may be important factors to consider in survivorship care planning. Copyright © 2014 John Wiley & Sons, Ltd.
JF - Psycho-Oncology
AU - Forsythe, Laura P
AU - Alfano, Catherine M
AU - Kent, Erin E
AU - Weaver, Kathryn E
AU - Bellizzi, Keith
AU - Arora, Neeraj
AU - Aziz, Noreen
AU - Keel, Gretchen
AU - Rowland, Julia H
AD - Patient-Centered Outcomes Research Institute (PCORI), Washington, DC, USA., Office of Cancer Survivorship, Division of Cancer Control and Population Sciences, National Cancer Institute, NIH/DHHS, Bethesda, MD, USA., Cancer Prevention Fellowship Program, Center for Cancer Training, National Cancer Institute, NIH/DHHS, Bethesda, MD, USA. ; Office of Cancer Survivorship, Division of Cancer Control and Population Sciences, National Cancer Institute, NIH/DHHS, Bethesda, MD, USA. ; Cancer Prevention Fellowship Program, Center for Cancer Training, National Cancer Institute, NIH/DHHS, Bethesda, MD, USA., Outcomes Research Branch, Applied Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, NIH/DHHS, Bethesda, MD, USA. ; Department of Social Sciences & Health Policy, Division of Public Health Sciences, Wake Forest School of Medicine, Winston-Salem, NC, USA. ; Human Development and Family Studies, University of Connecticut, Storrs, CT, USA. ; Outcomes Research Branch, Applied Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, NIH/DHHS, Bethesda, MD, USA. ; Office of Extramural Programs, National Institute of Nursing Research, NIH/DHHS, Bethesda, MD, USA. ; Information Management Services (IMS), Silver Spring, MD, USA. ; Patient-Centered Outcomes Research Institute (PCORI), Washington, DC, USA.; Office of Cancer Survivorship, Division of Cancer Control and Population Sciences, National Cancer Institute, NIH/DHHS, Bethesda, MD, USA.; Cancer Prevention Fellowship Program, Center for Cancer Training, National Cancer Institute, NIH/DHHS, Bethesda, MD, USA.
Y1 - 2014/07//
PY - 2014
DA - Jul 2014
SP - 788
EP - 796
CY - Chichester
PB - Wiley Subscription Services, Inc.
VL - 23
IS - 7
SN - 1057-9249
KW - Medical Sciences--Psychiatry And Neurology
KW - Breast cancer
KW - Care plans
KW - Selfefficacy
KW - Social support
KW - Sociodemographic aspects
KW - Survivors
KW - Cancer
KW - Care management
KW - Decision making
KW - Deviation
KW - Diagnosis
KW - Efficacy
KW - Emotional support
KW - Gynaecological cancer
KW - Health status
KW - Marital satisfaction
KW - Marital status
KW - Perceived social support
KW - Prostate
KW - Recurrence
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665162096?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Psycho-Oncology&rft.atitle=Social+support%2C+self-efficacy+for+decision-making%2C+and+follow-up+care+use+in+long-term+cancer+survivors&rft.au=Forsythe%2C+Laura+P%3BAlfano%2C+Catherine+M%3BKent%2C+Erin+E%3BWeaver%2C+Kathryn+E%3BBellizzi%2C+Keith%3BArora%2C+Neeraj%3BAziz%2C+Noreen%3BKeel%2C+Gretchen%3BRowland%2C+Julia+H&rft.aulast=Forsythe&rft.aufirst=Laura&rft.date=2014-07-01&rft.volume=23&rft.issue=7&rft.spage=788&rft.isbn=&rft.btitle=&rft.title=Psycho-Oncology&rft.issn=10579249&rft_id=info:doi/10.1002%2Fpon.3480
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Date revised - 2015-01-09
N1 - Last updated - 2016-08-17
DO - http://dx.doi.org/10.1002/pon.3480
ER -
TY - JOUR
T1 - Harmonization of Neuroticism and Extraversion phenotypes across inventories and cohorts in the Genetics of Personality Consortium: an application of Item Response Theory
AN - 1665150623
AB - Mega- or meta-analytic studies (e.g. genome-wide association studies) are increasingly used in behavior genetics. An issue in such studies is that phenotypes are often measured by different instruments across study cohorts, requiring harmonization of measures so that more powerful fixed effect meta-analyses can be employed. Within the Genetics of Personality Consortium, we demonstrate for two clinically relevant personality traits, Neuroticism and Extraversion, how Item-Response Theory (IRT) can be applied to map item data from different inventories to the same underlying constructs. Personality item data were analyzed in >160,000 individuals from 23 cohorts across Europe, USA and Australia in which Neuroticism and Extraversion were assessed by nine different personality inventories. Results showed that harmonization was very successful for most personality inventories and moderately successful for some. Neuroticism and Extraversion inventories were largely measurement invariant across cohorts, in particular when comparing cohorts from countries where the same language is spoken. The IRT-based scores for Neuroticism and Extraversion were heritable (48 and 49 %, respectively, based on a meta-analysis of six twin cohorts, total N = 29,496 and 29,501 twin pairs, respectively) with a significant part of the heritability due to non-additive genetic factors. For Extraversion, these genetic factors qualitatively differ across sexes. We showed that our IRT method can lead to a large increase in sample size and therefore statistical power. The IRT approach may be applied to any mega- or meta-analytic study in which item-based behavioral measures need to be harmonized.
JF - Behavior Genetics
AU - Berg, Stéphanie M
AU - Moor, Marleen H M
AU - McGue, Matt
AU - Pettersson, Erik
AU - Terracciano, Antonio
AU - Verweij, Karin J H
AU - Amin, Najaf
AU - Derringer, Jaime
AU - Esko, Tõnu
AU - Grootheest, Gerard
AU - Hansell, Narelle K
AU - Huffman, Jennifer
AU - Konte, Bettina
AU - Lahti, Jari
AU - Luciano, Michelle
AU - Matteson, Lindsay K
AU - Viktorin, Alexander
AU - Wouda, Jasper
AU - Agrawal, Arpana
AU - Allik, Jüri
AU - Bierut, Laura
AU - Broms, Ulla
AU - Campbell, Harry
AU - Smith, George Davey
AU - Eriksson, Johan G
AU - Ferrucci, Luigi
AU - Franke, Barbera
AU - Fox, Jean-Paul
AU - Geus, Eco J C
AU - Giegling, Ina
AU - Gow, Alan J
AU - Grucza, Richard
AU - Hartmann, Annette M
AU - Heath, Andrew C
AU - Heikkilä, Kauko
AU - Iacono, William G
AU - Janzing, Joost
AU - Jokela, Markus
AU - Kiemeney, Lambertus
AU - Lehtimäki, Terho
AU - Madden, Pamela A F
AU - Magnusson, Patrik K E
AU - Northstone, Kate
AU - Nutile, Teresa
AU - Ouwens, Klaasjan G
AU - Palotie, Aarno
AU - Pattie, Alison
AU - Pesonen, Anu-Katriina
AU - Polasek, Ozren
AU - Pulkkinen, Lea
AD - Department of Research Methodology, Measurement and Data-Analysis, University of Twente, Enschede, The Netherlands, Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden ; Department of Biological Psychology, VU University, Amsterdam, The Netherlands ; Department of Psychology, University of Minnesota, Elliott Hall, Minneapolis, MN, USA, Institute of Public Health, University of Southern Denmark, Odense, Denmark ; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden ; National Institute on Aging, NIH, Baltimore, MD, USA, College of Medicine, Florida State University, Tallahassee, FL, USA ; QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia, Department of Developmental Psychology and EMGO Institute for Health and Care Research, VU University Amsterdam, Amsterdam, The Netherlands ; Department of Research Methodology, Measurement and Data-Analysis, University of Twente, Enschede, The Netherlands, Department of Epidemiology, Erasmus University Medical Center, Rotterdam, The Netherlands ; Department of Research Methodology, Measurement and Data-Analysis, University of Twente, Enschede, The Netherlands, Department of Psychology, University of Illinois at Urbana-Champaign, Champaign, IL, USA ; Department of Research Methodology, Measurement and Data-Analysis, University of Twente, Enschede, The Netherlands, Estonian Genome Center, University of Tartu, Tartu, Estonia ; Department of Research Methodology, Measurement and Data-Analysis, University of Twente, Enschede, The Netherlands, Department of Psychiatry, EMGO+ Institute, Neuroscience Campus Amsterdam, VU University Medical Center Amsterdam, Amsterdam, The Netherlands ; QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia ; Department of Research Methodology, Measurement and Data-Analysis, University of Twente, Enschede, The Netherlands, MRC Human Genetics, MRC IGMM, Western General Hospital, University of Edinburgh, Edinburgh, Scotland, UK ; Department of Research Methodology, Measurement and Data-Analysis, University of Twente, Enschede, The Netherlands, Department of Psychiatry, University of Halle, Halle, Germany ; Department of Research Methodology, Measurement and Data-Analysis, University of Twente, Enschede, The Netherlands, Institute of Behavioural Sciences, University of Helsinki, Helsinki, Finland, Folkhälsan Research Center, Helsinki, Finland ; Department of Research Methodology, Measurement and Data-Analysis, University of Twente, Enschede, The Netherlands, Department of Psychology, University of Edinburgh, Edinburgh, UK, Centre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, Edinburgh, UK ; Department of Psychology, University of Minnesota, Elliott Hall, Minneapolis, MN, USA ; Department of Biological Psychology, VU University, Amsterdam, The Netherlands, Department of Psychiatry, Washington University School of Medicine, St. Louis, MO, USA ; Department of Biological Psychology, VU University, Amsterdam, The Netherlands, Department of Psychology, University of Tartu, Tartu, Estonia, Estonian Academy of Sciences, Tallinn, Estonia ; Department of Biological Psychology, VU University, Amsterdam, The Netherlands, Department of Public Health, Hjelt Institute, University of Helsinki, Helsinki, Finland, National Institute for Health and Welfare (THL), Helsinki, Finland ; Department of Biological Psychology, VU University, Amsterdam, The Netherlands, Centre for Population Health Sciences, Medical School, University of Edinburgh, Edinburgh, UK ; Department of Biological Psychology, VU University, Amsterdam, The Netherlands, MRC Integrative Epidemiology Unit, School of Social and Community Medicine, University of Bristol, Bristol, UK ; Department of Research Methodology, Measurement and Data-Analysis, University of Twente, Enschede, The Netherlands, Department of Biological Psychology, VU University, Amsterdam, The Netherlands, Folkhälsan Research Center, Helsinki, Finland, Vasa Central Hospital, Vaasa, Finland ; National Institute on Aging, NIH, Baltimore, MD, USA ; Department of Psychology, University of Minnesota, Elliott Hall, Minneapolis, MN, USA, Donders Institute for Cognitive Neuroscience, Radboud University Nijmegen, Nijmegen, The Netherlands, Department of Human Genetics, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands ; Department of Research Methodology, Measurement and Data-Analysis, University of Twente, Enschede, The Netherlands ; Department of Psychology, University of Minnesota, Elliott Hall, Minneapolis, MN, USA, Department of Psychology, School of Life Sciences, Heriot-Watt University, Edinburgh, UK ; Department of Biological Psychology, VU University, Amsterdam, The Netherlands, Department of Public Health, Hjelt Institute, University of Helsinki, Helsinki, Finland ; Department of Psychology, University of Minnesota, Elliott Hall, Minneapolis, MN, USA, Department of Psychiatry, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands ; Department of Research Methodology, Measurement and Data-Analysis, University of Twente, Enschede, The Netherlands, Department of Psychology, University of Minnesota, Elliott Hall, Minneapolis, MN, USA, Institute of Behavioural Sciences, University of Helsinki, Helsinki, Finland, Department of Clinical Chemistry, Fimlab Laboratories and School of Medicine, University of Tampere, Tampere, Finland ; Department of Psychology, University of Minnesota, Elliott Hall, Minneapolis, MN, USA, Department of Health Evidence, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands, Department of Urology, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands ; Department of Psychology, University of Minnesota, Elliott Hall, Minneapolis, MN, USA, Department of Clinical Chemistry, Fimlab Laboratories and School of Medicine, University of Tampere, Tampere, Finland ; Department of Psychology, University of Minnesota, Elliott Hall, Minneapolis, MN, USA, Institute of Genetics and Biophysics “A. Buzzati-Traverso" – CNR, Naples, Italy ; Department of Psychology, University of Minnesota, Elliott Hall, Minneapolis, MN, USA, Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, UK, Institute for Molecular Medicine Finland (FIMM), University of Helsinki, Helsinki, Finland ; Department of Research Methodology, Measurement and Data-Analysis, University of Twente, Enschede, The Netherlands, Institute of Behavioural Sciences, University of Helsinki, Helsinki, Finland ; Institute of Public Health, University of Southern Denmark, Odense, Denmark, Department of Public Health, Faculty of Medicine, University of Split, Split, Croatia ; Institute of Public Health, University of Southern Denmark, Odense, Denmark, Department of Psychology, University of Jyväskylä, Jyväskylä, Finland ; Department of Research Methodology, Measurement and Data-Analysis, University of Twente, Enschede, The Netherlands; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden
Y1 - 2014/07//
PY - 2014
DA - Jul 2014
SP - 295
EP - 313
CY - New York
PB - Springer Science & Business Media
VL - 44
IS - 4
SN - 0001-8244
KW - Biology
KW - Behaviour genetics
KW - Extraversion
KW - Genetic factors
KW - Harmonization
KW - Heritability
KW - Item response theory
KW - Measurement
KW - Neuroticism
KW - Personality
KW - Phenotypes
KW - Power
KW - Statistical power
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Behavior+Genetics&rft.atitle=Harmonization+of+Neuroticism+and+Extraversion+phenotypes+across+inventories+and+cohorts+in+the+Genetics+of+Personality+Consortium%3A+an+application+of+Item+Response+Theory&rft.au=Berg%2C+St%C3%A9phanie+M%3BMoor%2C+Marleen+H+M%3BMcGue%2C+Matt%3BPettersson%2C+Erik%3BTerracciano%2C+Antonio%3BVerweij%2C+Karin+J+H%3BAmin%2C+Najaf%3BDerringer%2C+Jaime%3BEsko%2C+T%C3%B5nu%3BGrootheest%2C+Gerard%3BHansell%2C+Narelle+K%3BHuffman%2C+Jennifer%3BKonte%2C+Bettina%3BLahti%2C+Jari%3BLuciano%2C+Michelle%3BMatteson%2C+Lindsay+K%3BViktorin%2C+Alexander%3BWouda%2C+Jasper%3BAgrawal%2C+Arpana%3BAllik%2C+J%C3%BCri%3BBierut%2C+Laura%3BBroms%2C+Ulla%3BCampbell%2C+Harry%3BSmith%2C+George+Davey%3BEriksson%2C+Johan+G%3BFerrucci%2C+Luigi%3BFranke%2C+Barbera%3BFox%2C+Jean-Paul%3BGeus%2C+Eco+J+C%3BGiegling%2C+Ina%3BGow%2C+Alan+J%3BGrucza%2C+Richard%3BHartmann%2C+Annette+M%3BHeath%2C+Andrew+C%3BHeikkil%C3%A4%2C+Kauko%3BIacono%2C+William+G%3BJanzing%2C+Joost%3BJokela%2C+Markus%3BKiemeney%2C+Lambertus%3BLehtim%C3%A4ki%2C+Terho%3BMadden%2C+Pamela+A+F%3BMagnusson%2C+Patrik+K+E%3BNorthstone%2C+Kate%3BNutile%2C+Teresa%3BOuwens%2C+Klaasjan+G%3BPalotie%2C+Aarno%3BPattie%2C+Alison%3BPesonen%2C+Anu-Katriina%3BPolasek%2C+Ozren%3BPulkkinen%2C+Lea&rft.aulast=Berg&rft.aufirst=St%C3%A9phanie&rft.date=2014-07-01&rft.volume=44&rft.issue=4&rft.spage=295&rft.isbn=&rft.btitle=&rft.title=Behavior+Genetics&rft.issn=00018244&rft_id=info:doi/10.1007%2Fs10519-014-9654-x
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Date revised - 2015-01-09
N1 - Last updated - 2015-12-14
DO - http://dx.doi.org/10.1007/s10519-014-9654-x
ER -
TY - JOUR
T1 - Inhibition of phosphoinositol 3 kinase contributes to nanoparticle-mediated exaggeration of endotoxin-induced leukocyte procoagulant activity
AN - 1660423612; PQ0001124109
AB - Aim: Disseminated intravascular coagulation is an increasing concern for certain types of engineered nanomaterials. Recent studies have shed some light on the nanoparticle physicochemical properties contributing to this toxicity; however, the mechanisms are poorly understood. Leukocyte procoagulant activity (PCA) is a key factor contributing to the initiation of this toxicity. We have previously reported on the exaggeration of endotoxin-induced PCA by cationic dendrimers. Herein, we report an effort to discern the mechanism. Materials & methods: Poly(amidoamine) dendrimers with various sizes and surface functionalities were studied in vitro by the recalcification test, flow cytometry and other relevant assays. Results & conclusion: Cationic dendrimers exaggerated endotoxin-induced PCA, but their anionic or neutral counterparts did not; the cationic charge prompts this phenomenon, but different cationic surface chemistries do not influence it. Cationic dendrimers and endotoxin differentially affect the PCA complex. The inhibition of phosphoinositol 3 kinase by dendrimers contributes to the exaggeration of the endotoxin-induced PCA. Original submitted: 4 February 2013; Revised submitted: 2 June 2013
JF - Nanomedicine
AU - Ilinskaya, Anna N
AU - Man, Sonny
AU - Patri, Anil K
AU - Clogston, Jeffrey D
AU - Crist, Rachael M
AU - Cachau, Raul E
AU - McNeil, Scott E
AU - Dobrovolskaia, Marina A
AD - super(1)Nanotechnology Characterization Laboratory, Advanced Technology Program, SAIC-Frederick Inc., NCI-Frederick, 1050 Boyles Street, Building 469, Frederick, MD 21702, USA
Y1 - 2014/07//
PY - 2014
DA - Jul 2014
SP - 1311
EP - 1326
PB - Future Science Group (FSG), Unitec House, 2 Albert Place London N3 1QB United Kingdom
VL - 9
IS - 9
SN - 1743-5889, 1743-5889
KW - Biotechnology and Bioengineering Abstracts
KW - coagulopathy
KW - dendrimer
KW - disseminated intravascular coagulation
KW - leukocyte
KW - nanoparticle
KW - procoagulant activity
KW - thrombosis
KW - Flow cytometry
KW - Endotoxins
KW - Disseminated intravascular coagulation
KW - Leukocytes
KW - Physicochemical properties
KW - Toxicity
KW - nanoparticles
KW - nanotechnology
KW - W 30900:Methods
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660423612?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nanomedicine&rft.atitle=Inhibition+of+phosphoinositol+3+kinase+contributes+to+nanoparticle-mediated+exaggeration+of+endotoxin-induced+leukocyte+procoagulant+activity&rft.au=Ilinskaya%2C+Anna+N%3BMan%2C+Sonny%3BPatri%2C+Anil+K%3BClogston%2C+Jeffrey+D%3BCrist%2C+Rachael+M%3BCachau%2C+Raul+E%3BMcNeil%2C+Scott+E%3BDobrovolskaia%2C+Marina+A&rft.aulast=Ilinskaya&rft.aufirst=Anna&rft.date=2014-07-01&rft.volume=9&rft.issue=9&rft.spage=1311&rft.isbn=&rft.btitle=&rft.title=Nanomedicine&rft.issn=17435889&rft_id=info:doi/
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-03-01
N1 - Number of references - 60
N1 - Last updated - 2015-11-16
N1 - SubjectsTermNotLitGenreText - Endotoxins; Flow cytometry; Disseminated intravascular coagulation; Physicochemical properties; Leukocytes; Toxicity; nanoparticles; nanotechnology
ER -
TY - JOUR
T1 - Depressive Symptoms in Young, Urban Schoolchildren: Environmental, Social, and Cognitive Risk
AN - 1660018774; 201501242
AB - This study examined relations among stressors, perceived social competence, attributional style, and depressive symptoms in young urban schoolchildren. Data were collected from 85 5- to 11-year-olds, mostly African American, who attended a public elementary school in a low-income urban area. Social competence was examined as a potential mediator, and attributional style was examined as a potential moderator of the relation between stressful life events and depressive symptoms. Separate analyses were conducted by age and gender. For older children and girls, main effects were found for stressful life events as predictors of depressive symptoms. Mediational analyses indicated that perceived peer acceptance served as a mediator of the relation between stressful life events and depressive symptoms for girls. In addition, attributional style moderated the relation between stressors and depressive symptoms in the older children. Together, findings suggest that significant relations exist among stressful life events, social and cognitive processes, and depressive symptoms in young urban children and that these relations are influenced by gender and development. Adapted from the source document.
JF - Journal of Prevention & Intervention in the Community
AU - Thurm, Audrey E
AU - Carlson, Ginger A
AU - Lyons, Aoife L
AU - Grant, Kathryn E
AU - Wagstaff, Amanda E
AD - Pediatrics and Developmental Neuroscience, National Institute of Mental Health, Bethesda, Maryland, USA athurm@mail.nih.gov
Y1 - 2014/07//
PY - 2014
DA - July 2014
SP - 169
EP - 182
PB - Taylor & Francis, Philadelphia PA
VL - 42
IS - 3
SN - 1085-2352, 1085-2352
KW - Depression (Psychology)
KW - Urban Areas
KW - Life Events
KW - Stress
KW - Social Competence
KW - Females
KW - Children
KW - Cognition
KW - Sex
KW - article
KW - 6143: child & family welfare
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Asocialservices&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Prevention+%26+Intervention+in+the+Community&rft.atitle=Depressive+Symptoms+in+Young%2C+Urban+Schoolchildren%3A+Environmental%2C+Social%2C+and+Cognitive+Risk&rft.au=Thurm%2C+Audrey+E%3BCarlson%2C+Ginger+A%3BLyons%2C+Aoife+L%3BGrant%2C+Kathryn+E%3BWagstaff%2C+Amanda+E&rft.aulast=Thurm&rft.aufirst=Audrey&rft.date=2014-07-01&rft.volume=42&rft.issue=3&rft.spage=169&rft.isbn=&rft.btitle=&rft.title=Journal+of+Prevention+%26+Intervention+in+the+Community&rft.issn=10852352&rft_id=info:doi/10.1080%2F10852352.2014.916574
LA - English
DB - Social Services Abstracts
N1 - Date revised - 2015-03-01
N1 - Last updated - 2016-09-28
N1 - SubjectsTermNotLitGenreText - Depression (Psychology); Urban Areas; Children; Social Competence; Females; Stress; Cognition; Sex; Life Events
DO - http://dx.doi.org/10.1080/10852352.2014.916574
ER -
TY - JOUR
T1 - Testicular Swelling Due to Lymphatic Filariasis After Brief Travel to Haiti
AN - 1647023029; 21189963
AB - After 6 months of a trip to Haiti, a 25-year-old healthy man presented with a 6-week history of a very slow progressive intermittent bilateral testicular pain and swelling. The biopsies in both testicles revealed the presence of a dead filarial parasite. Polymerase chain reaction products of the DNA from the biopsy were shown to have a 100% identity to Wuchereria bancrofti. Despite being uncommon in travelers, this presentation of W. bancrofti highlights the possibility of acquiring W. bancrofti during short-term trips to highly endemic regions of the world (i.e., Haiti).
JF - American Journal of Tropical Medicine and Hygiene
AU - Marcos, Luis A
AU - Shapley, Nathan P
AU - Eberhard, Mark
AU - Epstein, Jonathan I
AU - Fox, LeAnne M
AU - Magill, Alan
AU - Nutman, Thomas B
AD - Infectious Diseases, Hattiesburg Clinic, Hattiesburg, Mississippi; Urology Clinic, Wesley Medical Center, Hattiesburg, Mississippi; Division of Parasitic Diseases and Malaria, CDC, Atlanta, Georgia; Pathology Department, Johns Hopkins University, Baltimore, Maryland; Malaria, Global Health Program, Bill and Melinda Gates Foundation, Seattle, Washington; Laboratory of Parasitic Diseases, National Institutes of Health, Bethesda, Maryland, marcoslrz@yahoo.com
Y1 - 2014/07//
PY - 2014
DA - July 2014
SP - 89
EP - 91
PB - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States
VL - 91
IS - 1
SN - 0002-9637, 0002-9637
KW - Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts B: Bacteriology
KW - Testes
KW - Travel
KW - Parasites
KW - Wuchereria bancrofti
KW - Filariasis
KW - Polymerase chain reaction
KW - Biopsy
KW - Pain
KW - K 03400:Human Diseases
KW - J 02400:Human Diseases
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647023029?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.atitle=Testicular+Swelling+Due+to+Lymphatic+Filariasis+After+Brief+Travel+to+Haiti&rft.au=Marcos%2C+Luis+A%3BShapley%2C+Nathan+P%3BEberhard%2C+Mark%3BEpstein%2C+Jonathan+I%3BFox%2C+LeAnne+M%3BMagill%2C+Alan%3BNutman%2C+Thomas+B&rft.aulast=Marcos&rft.aufirst=Luis&rft.date=2014-07-01&rft.volume=91&rft.issue=1&rft.spage=89&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.14-0030
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-01-01
N1 - Last updated - 2016-02-18
N1 - SubjectsTermNotLitGenreText - Travel; Testes; Parasites; Filariasis; Polymerase chain reaction; Pain; Biopsy; Wuchereria bancrofti
DO - http://dx.doi.org/10.4269/ajtmh.14-0030
ER -
TY - JOUR
T1 - Does Social Capital Protect Against the Adverse Behavioural Outcomes of Child Neglect?
AN - 1627735339
AB - LONGSCAN was a longitudinal study of the risks and consequences of child abuse and neglect conducted between 1992 and 2012 among five sites across the US. Interviews with mothers of at-risk children began when the children were four years of age, and mothers and children from age six to age 18 years were interviewed every other year. Maltreatment reports were obtained from departments of social services, and subjects’ self-reported abuse was obtained at age 12. Generalised estimating equations were used to investigate the impact of informal social control, social cohesion and trust (SCT), and caregiver depression at ages 12, 14 and 16 years on externalising behaviours, smoking and alcohol use among 18-year olds who had been neglected prior to age 12. In models controlling for child age and gender, maltreatment types other than neglect, maternal education and study site, SCT significantly reduced the impact of caregiver depression on externalising behaviour and alcohol use among the neglected children at age 18. This moderating effect was not seen among non-neglected 18-year-old children. Copyright © 2014 John Wiley & Sons, Ltd. Key Practitioner Messages: * Child neglect is a significant predictor of adolescent health risk behaviours. * Caregiver depression increases the risk of neglect and increases the adverse behavioural outcomes of neglect. * Among children neglected before age 12, in the presence of caregiver depression, SCT reduce externalising behaviours and alcohol use at age 18. * Identification and treatment of caregiver depression, along with supporting community cohesion and neighbourhood trust, can ameliorate some of the negative outcomes associated with child neglect. ‘Child neglect is a significant predictor of adolescent health risk behaviours’
JF - Child Abuse Review
AU - Kotch, Jonathan B
AU - Smith, Jamie
AU - Margolis, Benyamin
AU - Black, Maureen M
AU - English, Diana
AU - Thompson, Richard
AU - Lee, Li-Ching
AU - Taneja, Gitanjali
AU - Bangdiwala, Shrikant I
AD - Department of Maternal and Child Health, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. ; Injury Prevention Research Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. ; Maternal and Child Health Bureau, Health Resources and Services Administration, US Department of Health and Human Services, Rockville, MD, USA. ; Department of Pediatrics, University of Maryland School of Medicine, Baltimore, MD, USA. ; School of Social Work, University of Washington, Seattle, WA, USA. ; Juvenile Protective Association, Chicago, IL, USA. ; Department of Epidemiology, Johns Hopkins University, Baltimore, MD, USA. ; National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA. ; Department of Biostatistics, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. ; Department of Maternal and Child Health, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Y1 - 2014/07//
PY - 2014
DA - Jul 2014
SP - 246
EP - 261
CY - Hoboken
PB - Wiley Subscription Services, Inc.
VL - 23
IS - 4
SN - 0952-9136
KW - Social Services And Welfare
KW - Neglected children
KW - Adolescents
KW - Age
KW - Alcohol related
KW - Child abuse
KW - Cohesion
KW - Health behaviour
KW - Identification
KW - Maltreated children
KW - Maltreatment
KW - Mothers
KW - Protective factors
KW - Risk behaviour
KW - Smoking
KW - Social capital
KW - Social cohesion
KW - Social control
KW - Social services
KW - Depression
KW - Child neglect
KW - Child maltreatment
KW - Carers
KW - At risk
KW - Alcohol consumption
KW - United States--US
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1627735339?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Child+Abuse+Review&rft.atitle=Does+Social+Capital+Protect+Against+the+Adverse+Behavioural+Outcomes+of+Child+Neglect%3F&rft.au=Kotch%2C+Jonathan+B%3BSmith%2C+Jamie%3BMargolis%2C+Benyamin%3BBlack%2C+Maureen+M%3BEnglish%2C+Diana%3BThompson%2C+Richard%3BLee%2C+Li-Ching%3BTaneja%2C+Gitanjali%3BBangdiwala%2C+Shrikant+I&rft.aulast=Kotch&rft.aufirst=Jonathan&rft.date=2014-07-01&rft.volume=23&rft.issue=4&rft.spage=246&rft.isbn=&rft.btitle=&rft.title=Child+Abuse+Review&rft.issn=09529136&rft_id=info:doi/10.1002%2Fcar.2345
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA); Social Services Abstracts
N1 - Date revised - 2014-11-10
N1 - Last updated - 2016-08-17
N1 - SubjectsTermNotLitGenreText - United States--US
DO - http://dx.doi.org/10.1002/car.2345
ER -
TY - JOUR
T1 - Nonresponse Bias in Survey Estimates of Alcohol Consumption and Its Association With Harm
AN - 1627731308
AB - Objective: Selective nonresponse represents a major source of potential bias in survey-based estimates of alcohol consumption and its association with harm. This study examined whether consumption differs for respondents and nonrespondents after correcting for their sociodemographic differences. Method: This study compared baseline consumption among initial respondents who did ( n = 34,653) and did not ( n = 5,306) respond to a 3-year follow-up interview in a prospective study of the U.S. general population. Differences in consumption measures were presented before and after adjustment or sociodemographic differences, and interactions of nonresponse with consumption were assessed in models predicting various types of harm. Results: After we adjusted for sociodemographic differences and factored in the overall level of nonresponse (13.3%), the degree to which the prevalence of drinking was underestimated in the total population was only 1.6%, and the extent to which consumption was overestimated among drinkers lay in the range of 1.7% to 2.4%. There was no consistent evidence that nonresponse moderated the association between consumption and alcohol-related harm. Sociodemographic differentials in nonresponse generally matched those reported for cross-sectional studies in the literature. Conclusions: The extent of nonresponse bias in survey estimates of alcohol consumption should not affect drinking guidelines and planning for prevention and treatment programs. The findings of this study are supportive of study designs that have been used to assess nonresponse bias, including the use of registry data on alcohol-related harms and secondary nonresponse data from prospective studies.
JF - Journal of Studies on Alcohol and Drugs
AU - DAWSON, DEBORAH A
AU - GOLDSTEIN, RISE B
AU - PICKERING, ROGER P
AU - GRANT, BRIDGET F
AD - Kelly Government Services, Bethesda, Maryland; Laboratory of Epidemiology and Biometry, Division of Intramural Clinical and Biological Research, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland ; Laboratory of Epidemiology and Biometry, Division of Intramural Clinical and Biological Research, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland ; Kelly Government Services, Bethesda, Maryland; Laboratory of Epidemiology and Biometry, Division of Intramural Clinical and Biological Research, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland
Y1 - 2014/07//
PY - 2014
DA - Jul 2014
SP - 695
EP - 703
CY - Piscataway
PB - Alcohol Research Documentation, Inc.
VL - 75
IS - 4
SN - 1937-1888
KW - Medical Sciences
KW - Alcohol consumption
KW - Alcohol related
KW - Associations
KW - Consumption
KW - Cross-sectional studies
KW - Moderated
KW - Nonresponse
KW - Preventive programmes
KW - Prospective studies
KW - Nonresponse bias
KW - Treatment methods
KW - Sociodemographic aspects
KW - United States--US
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1627731308?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Studies+on+Alcohol+and+Drugs&rft.atitle=Nonresponse+Bias+in+Survey+Estimates+of+Alcohol+Consumption+and+Its+Association+With+Harm&rft.au=DAWSON%2C+DEBORAH+A%3BGOLDSTEIN%2C+RISE+B%3BPICKERING%2C+ROGER+P%3BGRANT%2C+BRIDGET+F&rft.aulast=DAWSON&rft.aufirst=DEBORAH&rft.date=2014-07-01&rft.volume=75&rft.issue=4&rft.spage=695&rft.isbn=&rft.btitle=&rft.title=Journal+of+Studies+on+Alcohol+and+Drugs&rft.issn=19371888&rft_id=info:doi/
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Date revised - 2014-10-14
N1 - Last updated - 2016-05-16
N1 - SubjectsTermNotLitGenreText - United States--US
ER -
TY - JOUR
T1 - Multiyear Persistence of 2 Pandemic A/H1N1 Influenza Virus Lineages in West Africa
AN - 1618151794; 20800428
AB - Our understanding of the global ecology of influenza viruses is impeded by historically low levels of viral surveillance in Africa. Increased genetic sequencing of African A/H1N1 pandemic Influenza viruses during 2009-2013 revealed multiyear persistence of 2 viral lineages within West Africa, raising questions about the roles of reduced air traffic and the asynchrony of seasonal influenza epidemics among West African countries in the evolution of independent lineages. The potential for novel influenza virus lineages to evolve within Africa warrants Intensified influenza surveillance in Africa and other understudied areas.
JF - Journal of Infectious Diseases
AU - Nelson, Martha I
AU - Njouom, Richard
AU - Viboud, Cecile
AU - Niang, Mbayame N D
AU - Kadjo, Herve
AU - Ampofo, William
AU - Adebayo, Adedeji
AU - Tarnagda, Zekiba
AU - Miller, Mark A
AU - Holmes, Edward C
AU - Diop, Ousmane M
AD - Division of International Epidemiology and Population Studies, Fogarty International Center, National Institutes of Health, 16 Center Dr, Room 202, Bethesda, MD 20892, nelsonma@mail.nih.gov
Y1 - 2014/07/01/
PY - 2014
DA - 2014 Jul 01
SP - 121
EP - 125
PB - Oxford University Press, Oxford Journals, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL - 210
IS - 1
SN - 0022-1899, 0022-1899
KW - Health & Safety Science Abstracts; Virology & AIDS Abstracts
KW - human influenza A virus
KW - pandemic
KW - phylogenetic analysis
KW - Africa
KW - Historical account
KW - Epidemics
KW - Air traffic control
KW - Viruses
KW - Traffic
KW - Ecology
KW - Influenza
KW - pandemics
KW - Influenza virus
KW - Sulfur dioxide
KW - Infectious diseases
KW - Seasonal variations
KW - Evolution
KW - H 0500:General
KW - V 22310:Genetics, Taxonomy & Structure
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Infectious+Diseases&rft.atitle=Multiyear+Persistence+of+2+Pandemic+A%2FH1N1+Influenza+Virus+Lineages+in+West+Africa&rft.au=Nelson%2C+Martha+I%3BNjouom%2C+Richard%3BViboud%2C+Cecile%3BNiang%2C+Mbayame+N+D%3BKadjo%2C+Herve%3BAmpofo%2C+William%3BAdebayo%2C+Adedeji%3BTarnagda%2C+Zekiba%3BMiller%2C+Mark+A%3BHolmes%2C+Edward+C%3BDiop%2C+Ousmane+M&rft.aulast=Nelson&rft.aufirst=Martha&rft.date=2014-07-01&rft.volume=210&rft.issue=1&rft.spage=121&rft.isbn=&rft.btitle=&rft.title=Journal+of+Infectious+Diseases&rft.issn=00221899&rft_id=info:doi/10.1093%2Finfdis%2Fjiu047
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-10-01
N1 - Last updated - 2016-04-13
N1 - SubjectsTermNotLitGenreText - Influenza; pandemics; Epidemics; Evolution; Traffic; Ecology; Historical account; Sulfur dioxide; Infectious diseases; Air traffic control; Viruses; Seasonal variations; Influenza virus; Africa
DO - http://dx.doi.org/10.1093/infdis/jiu047
ER -
TY - JOUR
T1 - Cannabinoids in oral fluid by on-site immunoassay and by GC-MS using two different oral fluid collection devices
AN - 1567099119; 20555747
AB - Oral fluid (OF) enables non-invasive sample collection for on-site drug testing, but performance of on-site tests with occasional and frequent smokers' OF to identify cannabinoid intake requires further evaluation. Furthermore, as far as we are aware, no studies have evaluated differences between cannabinoid disposition among OF collection devices with authentic OF samples after controlled cannabis administration. Fourteen frequent and 10 occasional adult cannabis smokers smoked one 6.8% delta [sup 9]-tetrahydrocannabinol (THC) cigarette ad libitum over 10 min. OF was collected with the StatSure Saliva Sampler, Oral-Eze, and Draeger DrugTest 5000 test cassette before and up to 30 h after cannabis smoking. Test cassettes were analyzed within 15 min and gas chromatography-mass spectrometry cannabinoid results were obtained within 24 h. The DrugTest 5000 on-site device had high diagnostic sensitivity, specificity, and efficiency for cannabinoids.
JF - Analytical and Bioanalytical Chemistry
AU - Desrosiers, Nathalie A
AU - Milman, Garry
AU - Mendu, Damodara R
AU - Lee, Dayong
AU - Barnes, Allan J
AU - Gorelick, David A
AU - Huestis, Marilyn A
AD - Chemistry and Drug Metabolism Section, NIDA IRP, 251 Bayview Boulevard, Baltimore, MD 21224, USA; Program in Toxicology, University of Maryland Baltimore, 655 W. Baltimore Street, Baltimore, MD 21201, USA, mhuestis@intra.nida.nih.gov
PY - 2014
SP - 4117
EP - 4128
PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL - 406
IS - 17
SN - 1618-2642, 1618-2642
KW - Aqualine Abstracts; Water Resources Abstracts
KW - Cannabinoid
KW - Oral fluid
KW - On-site test
KW - Draeger DrugTest 5000
KW - Testing Procedures
KW - Samplers
KW - Evaluation
KW - On-site Tests
KW - Performance Evaluation
KW - Administration
KW - Drugs
KW - AQ 00001:Water Resources and Supplies
KW - SW 5040:Data acquisition
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1567099119?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aaqualine&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Analytical+and+Bioanalytical+Chemistry&rft.atitle=Cannabinoids+in+oral+fluid+by+on-site+immunoassay+and+by+GC-MS+using+two+different+oral+fluid+collection+devices&rft.au=Desrosiers%2C+Nathalie+A%3BMilman%2C+Garry%3BMendu%2C+Damodara+R%3BLee%2C+Dayong%3BBarnes%2C+Allan+J%3BGorelick%2C+David+A%3BHuestis%2C+Marilyn+A&rft.aulast=Desrosiers&rft.aufirst=Nathalie&rft.date=2014-07-01&rft.volume=406&rft.issue=17&rft.spage=4117&rft.isbn=&rft.btitle=&rft.title=Analytical+and+Bioanalytical+Chemistry&rft.issn=16182642&rft_id=info:doi/10.1007%2Fs00216-014-7813-9
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-12-01
N1 - Number of references - 27
N1 - Last updated - 2016-01-21
N1 - SubjectsTermNotLitGenreText - Evaluation; Testing Procedures; Performance Evaluation; On-site Tests; Administration; Drugs; Samplers
DO - http://dx.doi.org/10.1007/s00216-014-7813-9
ER -
TY - JOUR
T1 - First Report of Olpidium bornovanus and O. virulentus on Melon in Italy
AN - 1560114309; 20500663
AB - A survey for the presence of Olpidium spp. on melon (Cucumis melo L.) was conducted during the beginning of 2013 in central Italy in an unheated greenhouse, located in the melon-producing coastal area of north Latium (central Italy, Viterbo Province) (42 parallel 23'09.31" N, 11 parallel 30'46.10" E) with a history of monosporascus root rot and vine decline (MRRVD). For this aim, 10 soil samples were collected adjacent to the roots of plants symptomatic of MRRVD, represented by root lesions and rots and loss of smaller feeder roots. Olpidium was baited from collected infested soil by growing melon (cv. Dinero) plants for 45 days. Bait plants grown in sterilized soil were used as negative controls. All the baited melon roots were analyzed by morphological and molecular methods.
JF - Plant Disease
AU - Aleandri, M P
AU - Martignoni, D
AU - Reda, R
AU - Alfaro-Fernandez, A
AU - Font, M I
AU - Armengol, J
AU - Chilosi, G
AD - Dipartamento per la Innovazione nei Sistemi Biologici, Agroalimentari e Forestali (DIBAF), Universita degli Studi della Tuscia, Via S. Camillo de Lellis, 01100 Viterbo, Italy
PY - 2014
SP - 997
EP - 998
PB - American Phytopathological Society, 3340 Pilot Knob Road St. Paul MN 55121-2097 United States
VL - 98
IS - 7
SN - 0191-2917, 0191-2917
KW - Microbiology Abstracts A: Industrial & Applied Microbiology
KW - Soil
KW - Cucumis melo
KW - Plant diseases
KW - Vines
KW - Root rot
KW - Olpidium
KW - Greenhouses
KW - A 01360:Plant Diseases
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1560114309?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Plant+Disease&rft.atitle=First+Report+of+Olpidium+bornovanus+and+O.+virulentus+on+Melon+in+Italy&rft.au=Aleandri%2C+M+P%3BMartignoni%2C+D%3BReda%2C+R%3BAlfaro-Fernandez%2C+A%3BFont%2C+M+I%3BArmengol%2C+J%3BChilosi%2C+G&rft.aulast=Aleandri&rft.aufirst=M&rft.date=2014-07-01&rft.volume=98&rft.issue=7&rft.spage=997&rft.isbn=&rft.btitle=&rft.title=Plant+Disease&rft.issn=01912917&rft_id=info:doi/10.1094%2FPDIS-10-13-1041-PDN
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-09-01
N1 - Last updated - 2015-12-09
N1 - SubjectsTermNotLitGenreText - Soil; Plant diseases; Vines; Root rot; Greenhouses; Cucumis melo; Olpidium
DO - http://dx.doi.org/10.1094/PDIS-10-13-1041-PDN
ER -
TY - JOUR
T1 - Stability of Core Language Skill from Early Childhood to Adolescence: A Latent Variable Approach
AN - 1558997949; 201412781
AB - This four-wave prospective longitudinal study evaluated stability of language in 324 children from early childhood to adolescence. Structural equation modeling supported loadings of multiple age-appropriate multisource measures of child language on single-factor core language skills at 20 months and 4, 10, and 14 years. Large stability coefficients (standardized indirect effect = .46) were obtained between language latent variables from early childhood to adolescence even when accounting for child nonverbal intelligence and social competence and maternal verbal intelligence, education, speech, and social desirability. Stability coefficients were similar for girls and boys. Stability of core language skill was stronger from 4 to 10 to 14 years than from 20 months to 4 years, so early intervention to improve lagging language is recommended. Adapted from the source document
JF - Child Development
AU - Bornstein, Marc H
AU - Hahn, Chun-Shin
AU - Putnick, Diane L
AU - Suwalsky, Joan T D
AD - Eunice Kennedy Shriver National Institute of Child Health and Human Development
Y1 - 2014/07//
PY - 2014
DA - July 2014
SP - 1346
EP - 1356
VL - 85
IS - 4
SN - 0009-3920, 0009-3920
KW - Education (20900)
KW - Child Language (11800)
KW - Longitudinal Studies (49900)
KW - Intelligence (36450)
KW - Children (11850)
KW - article
KW - 4015: psycholinguistics; child language acquisition
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1558997949?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Allba&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Child+Development&rft.atitle=Stability+of+Core+Language+Skill+from+Early+Childhood+to+Adolescence%3A+A+Latent+Variable+Approach&rft.au=Bornstein%2C+Marc+H%3BHahn%2C+Chun-Shin%3BPutnick%2C+Diane+L%3BSuwalsky%2C+Joan+T+D&rft.aulast=Bornstein&rft.aufirst=Marc&rft.date=2014-07-01&rft.volume=85&rft.issue=4&rft.spage=1346&rft.isbn=&rft.btitle=&rft.title=Child+Development&rft.issn=00093920&rft_id=info:doi/
LA - English
DB - Linguistics and Language Behavior Abstracts (LLBA)
N1 - Date revised - 2014-09-01
N1 - Last updated - 2016-09-27
N1 - CODEN - CHDEAW
N1 - SubjectsTermNotLitGenreText - Children (11850); Intelligence (36450); Child Language (11800); Education (20900); Longitudinal Studies (49900)
ER -
TY - JOUR
T1 - Prioritizing practice in Ombudsman and ADR programs
AN - 1556292913; 4591999
AB - This article examines ways in which the Office of the Ombudsman/Center for Cooperative Resolution (OO/CCR) at the National Institutes of Health pursues activities that comprise an orientation toward practice and supports development of an 'activist' ombudsman orientation. The article opens by describing challenges that alternative dispute resolution (ADR) organizations face, contrasts them with the experience of OO/CCR, details elements of a practice orientation as experienced at OO/CCR, and suggests ways in which ADR and ombudsman organizations may address their own challenges and pursue a practice orientation.
JF - Conflict resolution quarterly
AU - Michael, David E
AD - National Institutes of Health
Y1 - 2014/07//
PY - 2014
DA - Jul 2014
SP - 463
EP - 476
VL - 31
IS - 4
SN - 1536-5581, 1536-5581
KW - Political Science
KW - Activists
KW - Co-operatives
KW - Ombudsman
KW - Conflict theory
KW - Alternation
KW - Conflict resolution
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Conflict+resolution+quarterly&rft.atitle=Prioritizing+practice+in+Ombudsman+and+ADR+programs&rft.au=Michael%2C+David+E&rft.aulast=Michael&rft.aufirst=David&rft.date=2014-07-01&rft.volume=31&rft.issue=4&rft.spage=463&rft.isbn=&rft.btitle=&rft.title=Conflict+resolution+quarterly&rft.issn=15365581&rft_id=info:doi/10.1002%2Fcrq.21098
LA - English
DB - International Bibliography of the Social Sciences (IBSS)
N1 - Date revised - 2014-08-26
N1 - Last updated - 2014-08-27
N1 - SubjectsTermNotLitGenreText - 2703 2698; 8925 10742; 934; 2704 9798; 2409; 553 9637
DO - http://dx.doi.org/10.1002/crq.21098
ER -
TY - JOUR
T1 - A tiered framework for risk-relevant characterization and ranking of chemical exposures: applications to the National Children's Study (NCS)
AN - 1556292738; 4591484
AB - A challenge for large-scale environmental health investigations such as the National Children's Study (NCS), is characterizing exposures to multiple, co-occurring chemical agents with varying spatiotemporal concentrations and consequences modulated by biochemical, physiological, behavioral, socioeconomic, and environmental factors. Such investigations can benefit from systematic retrieval, analysis, and integration of diverse extant information on both contaminant patterns and exposure-relevant factors. This requires development, evaluation, and deployment of informatics methods that support flexible access and analysis of multiattribute data across multiple spatiotemporal scales. A new 'Tiered Exposure Ranking' (TiER) framework, developed to support various aspects of risk-relevant exposure characterization, is described here, with examples demonstrating its application to the NCS. TiER utilizes advances in informatics computational methods, extant database content and availability, and integrative environmental/exposure/biological modeling to support both 'discovery-driven' and 'hypothesis-driven' analyses. 'Tier 1' applications focus on 'exposomic' pattern recognition for extracting information from multidimensional data sets, whereas second and higher tier applications utilize mechanistic models to develop risk-relevant exposure metrics for populations and individuals. In this article, 'tier 1' applications of TiER explore identification of potentially causative associations among risk factors, for prioritizing further studies, by considering publicly available demographic/socioeconomic, behavioral, and environmental data in relation to two health endpoints (preterm birth and low birth weight). A 'tier 2' application develops estimates of pollutant mixture inhalation exposure indices for NCS counties, formulated to support risk characterization for these endpoints. Applications of TiER demonstrate the feasibility of developing risk-relevant exposure characterizations for pollutants using extant environmental and demographic/socioeconomic data. Reprinted by permission of Blackwell Publishers
JF - Risk analysis
AU - Dellarco, Michael
AU - Landrigan, Philip J
AU - Lioy, Paul J
AU - Georgopoulos, Panos G
AU - Brinkerhoff, Christopher J
AU - Isukapalli, Sastry
AD - Rutgers, The State University of New Jersey ; National Institutes of Health ; Icahn School of Medicine at Mount Sinai
Y1 - 2014/07//
PY - 2014
DA - Jul 2014
SP - 1299
EP - 1316
VL - 34
IS - 7
SN - 0272-4332, 0272-4332
KW - Economics
KW - Pollutants
KW - Health care
KW - Computational methods
KW - Population
KW - Data analysis
KW - Risk theory
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Risk+analysis&rft.atitle=A+tiered+framework+for+risk-relevant+characterization+and+ranking+of+chemical+exposures%3A+applications+to+the+National+Children%27s+Study+%28NCS%29&rft.au=Dellarco%2C+Michael%3BLandrigan%2C+Philip+J%3BLioy%2C+Paul+J%3BGeorgopoulos%2C+Panos+G%3BBrinkerhoff%2C+Christopher+J%3BIsukapalli%2C+Sastry&rft.aulast=Dellarco&rft.aufirst=Michael&rft.date=2014-07-01&rft.volume=34&rft.issue=7&rft.spage=1299&rft.isbn=&rft.btitle=&rft.title=Risk+analysis&rft.issn=02724332&rft_id=info:doi/10.1111%2Frisa.12165
LA - English
DB - International Bibliography of the Social Sciences (IBSS)
N1 - Date revised - 2014-08-26
N1 - Last updated - 2014-08-27
N1 - SubjectsTermNotLitGenreText - 2671 10919; 11040 11035; 5775 13521; 9814; 3279 971 3286; 9846
DO - http://dx.doi.org/10.1111/risa.12165
ER -
TY - JOUR
T1 - Two perspectives on learning the organizational ombudsman role
AN - 1556291728; 4591998
AB - This article explores the challenges in learning the role of the organizational ombudsman from the perspectives of two practitioners-one an experienced workplace mediator, the other a student of conflict resolution. The discussion of the shift in thinking, as well as skills needed to transition into the various facets of organizational ombudsman work, combines concepts from ombudsman theory with insights on enhancing ombudsman practice. The authors provide observations and recommendations based on their own experiences assuming the roles of a new ombudsman, including reflective practice and partnering, coaching with employees, and expanding systemic engagements with and cultural knowledge of organizations.
JF - Conflict resolution quarterly
AU - Witzler, Lisa
AU - Myers, Linda
AD - National Institutes of Health
Y1 - 2014/07//
PY - 2014
DA - Jul 2014
SP - 447
EP - 462
VL - 31
IS - 4
SN - 1536-5581, 1536-5581
KW - Sociology
KW - Learning
KW - Organizations
KW - Engagement
KW - Students
KW - Knowledge
KW - Work place
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1556291728?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Conflict+resolution+quarterly&rft.atitle=Two+perspectives+on+learning+the+organizational+ombudsman+role&rft.au=Witzler%2C+Lisa%3BMyers%2C+Linda&rft.aulast=Witzler&rft.aufirst=Lisa&rft.date=2014-07-01&rft.volume=31&rft.issue=4&rft.spage=447&rft.isbn=&rft.btitle=&rft.title=Conflict+resolution+quarterly&rft.issn=15365581&rft_id=info:doi/10.1002%2Fcrq.21096
LA - English
DB - International Bibliography of the Social Sciences (IBSS)
N1 - Date revised - 2014-08-26
N1 - Last updated - 2014-08-27
N1 - SubjectsTermNotLitGenreText - 7278 12929 7073; 9030; 12334 4049; 7073; 4278; 13673 4214
DO - http://dx.doi.org/10.1002/crq.21096
ER -
TY - JOUR
T1 - The reflective observer model
AN - 1556285924; 4591995
AB - The reflective observer (RO) model is a unique process that incorporates live observation by a trained observer of an ombudsman during a mediation session, followed by an in-depth debriefing between the ombudsman and the RO. The clinical goal is to explore cognitive schema used by the ombudsman in decision making during critical moments of the mediation and to describe the underrecognized rationale behind seemingly intuitive expertise. During the debriefing, the exploration is guided by a protocol specifically designed to elicit personal associations, as well as tactical decisions of the ombudsman not frequently addressed in ombudsman practice or training. While research on reflective practice is common among mediators (Bronson ), less research has focused on the impact of reflective practice on the work of ombudsmen. The RO model shows promise as a personal and professional developmental tool for ombudsmen and is a novel approach for both deeper learning as well as developing higher-order clinical interviewing skills.
JF - Conflict resolution quarterly
AU - Kathleen moore, J
AD - US National Institutes of Health
Y1 - 2014/07//
PY - 2014
DA - Jul 2014
SP - 403
EP - 419
VL - 31
IS - 4
SN - 1536-5581, 1536-5581
KW - Political Science
KW - Decision making
KW - Skills
KW - Research methods
KW - Training
KW - Tactics
KW - Conflict resolution
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1556285924?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Conflict+resolution+quarterly&rft.atitle=The+reflective+observer+model&rft.au=Kathleen+moore%2C+J&rft.aulast=Kathleen+moore&rft.aufirst=J&rft.date=2014-07-01&rft.volume=31&rft.issue=4&rft.spage=403&rft.isbn=&rft.btitle=&rft.title=Conflict+resolution+quarterly&rft.issn=15365581&rft_id=info:doi/10.1002%2Fcrq.21094
LA - English
DB - International Bibliography of the Social Sciences (IBSS)
N1 - Date revised - 2014-08-26
N1 - Last updated - 2014-08-27
N1 - SubjectsTermNotLitGenreText - 11713; 12483; 12894; 3322 6071 1542 11325; 10919; 2703 2698
DO - http://dx.doi.org/10.1002/crq.21094
ER -
TY - JOUR
T1 - Toward the activist ombudsman: an introduction
AN - 1556284891; 4591994
AB - This introduction frames the articles in this mini-colloquy on the work of the Office of the Ombudsman at the National Institutes of Health, Center for Cooperative Resolution (OO/CCR). This office is unique in its size, experience, and approach to the work of the organizational ombudsman. Through this series of articles, we share our understandings of the potential for the role of the organizational conflict management specialists called ombudsmen and to assist other organizations and practitioners as they consider and enact similar roles within their workplaces.
JF - Conflict resolution quarterly
AU - Gadlin, Howard
AD - National Institutes of Health
Y1 - 2014/07//
PY - 2014
DA - Jul 2014
SP - 387
EP - 402
VL - 31
IS - 4
SN - 1536-5581, 1536-5581
KW - Political Science
KW - Organizations
KW - Cooperation
KW - Conflict resolution
KW - Institutions
KW - Framing
KW - Work place
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1556284891?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Conflict+resolution+quarterly&rft.atitle=Toward+the+activist+ombudsman%3A+an+introduction&rft.au=Gadlin%2C+Howard&rft.aulast=Gadlin&rft.aufirst=Howard&rft.date=2014-07-01&rft.volume=31&rft.issue=4&rft.spage=387&rft.isbn=&rft.btitle=&rft.title=Conflict+resolution+quarterly&rft.issn=15365581&rft_id=info:doi/10.1002%2Fcrq.21099
LA - English
DB - International Bibliography of the Social Sciences (IBSS)
N1 - Date revised - 2014-08-26
N1 - Last updated - 2014-08-27
N1 - SubjectsTermNotLitGenreText - 2703 2698; 13673 4214; 9030; 2859; Framing; 6590
DO - http://dx.doi.org/10.1002/crq.21099
ER -
TY - JOUR
T1 - Phenol-soluble modulins - critical determinants of staphylococcal virulence
AN - 1551645557; 20317181
AB - Phenol-soluble modulins (PSMs) are a recently discovered family of amphipathic, alpha-helical peptides that have multiple roles in staphylococcal pathogenesis and contribute to a large extent to the pathogenic success of virulent staphylococci, such as Staphylococcus aureus. PSMs may cause lysis of many human cell types including leukocytes and erythrocytes, stimulate inflammatory responses, and contribute to biofilm development. PSMs appear to have an original role in the commensal lifestyle of staphylococci, where they facilitate growth and spreading on epithelial surfaces. Aggressive, cytolytic PSMs seem to have evolved from that original role and are mainly expressed in highly virulent S. aureus. Here, we will review the biochemistry, genetics, and role of PSMs in the commensal and pathogenic lifestyles of staphylococci, discuss how diversification of PSMs defines the aggressiveness of staphylococcal species, and evaluate potential avenues to target PSMs for drug development against staphylococcal infections. Phenol-soluble modulins are newly recognized peptide toxins that define the virulence potential of Staphylococcus aureus and other staphylococci.
JF - FEMS Microbiology Reviews
AU - Cheung, Gordon YC
AU - Joo, Hwang-Soo
AU - Chatterjee, Som S
AU - Otto, Michael
AD - Pathogen Molecular Genetics Section Laboratory of Human Bacterial Pathogenesis. National Institute of Allergy and Infectious DiseasesThe National Institutes of Health
Y1 - 2014/07//
PY - 2014
DA - July 2014
SP - 698
EP - 719
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 38
IS - 4
SN - 0168-6445, 0168-6445
KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Microbiology Abstracts B: Bacteriology
KW - Virulence
KW - Spreading
KW - Erythrocytes
KW - Leukocytes
KW - Commensals
KW - Drug development
KW - Biofilms
KW - Staphylococcus aureus
KW - Infection
KW - Toxins
KW - Inflammation
KW - A 01450:Environmental Pollution & Waste Treatment
KW - J 02350:Immunology
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551645557?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=FEMS+Microbiology+Reviews&rft.atitle=Phenol-soluble+modulins+-+critical+determinants+of+staphylococcal+virulence&rft.au=Cheung%2C+Gordon+YC%3BJoo%2C+Hwang-Soo%3BChatterjee%2C+Som+S%3BOtto%2C+Michael&rft.aulast=Cheung&rft.aufirst=Gordon&rft.date=2014-07-01&rft.volume=38&rft.issue=4&rft.spage=698&rft.isbn=&rft.btitle=&rft.title=FEMS+Microbiology+Reviews&rft.issn=01686445&rft_id=info:doi/10.1111%2F1574-6976.12057
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-08-01
N1 - Last updated - 2016-03-17
N1 - SubjectsTermNotLitGenreText - Virulence; Spreading; Leukocytes; Erythrocytes; Commensals; Drug development; Biofilms; Infection; Toxins; Inflammation; Staphylococcus aureus
DO - http://dx.doi.org/10.1111/1574-6976.12057
ER -
TY - JOUR
T1 - Clinicopathological correlates of Gli1 expression in a population-based cohort of patients with newly diagnosed bladder cancer.
AN - 1549199396; 24856810
AB - Dysregulation of the hedgehog signaling pathway has been linked to the development and progression of a variety of different human tumors including cancers of the skin, brain, colon, prostate, blood, and pancreas. We assessed the clinicopathological factors that are potentially related to expression of Gli1, the transcription factor that is thought to be the most reliable marker of hedgehog pathway activation in bladder cancer.
Bladder cancer cases were identified from the New Hampshire State Cancer Registry as histologically confirmed primary bladder cancer diagnosed between January 1, 2002, and July 31, 2004. Immunohistochemical analysis was performed on a tissue microarray to detect Gli1 and p53 expression in these bladder tumors. We computed odds ratios (ORs) and their 95% CIs for Gli1 positivity for pathological category using T category (from TNM), invasiveness, and grade with both the World Health Organization 1973 and World Health Organization International Society of Urological Pathology criteria. We calculated hazard ratios and their 95% CI for Gli1 positivity and recurrence for both Ta-category and invasive bladder tumors (T1+). A total of 194 men and 67 women, whose tumors were assessable for Gli1 staining, were included in the study. No appreciable differences in Gli1 staining were noted by sex, age, smoking status, or high-risk occupation. Ta-category tumors were more likely to stain for Gli1 as compared with T1-category tumors (adjusted OR = 0.38, CI: 0.17-0.87). Similarly, low-grade (grades 1-2) tumors were more likely to stain for Gli1 as compared with high-grade tumors (grade 3) (adjusted OR = 0.44, CI: 0.21-0.93). In a Cox proportional hazards regression analysis, non-muscle-invasive bladder tumors expressing Gli1 were less likely to recur (adjusted hazard ratio = 0.48; CI: 0.28-0.82; P<0.05) than those in which Gli1 was absent.
Our findings indicate that Gli1 expression may be a marker of low-stage, low-grade bladder tumors and an indicator of a reduced risk of recurrence in this group. Copyright © 2014 Elsevier Inc. All rights reserved.
JF - Urologic oncology
AU - Sverrisson, Einar F
AU - Zens, Michael S
AU - Fei, Dennis Liang
AU - Andrews, Angeline
AU - Schned, Alan
AU - Robbins, David
AU - Kelsey, Karl T
AU - Li, Hua
AU - DiRenzo, James
AU - Karagas, Margaret R
AU - Seigne, John D
AD - Department of Surgery (Urology), Dartmouth-Hitchcock Medical Center, Lebanon, NH. ; Department of Community and Family Medicine, Geisel School of Medicine at Dartmouth, Hanover, NH. ; Cancer Biology Section, National Institutes of Health, Bethesda, MD. ; Department of Pathology (Urology), Dartmouth-Hitchcock Medical Center, Lebanon, NH. ; Molecular Oncology Program, Department of Surgery, University of Miami, Miami, FL. ; Department of Community Health, Brown University, Providence, RI. ; Center for Prostate Disease Research, Uniformed Services University of the Health Sciences, Bethesda, MD. ; Department of Pharmacology and Toxicology, Geisel School of Medicine at Dartmouth, Hanover, NH. ; Department of Surgery (Urology), Dartmouth-Hitchcock Medical Center, Lebanon, NH. Electronic address: john.d.seigne@hitchcock.org.
Y1 - 2014/07//
PY - 2014
DA - July 2014
SP - 539
EP - 545
VL - 32
IS - 5
KW - GLI1 protein, human
KW - 0
KW - Hedgehog Proteins
KW - TP53 protein, human
KW - Transcription Factors
KW - Tumor Suppressor Protein p53
KW - Zinc Finger Protein GLI1
KW - Index Medicus
KW - Gli1
KW - Bladder neoplasm
KW - Odds Ratio
KW - Humans
KW - Aged
KW - Tumor Suppressor Protein p53 -- metabolism
KW - Registries
KW - Hedgehog Proteins -- metabolism
KW - Tissue Array Analysis
KW - Adult
KW - Cohort Studies
KW - Treatment Outcome
KW - Middle Aged
KW - Neoplasm Recurrence, Local
KW - Time Factors
KW - Immunohistochemistry
KW - Female
KW - Male
KW - Proportional Hazards Models
KW - Gene Expression Regulation, Neoplastic
KW - Transcription Factors -- metabolism
KW - Urinary Bladder Neoplasms -- metabolism
KW - Transcription Factors -- genetics
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Urologic+oncology&rft.atitle=Clinicopathological+correlates+of+Gli1+expression+in+a+population-based+cohort+of+patients+with+newly+diagnosed+bladder+cancer.&rft.au=Sverrisson%2C+Einar+F%3BZens%2C+Michael+S%3BFei%2C+Dennis+Liang%3BAndrews%2C+Angeline%3BSchned%2C+Alan%3BRobbins%2C+David%3BKelsey%2C+Karl+T%3BLi%2C+Hua%3BDiRenzo%2C+James%3BKaragas%2C+Margaret+R%3BSeigne%2C+John+D&rft.aulast=Sverrisson&rft.aufirst=Einar&rft.date=2014-07-01&rft.volume=32&rft.issue=5&rft.spage=539&rft.isbn=&rft.btitle=&rft.title=Urologic+oncology&rft.issn=1873-2496&rft_id=info:doi/10.1016%2Fj.urolonc.2014.03.006
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-02-23
N1 - Date created - 2014-06-17
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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Urol Oncol. 2014 Jul;32(5):546-8 [24814405]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.urolonc.2014.03.006
ER -
TY - JOUR
T1 - Parenting in Fukushima City in the post-disaster period: short-term strategies and long-term perspectives
AN - 1548777860; 4579960
AB - Growing evidence indicates the adverse psychological and welfare consequences of nuclear power accidents particularly among parents of small children. However, little has been published about the public health experiences of and practical countermeasures to deal with such consequences for parents of small children in the aftermath of disasters. Based on our past research efforts to develop parenting support programmes in Fukushima City, we describe here the discussions and resulting strategies that developed from collaborative efforts between university researchers and public health nurses after the Fukushima nuclear plant accident caused by the Great East Japan Earthquake. The processes presented here may be useful to improve national and international preparedness to protect the health of parents and children in future nuclear disasters. Reprinted by permission of Blackwell Publishers
JF - Disasters
AU - Goto, Aya
AU - Reich, Michael R
AU - Suzuki, Yuriko
AU - Tsutomi, Hiroshi
AU - Watanabe, Eiko
AU - Yasumura, Seiji
AD - Fukushima Medical University ; Harvard University ; National Institute of Mental Health ; University of Shizuoka
Y1 - 2014/07//
PY - 2014
DA - Jul 2014
SP - s179
EP - s189
VL - 38
IS - s2
SN - 0361-3666, 0361-3666
KW - Sociology
KW - Parenting
KW - Nurses
KW - Nuclear accidents
KW - Nuclear energy
KW - Children
KW - Japan
KW - Public health
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1548777860?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Disasters&rft.atitle=Parenting+in+Fukushima+City+in+the+post-disaster+period%3A+short-term+strategies+and+long-term+perspectives&rft.au=Goto%2C+Aya%3BReich%2C+Michael+R%3BSuzuki%2C+Yuriko%3BTsutomi%2C+Hiroshi%3BWatanabe%2C+Eiko%3BYasumura%2C+Seiji&rft.aulast=Goto&rft.aufirst=Aya&rft.date=2014-07-01&rft.volume=38&rft.issue=s2&rft.spage=s179&rft.isbn=&rft.btitle=&rft.title=Disasters&rft.issn=03613666&rft_id=info:doi/10.1111%2Fdisa.12070
LA - English
DB - International Bibliography of the Social Sciences (IBSS)
N1 - Date revised - 2014-07-21
N1 - Last updated - 2014-07-29
N1 - SubjectsTermNotLitGenreText - 9183; 8759 4246; 8758 524; 2212; 10449 5772; 8806; 191 300 30
DO - http://dx.doi.org/10.1111/disa.12070
ER -
TY - JOUR
T1 - Web-based computational chemistry education with CHARMMing III: Reduction potentials of electron transfer proteins.
AN - 1548638615; 25058418
AB - A module for fast determination of reduction potentials, E°, of redox-active proteins has been implemented in the CHARMM INterface and Graphics (CHARMMing) web portal (www.charmming.org). The free energy of reduction, which is proportional to E°, is composed of an intrinsic contribution due to the redox site and an environmental contribution due to the protein and solvent. Here, the intrinsic contribution is selected from a library of pre-calculated density functional theory values for each type of redox site and redox couple, while the environmental contribution is calculated from a crystal structure of the protein using Poisson-Boltzmann continuum electrostatics. An accompanying lesson demonstrates a calculation of E°. In this lesson, an ionizable residue in a [4Fe-4S]-protein that causes a pH-dependent E° is identified, and the E° of a mutant that would test the identification is predicted. This demonstration is valuable to both computational chemistry students and researchers interested in predicting sequence determinants of E° for mutagenesis.
JF - PLoS computational biology
AU - Perrin, B Scott
AU - Miller, Benjamin T
AU - Schalk, Vinushka
AU - Woodcock, H Lee
AU - Brooks, Bernard R
AU - Ichiye, Toshiko
AD - Laboratory of Computational Biology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, United States of America. ; Department of Natural Sciences, New College of Florida, Sarasota, Florida, United States of America. ; Department of Chemistry, University of South Florida, Tampa, Florida, United States of America. ; Department of Chemistry, Georgetown University, Washington, D.C., United States of America.
Y1 - 2014/07//
PY - 2014
DA - July 2014
SP - 1
VL - 10
IS - 7
KW - Proteins
KW - 0
KW - Index Medicus
KW - Oxidation-Reduction
KW - Thermodynamics
KW - Computational Biology -- education
KW - Proteins -- chemistry
KW - Electron Transport
KW - Computational Biology -- methods
KW - Proteins -- metabolism
KW - Internet
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PLoS+computational+biology&rft.atitle=Web-based+computational+chemistry+education+with+CHARMMing+III%3A+Reduction+potentials+of+electron+transfer+proteins.&rft.au=Perrin%2C+B+Scott%3BMiller%2C+Benjamin+T%3BSchalk%2C+Vinushka%3BWoodcock%2C+H+Lee%3BBrooks%2C+Bernard+R%3BIchiye%2C+Toshiko&rft.aulast=Perrin&rft.aufirst=B&rft.date=2014-07-01&rft.volume=10&rft.issue=7&rft.spage=e1003739&rft.isbn=&rft.btitle=&rft.title=PLoS+computational+biology&rft.issn=1553-7358&rft_id=info:doi/10.1371%2Fjournal.pcbi.1003739
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-03-02
N1 - Date created - 2014-07-25
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1371/journal.pcbi.1003739
ER -
TY - JOUR
T1 - A Conserved Hydrogen-Bonding Network of P2 bis-Tetrahydrofuran-Containing HIV-1 Protease Inhibitors (PIs) with a Protease Active-Site Amino Acid Backbone Aids in Their Activity against PI-Resistant HIV
AN - 1547866920; 20207758
AB - In the present study, GRL008, a novel nonpeptidic human immunodeficiency virus type 1 (HIV-1) protease inhibitor (PI), and darunavir (DRV), both of which contain a P2-bis-tetrahydrofuranyl urethane (bis-THF) moiety, were found to exert potent antiviral activity (50% effective concentrations [EC50s], 0.029 and 0.002 mu M, respectively) against a multidrug-resistant clinical isolate of HIV-1 (HIVA02) compared to ritonavir (RTV; EC50, >1.0 mu M) and tipranavir (TPV; EC50, 0.364 mu M). Additionally, GRL008 showed potent antiviral activity against an HIV-1 variant selected in the presence of DRV over 20 passages (HIVDRVRP20), with a 2.6-fold increase in its EC50 (0.097 mu M) compared to its corresponding EC50 (0.038 mu M) against wild-type HIV-1NL4-3 (HIVWT). Based on X-ray crystallographic analysis, both GRL008 and DRV showed strong hydrogen bonds (H-bonds) with the backbone-amide nitrogen/carbonyl oxygen atoms of conserved active-site amino acids G27, D29, D30, and D30' of HIVA02 protease (PRA02) and wild-type PR in their corresponding crystal structures, while TPV lacked H-bonds with G27 and D30' due to an absence of polar groups. The P2' thiazolyl moiety of RTV showed two conformations in the crystal structure of the PRA02-RTV complex, one of which showed loss of contacts in the S2' binding pocket of PRA02, supporting RTV's compromised antiviral activity (EC50, >1 mu M). Thus, the conserved H-bonding network of P2-bis-THF-containing GRL008 with the backbone of G27, D29, D30, and D30' most likely contributes to its persistently greater antiviral activity against HIVWT, HIVA02, and HIVDRVRP20.
JF - Antimicrobial Agents & Chemotherapy
AU - Yedidi, Ravikiran S
AU - Garimella, Harisha
AU - Aoki, Manabu
AU - Aoki-Ogata, Hiromi
AU - Desai, Darshan V
AU - Chang, Simon B
AU - Davis, David A
AU - Fyvie, W Sean
AU - Kaufman, Joshua D
AU - Smith, David W
AD - Experimental Retrovirology Section, HIV and AIDS Malignancy Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA, mitsuyah@helix.nih.gov.
Y1 - 2014/07//
PY - 2014
DA - Jul 2014
SP - 3679
EP - 3688
PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL - 58
IS - 7
SN - 0066-4804, 0066-4804
KW - Virology & AIDS Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology
KW - Clinical isolates
KW - Amino acids
KW - Drug resistance
KW - Proteinase inhibitors
KW - Antiviral activity
KW - Oxygen
KW - Ritonavir
KW - Hydrogen bonding
KW - Ionizing radiation
KW - Human immunodeficiency virus 1
KW - Crystal structure
KW - carbonyls
KW - urethane
KW - Conformation
KW - Nitrogen
KW - A 01340:Antibiotics & Antimicrobials
KW - V 22360:AIDS and HIV
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1547866920?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Antimicrobial+Agents+%26+Chemotherapy&rft.atitle=A+Conserved+Hydrogen-Bonding+Network+of+P2+bis-Tetrahydrofuran-Containing+HIV-1+Protease+Inhibitors+%28PIs%29+with+a+Protease+Active-Site+Amino+Acid+Backbone+Aids+in+Their+Activity+against+PI-Resistant+HIV&rft.au=Yedidi%2C+Ravikiran+S%3BGarimella%2C+Harisha%3BAoki%2C+Manabu%3BAoki-Ogata%2C+Hiromi%3BDesai%2C+Darshan+V%3BChang%2C+Simon+B%3BDavis%2C+David+A%3BFyvie%2C+W+Sean%3BKaufman%2C+Joshua+D%3BSmith%2C+David+W&rft.aulast=Yedidi&rft.aufirst=Ravikiran&rft.date=2014-07-01&rft.volume=58&rft.issue=7&rft.spage=3679&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+Agents+%26+Chemotherapy&rft.issn=00664804&rft_id=info:doi/10.1128%2FAAC.00107-14
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-07-01
N1 - Number of references - 36
N1 - Last updated - 2014-10-02
N1 - SubjectsTermNotLitGenreText - Clinical isolates; Amino acids; Drug resistance; Proteinase inhibitors; Antiviral activity; Oxygen; Hydrogen bonding; Ritonavir; Ionizing radiation; Crystal structure; urethane; carbonyls; Nitrogen; Conformation; Human immunodeficiency virus 1
DO - http://dx.doi.org/10.1128/AAC.00107-14
ER -
TY - JOUR
T1 - Breast cancer risk in older women: results from the NIH-AARP Diet and Health Study
AN - 1547866051; 20116971
AB - Background: Divergent risk factors exist for premenopausal and postmenopausal breast cancers, but it is unclear whether differences by age exist among postmenopausal women. Methods: We examined relationships among 190,872 postmenopausal women, ages 50-71 years recruited during 1995-1996 for the NIH-AARP Diet and Health Study, in whom 7,384 incident invasive breast carcinomas were identified through 2006. Multivariable Cox regression hazard ratios (HRs) and 95 % confidence intervals (CIs) were estimated for breast cancer risk factors by age (50-59, 60-69, greater than or equal to 70 years). Results: The only factor showing significant statistical heterogeneity by age (p sub(het) = 0.001) was menopausal hormone therapy duration, but trends were apparent across all ages and the strongest association prevailed among women 60-69 years. Although other risk factors did not show statistically significant heterogeneity by age, we did observe attenuated relations for parity and late age at first birth among older women [e.g., HR for age at first birth greater than or equal to 30 vs. 20-24 = 1.62 (95 % CI 1.23-2.14) for women 50-59 years vs. 1.12 (0.96-1.31) for greater than or equal to 70 years]. In contrast, risk estimates associated with alcohol consumption and BMI tended to be slightly stronger among the oldest subjects [e.g., HR for BMI greater than or equal to 35 vs. 18.5-24.9 = 1.24 (95 % CI 0.97-1.58) for 50-59 years vs. 1.46 (1.26-1.70) for greater than or equal to 70 years]. These differences were somewhat more pronounced for estrogen receptor positive and ductal cancers, tumors predominating among older women. Breast cancer family history, physical activity, and previous breast biopsies did not show divergent associations by age. Conclusion: Although breast cancer risk factor differences among older women were not large, they may merit further consideration with respect to individualized risk prediction.
JF - Cancer Causes & Control
AU - Brinton, Louise A
AU - Smith, Llewellyn
AU - Gierach, Gretchen L
AU - Pfeiffer, Ruth M
AU - Nyante, Sarah J
AU - Sherman, Mark E
AU - Park, Yikyung
AU - Hollenbeck, Albert R
AU - Dallal, Cher M
AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, 20892, USA, brinton@nih.gov
Y1 - 2014/07//
PY - 2014
DA - Jul 2014
SP - 843
EP - 857
PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL - 25
IS - 7
SN - 0957-5243, 0957-5243
KW - Health & Safety Science Abstracts; Risk Abstracts
KW - Prediction
KW - Diets
KW - Alcohol
KW - Estrogens
KW - Age
KW - Physical activity
KW - Body mass
KW - Hormones
KW - Genetics
KW - Health risks
KW - Post-menopause
KW - Risk factors
KW - Breast cancer
KW - Females
KW - H 11000:Diseases/Injuries/Trauma
KW - R2 23060:Medical and environmental health
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1547866051?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Causes+%26+Control&rft.atitle=Breast+cancer+risk+in+older+women%3A+results+from+the+NIH-AARP+Diet+and+Health+Study&rft.au=Brinton%2C+Louise+A%3BSmith%2C+Llewellyn%3BGierach%2C+Gretchen+L%3BPfeiffer%2C+Ruth+M%3BNyante%2C+Sarah+J%3BSherman%2C+Mark+E%3BPark%2C+Yikyung%3BHollenbeck%2C+Albert+R%3BDallal%2C+Cher+M&rft.aulast=Brinton&rft.aufirst=Louise&rft.date=2014-07-01&rft.volume=25&rft.issue=7&rft.spage=843&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/10.1007%2Fs10552-014-0385-3
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-07-01
N1 - Number of references - 45
N1 - Last updated - 2014-10-02
N1 - SubjectsTermNotLitGenreText - Diets; Prediction; Alcohol; Age; Estrogens; Body mass; Physical activity; Hormones; Health risks; Genetics; Post-menopause; Risk factors; Breast cancer; Females
DO - http://dx.doi.org/10.1007/s10552-014-0385-3
ER -
TY - JOUR
T1 - African Green Monkeys Recapitulate the Clinical Experience with Replication of Live Attenuated Pandemic Influenza Virus Vaccine Candidates
AN - 1547865520; 20207856
AB - Live attenuated cold-adapted (ca) H5N1, H7N3, H6N1, and H9N2 influenza vaccine viruses replicated in the respiratory tract of mice and ferrets, and 2 doses of vaccines were immunogenic and protected these animals from challenge infection with homologous and heterologous wild-type (wt) viruses of the corresponding subtypes. However, when these vaccine candidates were evaluated in phase I clinical trials, there were inconsistencies between the observations in animal models and in humans. The vaccine viruses did not replicate well and immune responses were variable in humans, even though the study subjects were seronegative with respect to the vaccine viruses before vaccination. Therefore, we sought a model that would better reflect the findings in humans and evaluated African green monkeys (AGMs) as a nonhuman primate model. The distribution of sialic acid (SA) receptors in the respiratory tract of AGMs was similar to that in humans. We evaluated the replication of wt and ca viruses of avian influenza (AI) virus subtypes H5N1, H6N1, H7N3, and H9N2 in the respiratory tract of AGMs. All of the wt viruses replicated efficiently, while replication of the ca vaccine viruses was restricted to the upper respiratory tract. Interestingly, the patterns and sites of virus replication differed among the different subtypes. We also evaluated the immunogenicity and protective efficacy of H5N1, H6N1, H7N3, and H9N2 ca vaccines. Protection from wt virus challenge correlated well with the level of serum neutralizing antibodies. Immune responses were slightly better when vaccine was delivered by both intranasal and intratracheal delivery than when it was delivered intranasally by sprayer. We conclude that live attenuated pandemic influenza virus vaccines replicate similarly in AGMs and human subjects and that AGMs may be a useful model to evaluate the replication of ca vaccine candidates. IMPORTANCE Ferrets and mice are commonly used for preclinical evaluation of influenza vaccines. However, we observed significant inconsistencies between observations in humans and in these animal models. We used African green monkeys (AGMs) as a nonhuman primate (NHP) model for a comprehensive and comparative evaluation of pairs of wild-type and pandemic live attenuated influenza virus vaccines (pLAIV) representing four subtypes of avian influenza viruses and found that pLAIVs replicate similarly in AGMs and humans and that AGMs can be useful for evaluation of the protective efficacy of pLAIV.
JF - Journal of Virology
AU - Matsuoka, Yumiko
AU - Suguitan, Amorsolo Jr
AU - Orandle, Marlene
AU - Paskel, Myeisha
AU - Boonnak, Kobporn
AU - Gardner, Donald J
AU - Feldmann, Friederike
AU - Feldmann, Heinz
AU - Marino, Michael
AU - Jin, Hong
AD - Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA, ksubbarao@niaid.nih.gov.
Y1 - 2014/07//
PY - 2014
DA - Jul 2014
SP - 8139
EP - 8152
PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL - 88
IS - 14
SN - 0022-538X, 0022-538X
KW - Health & Safety Science Abstracts; Immunology Abstracts; Virology & AIDS Abstracts
KW - Viruses
KW - Animal models
KW - Infection
KW - Clinical trials
KW - Influenza
KW - pandemics
KW - Mustela
KW - Trachea
KW - Respiratory tract
KW - Replication
KW - Sprays
KW - Mice
KW - Primates
KW - Fowl plague
KW - Antibodies
KW - Influenza virus
KW - Immunogenicity
KW - Africa
KW - Immune response
KW - Vaccines
KW - Sialic acids
KW - V 22350:Immunology
KW - H 1000:Occupational Safety and Health
KW - F 06910:Microorganisms & Parasites
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Virology&rft.atitle=African+Green+Monkeys+Recapitulate+the+Clinical+Experience+with+Replication+of+Live+Attenuated+Pandemic+Influenza+Virus+Vaccine+Candidates&rft.au=Matsuoka%2C+Yumiko%3BSuguitan%2C+Amorsolo+Jr%3BOrandle%2C+Marlene%3BPaskel%2C+Myeisha%3BBoonnak%2C+Kobporn%3BGardner%2C+Donald+J%3BFeldmann%2C+Friederike%3BFeldmann%2C+Heinz%3BMarino%2C+Michael%3BJin%2C+Hong&rft.aulast=Matsuoka&rft.aufirst=Yumiko&rft.date=2014-07-01&rft.volume=88&rft.issue=14&rft.spage=8139&rft.isbn=&rft.btitle=&rft.title=Journal+of+Virology&rft.issn=0022538X&rft_id=info:doi/10.1128%2FJVI.00425-14
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-07-01
N1 - Number of references - 64
N1 - Last updated - 2015-04-02
N1 - SubjectsTermNotLitGenreText - Replication; Animal models; Infection; Clinical trials; Fowl plague; pandemics; Antibodies; Immunogenicity; Vaccines; Immune response; Trachea; Sialic acids; Respiratory tract; Influenza; Sprays; Viruses; Mice; Primates; Influenza virus; Mustela; Africa
DO - http://dx.doi.org/10.1128/JVI.00425-14
ER -
TY - JOUR
T1 - Inclusion of a universal tetanus toxoid CD4+ T cell epitope P2 significantly enhanced the immunogenicity of recombinant rotavirus Delta VP8* subunit parenteral vaccines
AN - 1547856102; 20297679
AB - Currently available live oral rotavirus vaccines, Rotarix registered and RotaTeq registered , are highly efficacious in developed countries. However, the immunogenicity and efficacy of such vaccines in some developing countries are low. We reported previously that bacterially-expressed rotavirus Delta VP8* subunit vaccine candidates with P[8], P[4] or P[6] specificity elicited high-titer virus neutralizing antibodies in animals immunized intramuscularly. Of note was the finding that antibodies induced with the P[8] Delta VP8* vaccine neutralized both homotypic P[8] and heterotypic P[4] rotavirus strains to high titer. To further improve its vaccine potential, a tetanus toxoid universal CD4+ T cell epitope P2 was introduced into P[8] or P[6] Delta VP8* construct. The resulting recombinant fusion proteins expressed in were of high solubility and were produced with high yield. Two doses (10 or 20 mu g/dose) of the P2-P[8] Delta VP8* vaccine or P2-P[6] Delta VP8* vaccine with aluminum phosphate adjuvant elicited significantly higher geometric mean homologous neutralizing antibody titers than the vaccines without P2 in intramuscularly immunized guinea pigs. Interestingly, high levels of neutralizing antibody responses induced in guinea pigs with 3 doses of the P2-P[8] Delta VP8* vaccine persisted for at least 6 months. Furthermore, in the gnotobiotic piglet challenge study, three intramuscular doses (50 mu g/dose) of the P2-P[8] Delta VP8* vaccine with aluminum phosphate adjuvant significantly delayed the onset of diarrhea and significantly reduced the duration of diarrhea and the cumulative diarrhea score after oral challenge with virulent human rotavirus Wa (G1P[8]) strain. The P2-P[8] Delta VP8* vaccine induced serum virus neutralizing antibody and VP4-specific IgG antibody production prechallenge, and primed the pigs for higher antibody and intestinal and systemic virus-specific IFN- gamma producing CD4+ T cell responses postchallenge. These two subunit vaccines could be used at a minimum singly or preferably in bivalent formulation to provide antigenic coverage of most of the G types of global importance.
JF - Vaccine
AU - Wen, Xiaobo
AU - Wen, Ke
AU - Cao, Dianjun
AU - Li, Guohua
AU - Jones, Ronald W
AU - Li, Jianping
AU - Szu, Shousun
AU - Hoshino, Yasutaka
AU - Yuan, Lijuan
AD - Rotavirus Vaccine Development Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, United States
Y1 - 2014/07//
PY - 2014
DA - Jul 2014
SP - 4420
EP - 4427
PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom
VL - 32
IS - 35
SN - 0264-410X, 0264-410X
KW - Virology & AIDS Abstracts; Microbiology Abstracts B: Bacteriology; Immunology Abstracts
KW - Human rotavirus
KW - Subunit vaccine
KW - T cell epitope
KW - Immunogenicity
KW - Protective efficacy
KW - Diarrhea
KW - Gnotobiotic pigs
KW - gamma -Interferon
KW - Solubility
KW - Adjuvants
KW - Tetanus
KW - CD4 antigen
KW - Phosphate
KW - Aluminum
KW - Lymphocytes T
KW - Intestine
KW - Gnotobiotics
KW - Immunoglobulin G
KW - Fusion protein
KW - Vaccines
KW - Developing countries
KW - Epitopes
KW - V 22350:Immunology
KW - F 06905:Vaccines
KW - J 02350:Immunology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Vaccine&rft.atitle=Inclusion+of+a+universal+tetanus+toxoid+CD4%2B+T+cell+epitope+P2+significantly+enhanced+the+immunogenicity+of+recombinant+rotavirus+Delta+VP8*+subunit+parenteral+vaccines&rft.au=Wen%2C+Xiaobo%3BWen%2C+Ke%3BCao%2C+Dianjun%3BLi%2C+Guohua%3BJones%2C+Ronald+W%3BLi%2C+Jianping%3BSzu%2C+Shousun%3BHoshino%2C+Yasutaka%3BYuan%2C+Lijuan&rft.aulast=Wen&rft.aufirst=Xiaobo&rft.date=2014-07-01&rft.volume=32&rft.issue=35&rft.spage=4420&rft.isbn=&rft.btitle=&rft.title=Vaccine&rft.issn=0264410X&rft_id=info:doi/10.1016%2Fj.vaccine.2014.06.060
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-07-01
N1 - Last updated - 2014-10-02
N1 - SubjectsTermNotLitGenreText - gamma -Interferon; Diarrhea; Solubility; Adjuvants; Tetanus; CD4 antigen; Phosphate; Immunogenicity; Aluminum; Immunoglobulin G; Gnotobiotics; Intestine; Lymphocytes T; Vaccines; Fusion protein; Developing countries; Epitopes; Human rotavirus
DO - http://dx.doi.org/10.1016/j.vaccine.2014.06.060
ER -
TY - JOUR
T1 - Chlamydia trachomatis Polymorphic Membrane Protein D Is a Virulence Factor Involved in Early Host-Cell Interactions
AN - 1547852776; 20296413
AB - Chlamydia trachomatis is an obligate intracellular mucosotropic pathogen of significant medical importance. It is the etiological agent of blinding trachoma and bacterial sexually transmitted diseases, infections that afflict hundreds of millions of people globally. The C. trachomatis polymorphic membrane protein D (PmpD) is a highly conserved autotransporter and the target of broadly cross-reactive neutralizing antibodies; however, its role in host-pathogen interactions is unknown. Here we employed a targeted reverse genetics approach to generate a pmpD null mutant that was used to define the role of PmpD in the pathogenesis of chlamydial infection. We show that pmpD is not an essential chlamydial gene and the pmpD null mutant has no detectable deficiency in cultured murine cells or in a murine mucosal infection model. Notably, however, the pmpD null mutant was significantly attenuated for macaque eyes and cultured human cells. A reduction in pmpD null infection of human endocervical cells was associated with a deficiency in chlamydial attachment to cells. Collectively, our results show that PmpD is a chlamydial virulence factor that functions in early host-cell interactions. This study is the first of its kind using reverse genetics to evaluate the contribution of a C. trachomatis gene to disease pathogenesis.
JF - Infection and Immunity
AU - Kari, Laszlo
AU - Southern, Timothy R
AU - Downey, Carey J
AU - Watkins, Heather S
AU - Randall, Linnell B
AU - Taylor, Lacey D
AU - Sturdevant, Gail L
AU - Whitmire, William M
AU - Caldwell, Harlan D
Y1 - 2014/07//
PY - 2014
DA - Jul 2014
SP - 2756
EP - 2762
PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL - 82
IS - 7
SN - 0019-9567, 0019-9567
KW - Microbiology Abstracts B: Bacteriology; Immunology Abstracts
KW - virulence factors
KW - Sexually-transmitted diseases
KW - Macaca
KW - Mucosa
KW - Animal models
KW - Chlamydia trachomatis
KW - Medical importance
KW - Membrane proteins
KW - Pathogens
KW - Infection
KW - Trachoma
KW - Antibodies
KW - Host-pathogen interactions
KW - J 02410:Animal Diseases
KW - F 06910:Microorganisms & Parasites
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+and+Immunity&rft.atitle=Chlamydia+trachomatis+Polymorphic+Membrane+Protein+D+Is+a+Virulence+Factor+Involved+in+Early+Host-Cell+Interactions&rft.au=Kari%2C+Laszlo%3BSouthern%2C+Timothy+R%3BDowney%2C+Carey+J%3BWatkins%2C+Heather+S%3BRandall%2C+Linnell+B%3BTaylor%2C+Lacey+D%3BSturdevant%2C+Gail+L%3BWhitmire%2C+William+M%3BCaldwell%2C+Harlan+D&rft.aulast=Kari&rft.aufirst=Laszlo&rft.date=2014-07-01&rft.volume=82&rft.issue=7&rft.spage=2756&rft.isbn=&rft.btitle=&rft.title=Infection+and+Immunity&rft.issn=00199567&rft_id=info:doi/10.1128%2FIAI.01686-14
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-07-01
N1 - Number of references - 34
N1 - Last updated - 2015-04-02
N1 - SubjectsTermNotLitGenreText - Antibodies; Sexually-transmitted diseases; virulence factors; Host-pathogen interactions; Mucosa; Animal models; Medical importance; Pathogens; Membrane proteins; Infection; Trachoma; Macaca; Chlamydia trachomatis
DO - http://dx.doi.org/10.1128/IAI.01686-14
ER -
TY - JOUR
T1 - Structural insight into exosite binding and discovery of novel exosite inhibitors of botulinum neurotoxin serotype A through in silico screening.
AN - 1545417329; 24958623
AB - Botulinum neurotoxin serotype A (BoNT/A) is the most lethal toxin among the Tier 1 Select Agents. Development of potent and selective small molecule inhibitors against BoNT/A zinc metalloprotease remains a challenging problem due to its exceptionally large substrate binding surface and conformational plasticity. The exosites of the catalytic domain of BoNT/A are intriguing alternative sites for small molecule intervention, but their suitability for inhibitor design remains largely unexplored. In this study, we employed two recently identified exosite inhibitors, D-chicoric acid and lomofungin, to probe the structural features of the exosites and molecular mechanisms of synergistic inhibition. The results showed that D-chicoric acid favors binding at the α-exosite, whereas lomofungin preferentially binds at the β-exosite by mimicking the substrate β-sheet binding interaction. Molecular dynamics simulations and binding interaction analysis of the exosite inhibitors with BoNT/A revealed key elements and hotspots that likely contribute to the inhibitor binding and synergistic inhibition. Finally, we performed database virtual screening for novel inhibitors of BoNT/A targeting the exosites. Hits C1 and C2 showed non-competitive inhibition and likely target the α- and β-exosites, respectively. The identified exosite inhibitors may provide novel candidates for structure-based development of therapeutics against BoNT/A intoxication.
JF - Journal of computer-aided molecular design
AU - Hu, Xin
AU - Legler, Patricia M
AU - Southall, Noel
AU - Maloney, David J
AU - Simeonov, Anton
AU - Jadhav, Ajit
AD - NIH Chemical Genomics Center, National Center for Advancing Translational Sciences, National Institutes of Health, 9800 Medical Center Drive, Rockville, MD, 20850, USA, hux61@mail.nih.gov.
Y1 - 2014/07//
PY - 2014
DA - July 2014
SP - 765
EP - 778
VL - 28
IS - 7
KW - Caffeic Acids
KW - 0
KW - Phenazines
KW - Succinates
KW - lomofungin
KW - 26786-84-5
KW - chicoric acid
KW - 70831-56-0
KW - Botulinum Toxins, Type A
KW - EC 3.4.24.69
KW - Index Medicus
KW - Computer Simulation
KW - Humans
KW - Molecular Dynamics Simulation
KW - Molecular Conformation
KW - Protein Binding
KW - Binding Sites
KW - Caffeic Acids -- chemistry
KW - Botulinum Toxins, Type A -- toxicity
KW - Botulinum Toxins, Type A -- antagonists & inhibitors
KW - Phenazines -- chemistry
KW - Succinates -- chemistry
KW - Structure-Activity Relationship
KW - Botulinum Toxins, Type A -- chemistry
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+computer-aided+molecular+design&rft.atitle=Structural+insight+into+exosite+binding+and+discovery+of+novel+exosite+inhibitors+of+botulinum+neurotoxin+serotype+A+through+in+silico+screening.&rft.au=Hu%2C+Xin%3BLegler%2C+Patricia+M%3BSouthall%2C+Noel%3BMaloney%2C+David+J%3BSimeonov%2C+Anton%3BJadhav%2C+Ajit&rft.aulast=Hu&rft.aufirst=Xin&rft.date=2014-07-01&rft.volume=28&rft.issue=7&rft.spage=765&rft.isbn=&rft.btitle=&rft.title=Journal+of+computer-aided+molecular+design&rft.issn=1573-4951&rft_id=info:doi/10.1007%2Fs10822-014-9758-7
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-03-30
N1 - Date created - 2014-07-15
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1007/s10822-014-9758-7
ER -
TY - JOUR
T1 - Dietary intake of a plant phospholipid/lipid conjugate reduces lung cancer growth and tumor angiogenesis.
AN - 1542652174; 24510111
AB - It is well recognized that early detection and cancer prevention are significant armaments in the 'war against cancer'. Changes in lifestyle and diet have significant impact on the global incidence of cancer. For over 30 years, many investigators have studied the concept of chemoprevention. More recently, with the demonstration that antiangiogenic activity reduces tumor growth, the concept of angioprevention has emerged as a novel strategy in the deterrence of cancer development (carcinogenesis). In this study, we utilized a fast growing, highly aggressive murine Lewis lung cancer model to examine the in vivo antitumor effects of a novel, dietary supplement, known as plant phospholipid/lipid conjugate (pPLC). Our goal was to determine if pPLC possessed direct antitumor activity with relatively little toxicity that could be developed as a chemoprevention therapy. We used pPLC directly in this in vivo model due to the lack of aqueous solubility of this novel formulation, which precludes in vitro experimentation. pPLC contains known antioxidants, ferulic acid and lipoic acid, as well as soy sterols, formulated in a unique aqueous-insoluble matrix. The pPLC dietary supplement was shown to suppress in vivo growth of this tumor model by 30%. We also demonstrated a significant decrease in tumor angiogenesis accompanied by increased apoptosis and present preliminary evidence of enhanced expression of the hypoxia-related genes pentraxin-3 and metallothionein-3, by 24.9-fold and 10.9-fold, respectively, compared with vehicle control. These findings lead us to propose using this plant phosolipid/lipid conjugate as a dietary supplement that may be useful in cancer prevention.
Published by Oxford University Press 2014.
JF - Carcinogenesis
AU - Shuman Moss, Laurie A
AU - Jensen-Taubman, Sandra
AU - Rubinstein, Danielle
AU - Viole, Gary
AU - Stetler-Stevenson, William G
AD - Radiation Oncology Branch, National Cancer Institute, Bethesda, MD 20895, USA, sstevenw@mail.nih.gov laurie.shumanmoss@nih.gov. ; Radiation Oncology Branch, National Cancer Institute, Bethesda, MD 20895, USA. ; Radiation Oncology Branch, National Cancer Institute, Bethesda, MD 20895, USA, Gettysburg College, Gettysburg, PA 17325, USA and. ; Conjugated Functional Foods, Hackensack, NJ 07601, USA. ; Radiation Oncology Branch, National Cancer Institute, Bethesda, MD 20895, USA, sstevenw@mail.nih.gov.
Y1 - 2014/07//
PY - 2014
DA - July 2014
SP - 1556
EP - 1563
VL - 35
IS - 7
KW - Biomarkers, Tumor
KW - 0
KW - Lipids
KW - Phospholipids
KW - Plant Preparations
KW - RNA, Messenger
KW - Index Medicus
KW - Real-Time Polymerase Chain Reaction
KW - Animals
KW - Biomarkers, Tumor -- genetics
KW - Apoptosis
KW - Oligonucleotide Array Sequence Analysis
KW - Humans
KW - Mice
KW - Reverse Transcriptase Polymerase Chain Reaction
KW - RNA, Messenger -- genetics
KW - Cell Proliferation
KW - Biomarkers, Tumor -- metabolism
KW - Gene Expression Profiling
KW - Blotting, Western
KW - Tumor Cells, Cultured
KW - Mice, Inbred C57BL
KW - Female
KW - Immunoenzyme Techniques
KW - Phytotherapy
KW - Plant Preparations -- therapeutic use
KW - Phospholipids -- chemistry
KW - Lipids -- chemistry
KW - Carcinoma, Lewis Lung -- diet therapy
KW - Carcinoma, Lewis Lung -- blood supply
KW - Carcinoma, Lewis Lung -- pathology
KW - Neovascularization, Pathologic -- prevention & control
KW - Diet
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-09-25
N1 - Date created - 2014-07-02
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Am J Clin Nutr. 2008 Apr;87(4):993-1001 [18400724]
Br J Nutr. 2007 Sep;98(3):550-5 [17459188]
Clin Dermatol. 2008 Jul-Aug;26(4):358-63 [18691515]
Nutr J. 2008;7:29 [18826565]
Nutr Rev. 2008 Nov;66(11):646-57 [19019027]
Eur J Immunol. 2009 Mar;39(3):843-57 [19224633]
Eur J Clin Nutr. 2009 Jul;63(7):813-20 [19491917]
Int J Cancer. 2009 Nov 1;125(9):1997-2003 [19551861]
Blood. 2009 Sep 10;114(11):2359-60 [19745081]
Biochim Biophys Acta. 2009 Oct;1790(10):1149-60 [19664690]
J Cardiovasc Pharmacol. 2009 Nov;54(5):391-8 [19998523]
Curr Pharm Des. 2010;16(7):877-83 [20388101]
Neuroscience. 2010 Sep 15;169(4):1575-88 [20600667]
Clin Cancer Res. 2011 Apr 15;17(8):2395-9 [21257721]
Cancer Lett. 2011 Sep 28;308(2):172-80 [21624767]
Mol Cancer Res. 2011 Jul;9(7):815-23 [21642390]
Pharmacol Rep. 2011;63(4):849-58 [22001972]
Odontology. 2012 Jul;100(2):215-21 [21932007]
Nat Rev Clin Oncol. 2012 Sep;9(9):498-509 [22850752]
Nutr Clin Pract. 2012 Oct;27(5):599-612 [22878362]
Anticancer Res. 2013 Mar;33(3):965-74 [23482768]
Nutr Cancer. 2000;37(2):140-4 [11142085]
Blood. 2002 Sep 1;100(5):1551-8 [12176869]
Behav Genet. 2002 Nov;32(6):435-43 [12467341]
Carcinogenesis. 2003 Jan;24(1):25-9 [12538345]
J Cell Physiol. 2003 Mar;194(3):325-40 [12548552]
J Lipid Res. 2003 May;44(5):994-1000 [12611905]
J Nutr. 2003 Jun;133(6):1937-42 [12771342]
J Lab Clin Med. 2004 Apr;143(4):255-62 [15085084]
J Nutr. 2004 May;134(5):1145-51 [15113961]
Blood. 2004 Jul 1;104(1):92-9 [15031207]
Nat Med. 2004 Jul;10(7):727-33 [15195087]
Fed Proc. 1976 May 1;35(6):1332-8 [770206]
Cancer Res. 1976 Jul;36(7 PT 2):2699-702 [1277177]
Drug Metab Rev. 1998 May;30(2):245-75 [9606603]
Lung Cancer. 1998 Jul;21(1):37-45 [9792052]
J Agric Food Chem. 2006 Jul 26;54(15):5375-81 [16848520]
Transl Res. 2007 Jan;149(1):22-30 [17196519]
Mol Nutr Food Res. 2007 Feb;51(2):161-70 [17266177]
Am J Physiol Cell Physiol. 2007 Mar;292(3):C987-95 [16943240]
J Exp Med. 2007 Apr 16;204(4):793-804 [17389238]
Curr Med Chem. 2008;15(11):1044-71 [18473802]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/carcin/bgu039
ER -
TY - JOUR
T1 - Tumor suppressor PDCD4 inhibits NF-κB-dependent transcription in human glioblastoma cells by direct interaction with p65.
AN - 1542650118; 24413684
AB - PDCD4 is a tumor suppressor induced by apoptotic stimuli that regulates both translation and transcription. Previously, we showed that overexpression of PDCD4 leads to decreased anchorage-independent growth in glioblastoma (GBM)-derived cell lines and decreased tumor growth in a GBM xenograft model. In inflammatory cells, PDCD4 stimulates tumor necrosis factor-induced activation of the transcription factor NF-κB, an oncogenic driver in many cancer sites. However, the effect of PDCD4 on NF-κB transcriptional activity in most cancers including GBM is still unknown. We studied the effect of PDCD4 on NF-κB-dependent transcriptional activity in GBM by stably overexpressing PDCD4 in U251 and LN229 cells. Stable PDCD4 expression inhibits NF-κB transcriptional activation measured by a luciferase reporter. The molecular mechanism by which PDCD4 inhibits NF-κB transcriptional activation does not involve inhibited expression of NF-κB p65 or p50 proteins. PDCD4 does not inhibit pathways upstream of NF-κB including the activation of IKKα and IKKβ kinases or degradation of IκBα, events needed for nuclear transport of p65 and p50. PDCD4 overexpression does inhibit localization of p65 but not p50 in the nucleus. PDCD4 protein interacts preferentially with p65 protein as shown by co-immunoprecipitation and confocal imaging. PDCD4 overexpression inhibits the mRNA expression of two NF-κB target genes in a p65-dependent manner. These results suggest that PDCD4 can significantly inhibit NF-κB activity in GBM cells by a mechanism that involves direct or indirect protein-protein interaction independent of the expected mRNA-selective translational inhibition. These findings offer novel opportunities for NF-κB-targeted interventions to prevent or treat cancer. © The Author 2014. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.
JF - Carcinogenesis
AU - Hwang, Soon-Kyung
AU - Baker, Alyson R
AU - Young, Matthew R
AU - Colburn, Nancy H
AD - Laboratory of Cancer Prevention, Center for Cancer Research, National Cancer Institute, Frederick National Laboratory, 1050 Boyles Street, Bldg 576, Rm 101, Frederick, MD 21702, USA police042@naver.com. ; Laboratory of Cancer Prevention, Center for Cancer Research, National Cancer Institute, Frederick National Laboratory, 1050 Boyles Street, Bldg 576, Rm 101, Frederick, MD 21702, USA.
Y1 - 2014/07//
PY - 2014
DA - July 2014
SP - 1469
EP - 1480
VL - 35
IS - 7
KW - Apoptosis Regulatory Proteins
KW - 0
KW - NF-kappa B p50 Subunit
KW - PDCD4 protein, human
KW - RNA, Messenger
KW - RNA-Binding Proteins
KW - Transcription Factor RelA
KW - Index Medicus
KW - Real-Time Polymerase Chain Reaction
KW - Cell Movement
KW - Blotting, Western
KW - Apoptosis
KW - Tumor Cells, Cultured
KW - Humans
KW - Immunoprecipitation
KW - Chromatin Immunoprecipitation
KW - Transcription, Genetic
KW - Reverse Transcriptase Polymerase Chain Reaction
KW - RNA, Messenger -- genetics
KW - Cell Proliferation
KW - Gene Expression Regulation, Neoplastic
KW - Glioblastoma -- genetics
KW - Apoptosis Regulatory Proteins -- genetics
KW - RNA-Binding Proteins -- metabolism
KW - RNA-Binding Proteins -- genetics
KW - Transcription Factor RelA -- metabolism
KW - Transcription Factor RelA -- genetics
KW - NF-kappa B p50 Subunit -- genetics
KW - Glioblastoma -- pathology
KW - Glioblastoma -- metabolism
KW - Apoptosis Regulatory Proteins -- metabolism
KW - NF-kappa B p50 Subunit -- metabolism
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-09-25
N1 - Date created - 2014-07-02
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Proc Natl Acad Sci U S A. 1999 Nov 23;96(24):14037-42 [10570194]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/carcin/bgu008
ER -
TY - JOUR
T1 - Modulation of aryl hydrocarbon receptor (AHR)-dependent signaling by peroxisome proliferator-activated receptor β/δ (PPARβ/δ) in keratinocytes.
AN - 1542649766; 24639079
AB - Whether peroxisome proliferator-activated receptor β/δ (PPARβ/δ) reduces skin tumorigenesis by altering aryl hydrocarbon receptor (AHR)-dependent activities was examined. Polycyclic aromatic hydrocarbons (PAH) increased expression of cytochrome P4501A1 (CYP1A1), CYP1B1 and phase II xenobiotic metabolizing enzymes in wild-type skin and keratinocytes. Surprisingly, this effect was not found in Pparβ/δ-null skin and keratinocytes. Pparβ/δ-null keratinocytes exhibited decreased AHR occupancy and histone acetylation on the Cyp1a1 promoter in response to a PAH compared with wild-type keratinocytes. Bisulfite sequencing of the Cyp1a1 promoter and studies using a DNA methylation inhibitor suggest that PPARβ/δ promotes demethylation of the Cyp1a1 promoter. Experiments with human HaCaT keratinocytes stably expressing shRNA against PPARβ/δ also support this conclusion. Consistent with the lower AHR-dependent activities in Pparβ/δ-null mice compared with wild-type mice, 7,12-dimethylbenz[a]anthracene (DMBA)-induced skin tumorigenesis was inhibited in Pparβ/δ-null mice compared with wild-type. Results from these studies demonstrate that PPARβ/δ is required to mediate complete carcinogenesis by DMBA. The mechanisms underlying this PPARβ/δ-dependent reduction of AHR signaling by PAH are not due to alterations in the expression of AHR auxiliary proteins, ligand binding or AHR nuclear translocation between genotypes, but are likely influenced by PPARβ/δ-dependent demethylation of AHR target gene promoters including Cyp1a1 that reduces AHR accessibility as shown by reduced promoter occupancy. This PPARβ/δ/AHR crosstalk is unique to keratinocytes and conserved between mice and humans. Published by Oxford University Press 2014.
JF - Carcinogenesis
AU - Borland, Michael G
AU - Krishnan, Prasad
AU - Lee, Christina
AU - Albrecht, Prajakta P
AU - Shan, Weiwei
AU - Bility, Moses T
AU - Marcus, Craig B
AU - Lin, Jyh M
AU - Amin, Shantu
AU - Gonzalez, Frank J
AU - Perdew, Gary H
AU - Peters, Jeffrey M
AD - Department of Veterinary and Biomedical Sciences and the Center of Molecular Toxicology and Carcinogenesis and The Graduate Program in Biochemistry, Microbiology, and Molecular Biology, The Pennsylvania State University, University Park, PA 16802, USA. ; Department of Veterinary and Biomedical Sciences and the Center of Molecular Toxicology and Carcinogenesis and. ; Department of Environmental and Molecular Toxicology, Oregon State University, Corvallis, OR 97331, USA. ; Department of Pharmacology, Penn State Cancer Institute, The Pennsylvania State University, Milton S. Hershey Medical Center, Hershey, PA 17033, USA and. ; Laboratory of Metabolism, National Cancer Institute, Bethesda, MD 20892, USA. ; Department of Veterinary and Biomedical Sciences and the Center of Molecular Toxicology and Carcinogenesis and The Graduate Program in Biochemistry, Microbiology, and Molecular Biology, The Pennsylvania State University, University Park, PA 16802, USA, jmp21@psu.edu.
Y1 - 2014/07//
PY - 2014
DA - July 2014
SP - 1602
EP - 1612
VL - 35
IS - 7
KW - Ahr protein, mouse
KW - 0
KW - Basic Helix-Loop-Helix Transcription Factors
KW - Carcinogens
KW - PPAR delta
KW - PPAR-beta
KW - RNA, Messenger
KW - Receptors, Aryl Hydrocarbon
KW - 9,10-Dimethyl-1,2-benzanthracene
KW - 57-97-6
KW - Index Medicus
KW - Real-Time Polymerase Chain Reaction
KW - Animals
KW - Cell Transformation, Neoplastic -- pathology
KW - Dermis -- cytology
KW - Humans
KW - Cell Transformation, Neoplastic -- metabolism
KW - Carcinogens -- toxicity
KW - Skin Neoplasms -- pathology
KW - Mice
KW - Fibroblasts -- cytology
KW - Reverse Transcriptase Polymerase Chain Reaction
KW - RNA, Messenger -- genetics
KW - Skin Neoplasms -- metabolism
KW - Fibroblasts -- metabolism
KW - Dermis -- metabolism
KW - Mice, Knockout
KW - Blotting, Western
KW - 9,10-Dimethyl-1,2-benzanthracene -- toxicity
KW - Cells, Cultured
KW - Skin Neoplasms -- chemically induced
KW - Cell Transformation, Neoplastic -- chemically induced
KW - Chromatin Immunoprecipitation
KW - Signal Transduction
KW - Immunoenzyme Techniques
KW - Female
KW - PPAR delta -- physiology
KW - Receptors, Aryl Hydrocarbon -- physiology
KW - Basic Helix-Loop-Helix Transcription Factors -- physiology
KW - Keratinocytes -- cytology
KW - Keratinocytes -- metabolism
KW - PPAR-beta -- physiology
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1542649766?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Modulation+of+aryl+hydrocarbon+receptor+%28AHR%29-dependent+signaling+by+peroxisome+proliferator-activated+receptor+%CE%B2%2F%CE%B4+%28PPAR%CE%B2%2F%CE%B4%29+in+keratinocytes.&rft.au=Borland%2C+Michael+G%3BKrishnan%2C+Prasad%3BLee%2C+Christina%3BAlbrecht%2C+Prajakta+P%3BShan%2C+Weiwei%3BBility%2C+Moses+T%3BMarcus%2C+Craig+B%3BLin%2C+Jyh+M%3BAmin%2C+Shantu%3BGonzalez%2C+Frank+J%3BPerdew%2C+Gary+H%3BPeters%2C+Jeffrey+M&rft.aulast=Borland&rft.aufirst=Michael&rft.date=2014-07-01&rft.volume=35&rft.issue=7&rft.spage=1602&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgu067
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-09-25
N1 - Date created - 2014-07-02
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/carcin/bgu067
ER -
TY - JOUR
T1 - CRBP-1 expression in ovarian cancer: a potential therapeutic target.
AN - 1542299828; 24982334
AB - Cellular retinol binding protein-1 regulates retinol bioavailability and contributes to cell differentiation maintenance, but its role in ovarian carcinogenesis remains uncertain. We investigated CRBP-1 expression in ovarian tumors and CRBP-1 signaling-regulated pathways.
We performed immunohistochemistry, methylation-specific PCR, gene copy number analysis in ovarian tumors and proliferation/apoptosis evaluation, gene array, blot and real-time PCR in CRBP-1-transfected A2780 ovarian cancer cells. CRBP-1 expression was reduced or absent in G2 and G3 ovarian carcinomas. CRBP-1 silencing in 60% of G2 and 66.7% of G3 carcinomas was due to CRBP-1 promoter methylation. A2780 CRBP-1-transfected cells showed increased retinol-induced apoptosis, retinoid-induced reduced clonogenicity and down-regulation of proliferation and transcription genes, including AKT1, AKT3, EGFR, FOS, JUN, STAT1 and STAT5A.
CRBP-1 loss in G2/G3 ovarian carcinomas and increased apoptotic susceptibility to retinoids in CRBP-1-transfected-A2780 cells suggest CRBP-1 screening as a target to ensure efficacy of an adjuvant retinoid therapy. Copyright© 2014 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved.
JF - Anticancer research
AU - Doldo, Elena
AU - Costanza, Gaetana
AU - Ferlosio, Amedeo
AU - Passeri, Daniela
AU - Bernardini, Sergio
AU - Scioli, Maria Giovanna
AU - Mazzaglia, Donatella
AU - Agostinelli, Sara
AU - Del Bufalo, Donatella
AU - Czernobilsky, Bernard
AU - Orlandi, Augusto
AD - Anatomic Pathology, Department of Biomedicine and Prevention, Tor Vergata University of Rome, Rome, Italy. ; Department of Laboratory Medicine, Tor Vergata University of Rome, Rome, Italy. ; Experimental Chemotherapy Laboratory, Regina Elena National Cancer Institute, Rome, Italy. ; Patho-Lab Diagnostics, Ness-Zione, Israel. ; Anatomic Pathology, Department of Biomedicine and Prevention, Tor Vergata University of Rome, Rome, Italy orlandi@uniroma2.it.
Y1 - 2014/07//
PY - 2014
DA - July 2014
SP - 3303
EP - 3312
VL - 34
IS - 7
KW - Retinol-Binding Proteins, Cellular
KW - 0
KW - Vitamin A
KW - 11103-57-4
KW - Proteasome Endopeptidase Complex
KW - EC 3.4.25.1
KW - Index Medicus
KW - Retinol
KW - apoptosis
KW - ovarian tumor
KW - gynecological cancer
KW - retinol binding protein
KW - Humans
KW - Vitamin A -- pharmacology
KW - Aged
KW - Cell Line, Tumor
KW - Cell Growth Processes -- genetics
KW - Gene Expression Regulation, Neoplastic
KW - Promoter Regions, Genetic
KW - Tissue Array Analysis
KW - Proteasome Endopeptidase Complex -- metabolism
KW - DNA Methylation
KW - Aged, 80 and over
KW - Adult
KW - MCF-7 Cells
KW - Middle Aged
KW - Gene Dosage
KW - Immunohistochemistry
KW - Signal Transduction
KW - Female
KW - Ovarian Neoplasms -- metabolism
KW - Retinol-Binding Proteins, Cellular -- genetics
KW - Ovarian Neoplasms -- genetics
KW - Retinol-Binding Proteins, Cellular -- biosynthesis
KW - Ovarian Neoplasms -- drug therapy
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1542299828?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Anticancer+research&rft.atitle=CRBP-1+expression+in+ovarian+cancer%3A+a+potential+therapeutic+target.&rft.au=Doldo%2C+Elena%3BCostanza%2C+Gaetana%3BFerlosio%2C+Amedeo%3BPasseri%2C+Daniela%3BBernardini%2C+Sergio%3BScioli%2C+Maria+Giovanna%3BMazzaglia%2C+Donatella%3BAgostinelli%2C+Sara%3BDel+Bufalo%2C+Donatella%3BCzernobilsky%2C+Bernard%3BOrlandi%2C+Augusto&rft.aulast=Doldo&rft.aufirst=Elena&rft.date=2014-07-01&rft.volume=34&rft.issue=7&rft.spage=3303&rft.isbn=&rft.btitle=&rft.title=Anticancer+research&rft.issn=1791-7530&rft_id=info:doi/
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-08-21
N1 - Date created - 2014-07-01
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
ER -
TY - JOUR
T1 - Stable enhanced green fluorescent protein expression after differentiation and transplantation of reporter human induced pluripotent stem cells generated by AAVS1 transcription activator-like effector nucleases.
AN - 1542009553; 24833591
AB - Human induced pluripotent stem (hiPS) cell lines with tissue-specific or ubiquitous reporter genes are extremely useful for optimizing in vitro differentiation conditions as well as for monitoring transplanted cells in vivo. The adeno-associated virus integration site 1 (AAVS1) locus has been used as a "safe harbor" locus for inserting transgenes because of its open chromatin structure, which permits transgene expression without insertional mutagenesis. However, it is not clear whether targeted transgene expression at the AAVS1 locus is always protected from silencing when driven by various promoters, especially after differentiation and transplantation from hiPS cells. In this paper, we describe a pair of transcription activator-like effector nucleases (TALENs) that enable more efficient genome editing than the commercially available zinc finger nuclease at the AAVS1 site. Using these TALENs for targeted gene addition, we find that the cytomegalovirus-immediate early enhancer/chicken β-actin/rabbit β-globin (CAG) promoter is better than cytomegalovirus 7 and elongation factor 1α short promoters in driving strong expression of the transgene. The two independent AAVS1, CAG, and enhanced green fluorescent protein (EGFP) hiPS cell reporter lines that we have developed do not show silencing of EGFP either in undifferentiated hiPS cells or in randomly and lineage-specifically differentiated cells or in teratomas. Transplanting cardiomyocytes from an engineered AAVS1-CAG-EGFP hiPS cell line in a myocardial infarcted mouse model showed persistent expression of the transgene for at least 7 weeks in vivo. Our results show that high-efficiency targeting can be obtained with open-source TALENs and that careful optimization of the reporter and transgene constructs results in stable and persistent expression in vitro and in vivo.
©AlphaMed Press.
JF - Stem cells translational medicine
AU - Luo, Yongquan
AU - Liu, Chengyu
AU - Cerbini, Trevor
AU - San, Hong
AU - Lin, Yongshun
AU - Chen, Guokai
AU - Rao, Mahendra S
AU - Zou, Jizhong
AD - NIH Center for Regenerative Medicine, Laboratory of Stem Cell Biology, National Institute of Arthritis, Musculoskeletal and Skin Diseases, Bethesda, Maryland, USA; Center for Molecular Medicine, Division of Intramural Research, National Heart, Lung, and Blood Institute, Bethesda, Maryland, USA. ; NIH Center for Regenerative Medicine, Laboratory of Stem Cell Biology, National Institute of Arthritis, Musculoskeletal and Skin Diseases, Bethesda, Maryland, USA; Center for Molecular Medicine, Division of Intramural Research, National Heart, Lung, and Blood Institute, Bethesda, Maryland, USA zouj2@mail.nih.gov.
Y1 - 2014/07//
PY - 2014
DA - July 2014
SP - 821
EP - 835
VL - 3
IS - 7
SN - 2157-6564, 2157-6564
KW - Actins
KW - 0
KW - Peptide Elongation Factor 1
KW - enhanced green fluorescent protein
KW - Green Fluorescent Proteins
KW - 147336-22-9
KW - NADH Dehydrogenase
KW - EC 1.6.99.3
KW - Deoxyribonucleases
KW - EC 3.1.-
KW - Index Medicus
KW - Differentiation
KW - Transplantation
KW - Human induced pluripotent stem cells
KW - Transcription activator-like effector nuclease (TALEN)
KW - Genome editing
KW - AAVS1
KW - Myocardial Infarction -- pathology
KW - Animals
KW - Myocardial Infarction -- surgery
KW - Cell Lineage
KW - Myocardium -- pathology
KW - Cell Tracking
KW - Gene Silencing
KW - Humans
KW - Myocardial Infarction -- genetics
KW - Disease Models, Animal
KW - Mice
KW - Myocytes, Cardiac -- pathology
KW - Myocardium -- metabolism
KW - Myocytes, Cardiac -- transplantation
KW - NADH Dehydrogenase -- genetics
KW - Myocardial Infarction -- metabolism
KW - Promoter Regions, Genetic
KW - Actins -- genetics
KW - Cells, Cultured
KW - Cytomegalovirus -- genetics
KW - NADH Dehydrogenase -- biosynthesis
KW - Gene Expression Regulation
KW - Time Factors
KW - Peptide Elongation Factor 1 -- genetics
KW - Myocytes, Cardiac -- metabolism
KW - Induced Pluripotent Stem Cells -- metabolism
KW - Transfection -- methods
KW - Green Fluorescent Proteins -- biosynthesis
KW - Transduction, Genetic
KW - Induced Pluripotent Stem Cells -- transplantation
KW - Genes, Reporter
KW - Dependovirus -- genetics
KW - Cell Differentiation
KW - Deoxyribonucleases -- metabolism
KW - Green Fluorescent Proteins -- genetics
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Stem+cells+translational+medicine&rft.atitle=Stable+enhanced+green+fluorescent+protein+expression+after+differentiation+and+transplantation+of+reporter+human+induced+pluripotent+stem+cells+generated+by+AAVS1+transcription+activator-like+effector+nucleases.&rft.au=Luo%2C+Yongquan%3BLiu%2C+Chengyu%3BCerbini%2C+Trevor%3BSan%2C+Hong%3BLin%2C+Yongshun%3BChen%2C+Guokai%3BRao%2C+Mahendra+S%3BZou%2C+Jizhong&rft.aulast=Luo&rft.aufirst=Yongquan&rft.date=2014-07-01&rft.volume=3&rft.issue=7&rft.spage=821&rft.isbn=&rft.btitle=&rft.title=Stem+cells+translational+medicine&rft.issn=21576564&rft_id=info:doi/10.5966%2Fsctm.2013-0212
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-10-07
N1 - Date created - 2014-06-28
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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Stem Cells. 2008 Feb;26(2):496-504 [18024421]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.5966/sctm.2013-0212
ER -
TY - JOUR
T1 - Efficient generation of integration-free human induced pluripotent stem cells from keratinocytes by simple transfection of episomal vectors.
AN - 1542009230; 24904173
AB - Keratinocytes represent an easily accessible cell source for derivation of human induced pluripotent stem (hiPS) cells, reportedly achieving higher reprogramming efficiency than fibroblasts. However, most studies utilized a retroviral or lentiviral method for reprogramming of keratinocytes, which introduces undesirable transgene integrations into the host genome. Moreover, current protocols of generating integration-free hiPS cells from keratinocytes are mostly inefficient. In this paper, we describe a more efficient, simple-to-use, and cost-effective method for generating integration-free hiPS cells from keratinocytes. Our improved method using lipid-mediated transfection achieved a reprogramming efficiency of ∼0.14% on average. Keratinocyte-derived hiPS cells showed no integration of episomal vectors, expressed stem cell-specific markers and possessed potentials to differentiate into all three germ layers by in vitro embryoid body formation as well as in vivo teratoma formation. To our knowledge, this represents the most efficient method to generate integration-free hiPS cells from keratinocytes.
©AlphaMed Press.
JF - Stem cells translational medicine
AU - Piao, Yulan
AU - Hung, Sandy Shen-Chi
AU - Lim, Shiang Y
AU - Wong, Raymond Ching-Bong
AU - Ko, Minoru S H
AD - Laboratory of Genetics, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, USA; ; Laboratory of Genetics, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, USA; Centre for Eye Research Australia, Department of Ophthalmology, University of Melbourne, Australia; ; O'Brien Institute and University of Melbourne, Department of Surgery, St. Vincent's Hospital, Australia; ; Laboratory of Genetics, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, USA; Department of Systems Medicine, Sakaguchi Laboratory, Keio University School of Medicine, Shinjuku, Tokyo, Japan KoM@z7.keio.jp.
Y1 - 2014/07//
PY - 2014
DA - July 2014
SP - 787
EP - 791
VL - 3
IS - 7
SN - 2157-6564, 2157-6564
KW - Transcription Factors
KW - 0
KW - Index Medicus
KW - Lipid mediated transfection
KW - Episomal vectors
KW - Integration-free
KW - Keratinocytes
KW - Derivation of human induced pluripotent stem cells
KW - Embryoid Bodies -- metabolism
KW - Teratoma -- metabolism
KW - Teratoma -- genetics
KW - Coculture Techniques
KW - Animals
KW - Cellular Reprogramming
KW - Humans
KW - Cell Differentiation
KW - Mice
KW - Fibroblasts -- metabolism
KW - Feeder Cells
KW - Gene Expression Regulation, Developmental
KW - Induced Pluripotent Stem Cells -- metabolism
KW - Transfection -- methods
KW - Transcription Factors -- metabolism
KW - Plasmids -- genetics
KW - Genetic Vectors
KW - Keratinocytes -- metabolism
KW - Transcription Factors -- genetics
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Stem+cells+translational+medicine&rft.atitle=Efficient+generation+of+integration-free+human+induced+pluripotent+stem+cells+from+keratinocytes+by+simple+transfection+of+episomal+vectors.&rft.au=Piao%2C+Yulan%3BHung%2C+Sandy+Shen-Chi%3BLim%2C+Shiang+Y%3BWong%2C+Raymond+Ching-Bong%3BKo%2C+Minoru+S+H&rft.aulast=Piao&rft.aufirst=Yulan&rft.date=2014-07-01&rft.volume=3&rft.issue=7&rft.spage=787&rft.isbn=&rft.btitle=&rft.title=Stem+cells+translational+medicine&rft.issn=21576564&rft_id=info:doi/10.5966%2Fsctm.2013-0036
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-10-07
N1 - Date created - 2014-06-28
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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Fertil Steril. 2012 Jun;97(6):1250-9 [22656305]
Stem Cells Transl Med. 2013 Sep;2(9):715-25 [23884641]
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Science. 2009 May 8;324(5928):797-801 [19325077]
PLoS One. 2009;4(9):e7076 [19763270]
Nat Biotechnol. 2009 Nov;27(11):1033-7 [19826408]
Cell Res. 2011 Mar;21(3):518-29 [21243013]
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Biochem Biophys Res Commun. 2012 May 25;422(1):75-9 [22560904]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.5966/sctm.2013-0036
ER -
TY - JOUR
T1 - Mechanism and Significance of Cell Type-Dependent Neutralization of Flaviviruses
AN - 1540231965; 20124367
AB - The production of neutralizing antibodies (NAbs) is a correlate of protection for many human vaccines, including currently licensed vaccines against flaviviruses. NAbs are typically measured using a plaque reduction neutralization test (PRNT). Despite its extensive use, parameters that impact the performance of the PRNT have not been investigated from a mechanistic perspective. The results of a recent phase IIb clinical trial of a tetravalent dengue virus (DENV) vaccine suggest that NAbs, as measured using a PRNT performed with Vero cells, do not correlate with protection. This surprising finding highlights the importance of understanding how well the PRNT captures the complexity of the NAb response to DENV. In this study, we demonstrated that the structural heterogeneity of flaviviruses arising from inefficient virion maturation impacts the results of neutralization assays in a cell type-dependent manner. Neutralization titers of several monoclonal antibodies were significantly reduced when assayed on Vero cells compared to Raji cells expressing DC-SIGNR. This pattern can be explained by differences in the efficiency with which partially mature flaviviruses attach to each cell type, rather than a differential capacity of antibody to block infection. Vero cells are poorly permissive to the fraction of virions that are most sensitive to neutralization. Analysis of sera from recipients of live-attenuated monovalent DENV vaccine candidates revealed a strong correlation between the sensitivity of serum antibodies to the maturation state of DENV and cell type-dependent patterns of neutralization. Cross-reactive patterns of neutralization may be underrepresented by the "gold-standard" PRNT that employs Vero cells. IMPORTANCE Cell type-dependent patterns of neutralization describe a differential capacity of antibodies to inhibit virus infection when assayed on multiple cellular substrates. In this study, we established a link between antibodies that neutralize infection in a cell type-dependent fashion and those sensitive to the maturation state of the flavivirus virion. We demonstrated that cell type-dependent neutralization reflects a differential capacity to measure neutralization of viruses that are incompletely mature. Partially mature virions that most efficiently bind maturation state-sensitive antibodies are poorly represented by assays typically used in support of flavivirus vaccine development. The selection of cellular substrate for neutralization assays may significantly impact evaluation of the neutralization potency of the polyclonal response. These data suggest that current assays do not adequately capture the full complexity of the neutralizing antibody response and may hinder the identification of correlates of protection following flavivirus vaccination.
JF - Journal of Virology
AU - Mukherjee, Swati
AU - Dowd, Kimberly A
AU - Manhart, Carolyn J
AU - Ledgerwood, Julie E
AU - Durbin, Anna P
AU - Whitehead, Stephen S
AU - Pierson, Theodore C
AD - Viral Pathogenesis Section, Laboratory of Viral Diseases, National Institutes of Health, Bethesda, Maryland, USA, piersontc@mail.nih.gov.
Y1 - 2014/07//
PY - 2014
DA - July 2014
SP - 7210
EP - 7220
PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL - 88
IS - 13
SN - 0022-538X, 0022-538X
KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Virology & AIDS Abstracts
KW - Dengue virus
KW - Virions
KW - Virology
KW - Data processing
KW - Vero cells
KW - Monoclonal antibodies
KW - Viruses
KW - Disease control
KW - Antibody response
KW - Infection
KW - Clinical trials
KW - Vaccination
KW - Flavivirus
KW - Antibodies
KW - Viral diseases
KW - Substrate preferences
KW - Sexual maturity
KW - Plaques
KW - Vaccines
KW - Q1 08484:Species interactions: parasites and diseases
KW - V 22320:Replication
KW - Q5 08524:Public health, medicines, dangerous organisms
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Virology&rft.atitle=Mechanism+and+Significance+of+Cell+Type-Dependent+Neutralization+of+Flaviviruses&rft.au=Mukherjee%2C+Swati%3BDowd%2C+Kimberly+A%3BManhart%2C+Carolyn+J%3BLedgerwood%2C+Julie+E%3BDurbin%2C+Anna+P%3BWhitehead%2C+Stephen+S%3BPierson%2C+Theodore+C&rft.aulast=Mukherjee&rft.aufirst=Swati&rft.date=2014-07-01&rft.volume=88&rft.issue=13&rft.spage=7210&rft.isbn=&rft.btitle=&rft.title=Journal+of+Virology&rft.issn=0022538X&rft_id=info:doi/10.1128%2FJVI.03690-13
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-01
N1 - Number of references - 63
N1 - Last updated - 2016-10-12
N1 - SubjectsTermNotLitGenreText - Virology; Antibodies; Substrate preferences; Viral diseases; Monoclonal antibodies; Sexual maturity; Viruses; Disease control; Vaccines; Virions; Data processing; Vero cells; Plaques; Antibody response; Infection; Vaccination; Clinical trials; Dengue virus; Flavivirus
DO - http://dx.doi.org/10.1128/JVI.03690-13
ER -
TY - JOUR
T1 - PET imaging of neuroinflammation in a rat traumatic brain injury model with radiolabeled TSPO ligand DPA-714
AN - 1540229425; 20130323
AB - Purpose: The inflammatory response in injured brain parenchyma after traumatic brain injury (TBI) is crucial in the pathological process. In order to follow microglia activation and neuroinflammation after TBI, we performed PET imaging in a rat model of TBI using super(18)F-labeled DPA-714, a ligand of the 18-kDa translocator protein (TSPO). Methods: TBI was induced in male SD rats by a controlled cortical impact. The success of the TBI model was confirmed by MRI. [ super(18)F]DPA-714 was synthesized using a slightly modified TRACERLab FX-FN module and an automated procedure. In vivo PET imaging was performed at different time points after surgery using an Inveon small-animal PET scanner. The specificity of [ super(18)F]DPA-714 was confirmed by a displacement study with an unlabeled competitive TSPO ligand, PK11195. Ex vivo autoradiography as well as immunofluorescence staining was carried out to confirm the in vivo PET results. Results: Both in vivo T sub(2)-weighted MR images and ex vivo TTC staining results revealed successful establishment of the TBI model. Compared with the sham-treated group, [ super(18)F]DPA-714 uptake was significantly higher in the injured brain area on PET images. Increased lesion-to-normal ratios of [ super(18)F]DPA-714 were observed in the brain of TBI rats on day 2 after surgery. Ratios peaked around day 6 (2.65 plus or minus 0.36) and then decreased gradually to nearly normal levels on day 28. The displacement study using PK11195 confirmed the specific binding of [ super(18)F]DPA-714 to TSPO. The results of ex vivo autoradiography were consistent with in vivo PET results. Immunofluorescence staining showed the time course of TSPO expression after TBI and the temporal and the spatial distribution of microglia in the damaged brain area. Conclusion: TSPO-targeted PET using [ super(18)F]DPA-714 as the imaging probe can be used to dynamically monitor the inflammatory response after TBI in a noninvasive manner. This method will not only facilitate a better understanding of the inflammatory process after TBI, but also provide a useful in vivo monitoring strategy for antiinflammation therapy of TBI.
JF - European Journal of Nuclear Medicine and Molecular Imaging
AU - Wang, Yu
AU - Yue, Xuyi
AU - Kiesewetter, Dale O
AU - Niu, Gang
AU - Teng, Gaojun
AU - Chen, Xiaoyuan
AD - Jiangsu Key Laboratory of Molecular Imaging and Functional Imaging, Department of Radiology, Zhongda Hospital, Medical School of Southeast University, Nanjing, 210009, China, niug@mail.nih.gov
Y1 - 2014/07//
PY - 2014
DA - Jul 2014
SP - 1440
EP - 1449
PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL - 41
IS - 7
SN - 1619-7070, 1619-7070
KW - CSA Neurosciences Abstracts; Biotechnology and Bioengineering Abstracts
KW - Parenchyma
KW - Neuroimaging
KW - Spatial distribution
KW - Magnetic resonance imaging
KW - Brain
KW - Animal models
KW - Probes
KW - Immunofluorescence
KW - Autoradiography
KW - Microglia
KW - Inflammation
KW - Surgery
KW - Positron emission tomography
KW - Nuclear medicine
KW - Traumatic brain injury
KW - W 30910:Imaging
KW - N3 11145:Methodology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+Journal+of+Nuclear+Medicine+and+Molecular+Imaging&rft.atitle=PET+imaging+of+neuroinflammation+in+a+rat+traumatic+brain+injury+model+with+radiolabeled+TSPO+ligand+DPA-714&rft.au=Wang%2C+Yu%3BYue%2C+Xuyi%3BKiesewetter%2C+Dale+O%3BNiu%2C+Gang%3BTeng%2C+Gaojun%3BChen%2C+Xiaoyuan&rft.aulast=Wang&rft.aufirst=Yu&rft.date=2014-07-01&rft.volume=41&rft.issue=7&rft.spage=1440&rft.isbn=&rft.btitle=&rft.title=European+Journal+of+Nuclear+Medicine+and+Molecular+Imaging&rft.issn=16197070&rft_id=info:doi/10.1007%2Fs00259-014-2727-5
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-01
N1 - Number of references - 34
N1 - Last updated - 2014-10-30
N1 - SubjectsTermNotLitGenreText - Parenchyma; Neuroimaging; Spatial distribution; Magnetic resonance imaging; Probes; Animal models; Brain; Immunofluorescence; Microglia; Autoradiography; Inflammation; Surgery; Positron emission tomography; Nuclear medicine; Traumatic brain injury
DO - http://dx.doi.org/10.1007/s00259-014-2727-5
ER -
TY - JOUR
T1 - Idiosyncratic drug-induced liver injury is associated with substantial morbidity and mortality within 6 months from onset.
AN - 1539711230; 24681128
AB - Little is known about the incidence of drug-induced liver injury (DILI) and risk factors for adverse outcomes. We evaluated short-term outcomes of a large cohort of patients with DILI enrolled in an ongoing multicenter prospective study.
Data were collected from 660 adults with definite, highly likely, or probable DILI. Regression methods were used to identify risk factors for early liver-related death or liver transplantation and chronic liver injury. Patients' median age was 51.4 years; 59.5% were female and 59.1% required hospitalization. Within 6 months of DILI onset, 30 patients received liver transplants (4.5%; 95% confidence interval [CI], 3.0%-6.1%) and 32 died (5%; 95% CI, 3.2%-6.5%); 53% of the deaths were liver related. Asian race, absence of itching, lung disease, low serum albumin levels, low platelet counts, and high serum levels of alanine aminotransferase and total bilirubin at presentation were independent risk factors for reduced times to liver-related death or liver transplantation (C-statistic = 0.87). At 6 months after DILI onset, 18.9% of the 598 evaluable subjects had persistent liver damage. African-American race, higher serum levels of alkaline phosphatase, and prior heart disease or malignancy requiring treatment were independent risk factors for chronic DILI (C-statistic = 0.71). Nearly 1 in 10 patients die or undergo liver transplantation within 6 months of DILI onset and nearly 1 in 5 of the remaining patients have evidence of persistent liver injury at 6 months. The profile of liver injury at presentation, initial severity, patient's race, and medical comorbidities are important determinants of the likelihood of death/transplantation or persistent liver injury within 6 months.
Copyright © 2014 AGA Institute. Published by Elsevier Inc. All rights reserved.
JF - Gastroenterology
AU - Fontana, Robert J
AU - Hayashi, Paul H
AU - Gu, Jiezhun
AU - Reddy, K Rajender
AU - Barnhart, Huiman
AU - Watkins, Paul B
AU - Serrano, Jose
AU - Lee, William M
AU - Chalasani, Naga
AU - Stolz, Andrew
AU - Davern, Timothy
AU - Talwakar, Jayant A
AU - DILIN Network
AD - Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan. Electronic address: rfontana@med.umich.edu. ; University of North Carolina, Chapel Hill, North Carolina. ; Duke Clinical Research Institute, Durham, North Carolina. ; Division of Gastroenterology and Hepatology, University of Pennsylvania, Philadelphia, Pennsylvania. ; Liver Disease Research Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland. ; Division of Digestive and Liver Diseases, University of Texas Southwestern Medical Center, Dallas, Texas. ; Department of Medicine, Indiana University, Indianapolis, Indiana. ; University of Southern California, Los Angeles, California. ; California Pacific Medical Center, San Francisco, California. ; Mayo Clinic, Rochester, Minnesota. ; DILIN Network
Y1 - 2014/07//
PY - 2014
DA - July 2014
SP - 96
EP - 108.e4
VL - 147
IS - 1
KW - Abridged Index Medicus
KW - Index Medicus
KW - Causality
KW - Transplantation
KW - Acute Liver Failure
KW - Hepatotoxicity
KW - United States
KW - Prospective Studies
KW - Survival Rate
KW - Humans
KW - Cohort Studies
KW - Adult
KW - Aged
KW - Middle Aged
KW - Time Factors
KW - Male
KW - Liver Transplantation
KW - Female
KW - Comorbidity
KW - Chemical and Drug Induced Liver Injury -- mortality
KW - Chemical and Drug Induced Liver Injury -- epidemiology
KW - Chemical and Drug Induced Liver Injury -- surgery
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gastroenterology&rft.atitle=Idiosyncratic+drug-induced+liver+injury+is+associated+with+substantial+morbidity+and+mortality+within+6+months+from+onset.&rft.au=Fontana%2C+Robert+J%3BHayashi%2C+Paul+H%3BGu%2C+Jiezhun%3BReddy%2C+K+Rajender%3BBarnhart%2C+Huiman%3BWatkins%2C+Paul+B%3BSerrano%2C+Jose%3BLee%2C+William+M%3BChalasani%2C+Naga%3BStolz%2C+Andrew%3BDavern%2C+Timothy%3BTalwakar%2C+Jayant+A%3BDILIN+Network&rft.aulast=Fontana&rft.aufirst=Robert&rft.date=2014-07-01&rft.volume=147&rft.issue=1&rft.spage=96&rft.isbn=&rft.btitle=&rft.title=Gastroenterology&rft.issn=1528-0012&rft_id=info:doi/10.1053%2Fj.gastro.2014.03.045
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-09-30
N1 - Date created - 2014-06-23
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Hepatology. 2001 Jan;33(1):123-30 [11124828]
Hepatology. 2002 Aug;36(2):451-5 [12143055]
Ann Intern Med. 2002 Dec 17;137(12):947-54 [12484709]
Clin Gastroenterol Hepatol. 2004 Mar;2(3):262-5 [15017611]
Liver Transpl. 2004 Aug;10(8):1018-23 [15390328]
Cleve Clin J Med. 1999 Apr;66(4):239-45 [10199060]
Gut. 1999 May;44(5):731-5 [10205214]
J Clin Gastroenterol. 2005 Jan;39(1):64-7 [15599214]
Hepatology. 2005 Aug;42(2):481-9 [16025496]
Gastroenterology. 2005 Aug;129(2):512-21 [16083708]
Hepatology. 2006 Dec;44(6):1581-8 [17133470]
Am J Gastroenterol. 2007 Mar;102(3):558-62; quiz 693 [17156142]
Aliment Pharmacol Ther. 2007 Jul 1;26(1):79-85 [17555424]
Gastroenterology. 2008 Dec;135(6):1924-34, 1934.e1-4 [18955056]
Drug Saf. 2009;32(1):55-68 [19132805]
J Hepatol. 2009 Mar;50(3):511-7 [19155082]
Clin Gastroenterol Hepatol. 2010 May;8(5):463-70 [20170750]
Hepatology. 2010 Jun;51(6):2117-26 [20512999]
Hepatology. 2010 Aug;52(2):730-42 [20564754]
Hepatology. 2010 Dec;52(6):2065-76 [20949552]
Gastroenterology. 2011 Nov;141(5):1665-72.e1-9 [21855518]
Dig Dis Sci. 2013 Sep;58(9):2682-90 [23625293]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1053/j.gastro.2014.03.045
ER -
TY - JOUR
T1 - Tofacitinib suppresses antibody responses to protein therapeutics in murine hosts.
AN - 1539475996; 24890727
AB - Immunogenicity remains the "Achilles' heel" of protein-based therapeutics. Anti-drug Abs produced in response to protein therapeutics can severely limit both the safety and efficacy of this expanding class of agent. In this article, we report that monotherapy of mice with tofacitinib (the JAK inhibitor) quells Ab responses to an immunotoxin derived from the bacterial protein Pseudomonas exotoxin A, as well as to the model Ag keyhole limpet hemocyanin. Thousand-fold reductions in IgG1 titers to both Ags were observed 21 d post immunization. In fact, suppression was evident for all IgG isotypes and IgM. A reduction in IgG3 production was also noted with a thymus-independent type II Ag. Mechanistic investigations revealed that tofacitinib treatment led to reduced numbers of CD127+ pro-B cells. Furthermore, we observed fewer germinal center B cells and the impaired formation of germinal centers of mice treated with tofacitinib. Because normal Ig levels were still present during tofacitinib treatment, this agent specifically reduced anti-drug Abs, thus preserving the potential efficacy of biological therapeutics, including those used as cancer therapeutics.
JF - Journal of immunology (Baltimore, Md. : 1950)
AU - Onda, Masanori
AU - Ghoreschi, Kamran
AU - Steward-Tharp, Scott
AU - Thomas, Craig
AU - O'Shea, John J
AU - Pastan, Ira H
AU - FitzGerald, David J
AD - Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892; ondam@mail.nih.gov fitzgerd@helix.nih.gov. ; Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892; and. ; Division of Pre-Clinical Innovation, National Center for Advancing Translational Sciences, National Institutes of Health, Bethesda, MD 20892. ; Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892;
Y1 - 2014/07/01/
PY - 2014
DA - 2014 Jul 01
SP - 48
EP - 55
VL - 193
IS - 1
KW - Bacterial Toxins
KW - 0
KW - Exotoxins
KW - Immunoglobulin G
KW - Immunoglobulin M
KW - Immunotoxins
KW - Piperidines
KW - Protein Kinase Inhibitors
KW - Pyrimidines
KW - Pyrroles
KW - Virulence Factors
KW - tofacitinib
KW - 87LA6FU830
KW - Hemocyanin
KW - 9013-72-3
KW - ADP Ribose Transferases
KW - EC 2.4.2.-
KW - toxA protein, Pseudomonas aeruginosa
KW - EC 2.4.2.31
KW - Janus Kinases
KW - EC 2.7.10.2
KW - keyhole-limpet hemocyanin
KW - FV4Y0JO2CX
KW - Abridged Index Medicus
KW - Index Medicus
KW - Animals
KW - Janus Kinases -- antagonists & inhibitors
KW - Janus Kinases -- immunology
KW - Immunoglobulin M -- immunology
KW - Mice
KW - B-Lymphocytes -- immunology
KW - Germinal Center -- immunology
KW - Mice, Inbred BALB C
KW - Immunoglobulin G -- immunology
KW - Female
KW - Virulence Factors -- pharmacology
KW - Piperidines -- pharmacology
KW - Exotoxins -- pharmacology
KW - Protein Kinase Inhibitors -- pharmacology
KW - Hemocyanin -- pharmacology
KW - Pyrimidines -- pharmacology
KW - Bacterial Toxins -- pharmacology
KW - Pyrroles -- pharmacology
KW - Immunotoxins -- pharmacology
KW - ADP Ribose Transferases -- pharmacology
KW - Antibody Formation -- drug effects
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-08-18
N1 - Date created - 2014-06-21
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.4049/jimmunol.1400063
ER -
TY - JOUR
T1 - Exceptionally potent neutralization of Middle East respiratory syndrome coronavirus by human monoclonal antibodies.
AN - 1539475796; 24789777
AB - The recently discovered Middle East respiratory syndrome coronavirus (MERS-CoV) continues to infect humans, with high mortality. Specific, highly effective therapeutics and vaccines against the MERS-CoV are urgently needed to save human lives and address the pandemic concerns. We identified three human monoclonal antibodies (MAbs), m336, m337, and m338, targeting the receptor (CD26/DPP4) binding domain (RBD) of the MERS-CoV spike glycoprotein from a very large naïve-antibody library (containing ∼10(11) antibodies). They bound with high affinity: equilibrium dissociation constants for the three MAbs were equal to 4.2, 9.3, and 15 nM, respectively, as measured by Biacore for Fabs binding to RBD. The avidity for IgG1 m336, m337, and m338 was even higher: 99, 820, and 560 pM, respectively. The antibodies bound to overlapping epitopes that overlap the receptor binding site on the RBD as suggested by competition experiments and further supported by site-directed mutagenesis of the RBD and a docking model of the m336-RBD complex. The highest-affinity MAb, m336, neutralized both pseudotyped and live MERS-CoV with exceptional potency, 50% neutralization at 0.005 and 0.07 μg/ml, respectively, likely by competing with DPP4 for binding to the S glycoprotein. The exceptionally high neutralization activity of these antibodies and especially m336 suggests that they have great potential for prophylaxis and therapy of MERS-CoV infection in humans and as a tool for development of vaccine immunogens. The rapid identification (within several weeks) of potent MAbs suggests a possibility to use the new large antibody library and related methodology for a quick response to the public threat resulting from emerging coronaviruses. Importance: A novel human coronavirus, the Middle East respiratory syndrome coronavirus (MERS-CoV), was found to infect humans with a high mortality rate in 2012, just 1 decade after the appearance of the first highly pathogenic coronavirus, severe acute respiratory syndrome coronavirus (SARS-CoV). There are no effective therapeutics available. It is highly desirable to find an approach for rapidly developing potent therapeutics against MERS-CoV, which not only can be implemented for MERS treatment but also can help to develop a platform strategy to combat future emerging coronaviruses. We report here the identification of human monoclonal antibodies (MAbs) from a large nonimmune antibody library that target MERS-CoV. One of the antibodies, m336, neutralized the virus with exceptional potency. It therefore may have great potential as a candidate therapeutic and as a reagent to facilitate the development of vaccines against MERS-CoV.
Copyright © 2014, American Society for Microbiology. All Rights Reserved.
JF - Journal of virology
AU - Ying, Tianlei
AU - Du, Lanying
AU - Ju, Tina W
AU - Prabakaran, Ponraj
AU - Lau, Candy C Y
AU - Lu, Lu
AU - Liu, Qi
AU - Wang, Lili
AU - Feng, Yang
AU - Wang, Yanping
AU - Zheng, Bo-Jian
AU - Yuen, Kwok-Yung
AU - Jiang, Shibo
AU - Dimitrov, Dimiter S
AD - Protein Interactions Group, Laboratory of Experimental Immunology, Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Frederick, Maryland, USA yingt@mail.nih.gov dimiter.dimitrov@nih.gov. ; Lindsley F. Kimball Research Institute, New York Blood Center, New York, New York, USA. ; Protein Interactions Group, Laboratory of Experimental Immunology, Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Frederick, Maryland, USA. ; Protein Interactions Group, Laboratory of Experimental Immunology, Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Frederick, Maryland, USA Basic Science Program, Leidos Biomedical Research, Inc., Frederick National Laboratory, Frederick, Maryland, USA. ; Department of Microbiology, University of Hong Kong, Pokfulam, Hong Kong. ; Key Laboratory of Medical Molecular Virology of Ministries of Education and Health, Shanghai Medical College and Institute of Medical Microbiology, Fudan University, Shanghai, China. ; Basic Science Program, Leidos Biomedical Research, Inc., Frederick National Laboratory, Frederick, Maryland, USA. ; Lindsley F. Kimball Research Institute, New York Blood Center, New York, New York, USA Key Laboratory of Medical Molecular Virology of Ministries of Education and Health, Shanghai Medical College and Institute of Medical Microbiology, Fudan University, Shanghai, China.
Y1 - 2014/07//
PY - 2014
DA - July 2014
SP - 7796
EP - 7805
VL - 88
IS - 14
KW - Antibodies, Monoclonal
KW - 0
KW - Antibodies, Neutralizing
KW - Antibodies, Viral
KW - Immunoglobulin G
KW - Peptide Library
KW - Index Medicus
KW - Mutagenesis, Site-Directed
KW - Molecular Docking Simulation
KW - Kinetics
KW - Immunoglobulin G -- isolation & purification
KW - Humans
KW - Neutralization Tests
KW - Antibody Affinity
KW - Immunoglobulin G -- immunology
KW - Protein Binding
KW - Epitope Mapping
KW - Binding Sites
KW - Antibodies, Viral -- isolation & purification
KW - Antibodies, Monoclonal -- isolation & purification
KW - Coronavirus -- immunology
KW - Antibodies, Neutralizing -- immunology
KW - Antibodies, Viral -- immunology
KW - Antibodies, Neutralizing -- isolation & purification
KW - Antibodies, Monoclonal -- immunology
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1539475796?accountid=14244
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-08-22
N1 - Date created - 2014-06-21
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Blood. 2001 Feb 15;97(4):1023-6 [11159532]
Lancet Infect Dis. 2014 Feb;14(2):140-5 [24355866]
Nat Rev Microbiol. 2004 Sep;2(9):695-703 [15372080]
Drugs. 1999 Aug;58(2):305-11; discussion 312-3 [10473022]
J Virol. 2006 Jan;80(2):891-9 [16378991]
Nat Rev Drug Discov. 2006 Feb;5(2):147-59 [16424916]
Nat Rev Immunol. 2006 May;6(5):343-57 [16622479]
Proc Natl Acad Sci U S A. 2007 Jul 17;104(29):12123-8 [17620608]
Nat Biotechnol. 2007 Dec;25(12):1421-34 [18066039]
Virology. 2008 Mar 15;372(2):357-71 [18054977]
Bioinformatics. 2008 Sep 1;24(17):1953-4 [18641403]
Expert Opin Biol Ther. 2009 Mar;9(3):355-68 [19216624]
PLoS Pathog. 2009 Oct;5(10):e1000642 [19888339]
J Virol. 2011 Nov;85(21):11048-57 [21865387]
Sci Transl Med. 2011 Oct 19;3(105):105ra103 [22013123]
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Immunity. 2012 Sep 21;37(3):412-25 [22999947]
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Virol Sin. 2013 Apr;28(2):71-80 [23575729]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1128/JVI.00912-14
ER -
TY - JOUR
T1 - Heme-related gene expression signatures of meat intakes in lung cancer tissues.
AN - 1537592543; 23681825
AB - Lung cancer causes more deaths worldwide than any other cancer. In addition to cigarette smoking, dietary factors may contribute to lung carcinogenesis. Epidemiologic studies, including the environment and genetics in lung cancer etiology (EAGLE), have reported increased consumption of red/processed meats to be associated with higher risk of lung cancer. Heme-iron toxicity may link meat intake with cancer. We investigated this hypothesis in meat-related lung carcinogenesis using whole genome expression. We measured genome-wide expression (HG-U133A) in 49 tumor and 42 non-involved fresh frozen lung tissues of 64 adenocarcinoma EAGLE patients. We studied gene expression profiles by high-versus-low meat consumption, with and without adjustment by sex, age, and smoking. Threshold for significance was a false discovery rate (FDR) ≤ 0.15. We studied whether the identified genes played a role in heme-iron related processes by means of manually curated literature search and gene ontology-based pathway analysis. We found that gene expression of 232 annotated genes in tumor tissue significantly distinguished lung adenocarcinoma cases who consumed above/below the median intake of fresh red meats (FDR = 0.12). Sixty-three (∼ 28%) of the 232 identified genes (12 expected by chance, P-value < 0.001) were involved in heme binding, absorption, transport, and Wnt signaling pathway (e.g., CYPs, TPO, HPX, HFE, SLCs, and WNTs). We also identified several genes involved in lipid metabolism (e.g., NCR1, TNF, and UCP3) and oxidative stress (e.g., TPO, SGK2, and MTHFR) that may be indirectly related to heme-toxicity. The study's results provide preliminary evidence that heme-iron toxicity might be one underlying mechanism linking fresh red meat intake and lung cancer.
© 2013 Wiley Periodicals, Inc.
JF - Molecular carcinogenesis
AU - Lam, Tram Kim
AU - Rotunno, Melissa
AU - Ryan, Brid M
AU - Pesatori, Angela C
AU - Bertazzi, Pier Alberto
AU - Spitz, Margaret
AU - Caporaso, Neil E
AU - Landi, Maria Teresa
AD - Cancer Prevention Fellowship Program, Office of Preventive Oncology, Genetic Epidemiology Branch, National Cancer Institute, National Institutes of Health (NIH), DHHS, Bethesda, Maryland; Division of Cancer Epidemiology and Genetics, Genetic Epidemiology Branch, National Cancer Institute, National Institutes of Health (NIH), DHHS, Bethesda, Maryland.
Y1 - 2014/07//
PY - 2014
DA - July 2014
SP - 548
EP - 556
VL - 53
IS - 7
KW - Iron, Dietary
KW - 0
KW - Heme
KW - 42VZT0U6YR
KW - Index Medicus
KW - heme-iron
KW - lung cancer
KW - gene expression
KW - Humans
KW - Aged
KW - Lipid Metabolism -- genetics
KW - Oxidative Stress -- genetics
KW - Feeding Behavior
KW - Risk
KW - Gene Expression Profiling
KW - Protein Transport -- genetics
KW - Risk Factors
KW - Case-Control Studies
KW - Middle Aged
KW - Protein Binding -- genetics
KW - Wnt Signaling Pathway -- genetics
KW - Diet
KW - Female
KW - Male
KW - Eating
KW - Carcinogenesis -- genetics
KW - Meat -- adverse effects
KW - Lung Neoplasms -- genetics
KW - Iron, Dietary -- adverse effects
KW - Adenocarcinoma -- genetics
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-08-19
N1 - Date created - 2014-06-18
N1 - Date revised - 2017-01-13
N1 - SuppNotes - Cited By:
Drug Metab Rev. 1993;25(1-2):49-152 [8449148]
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Bioinformatics. 2006 Apr 15;22(8):943-9 [16473874]
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Carcinogenesis. 2010 Dec;31(12):2091-6 [20935060]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1002/mc.22006
ER -
TY - JOUR
T1 - Impact of subdomain D1 of the short form S1b of the human prolactin receptor on its inhibitory action on the function of the long form of the receptor induced by prolactin.
AN - 1536685111; 24735798
AB - Long-form (LF) homodimers of the human prolactin receptor (PRLR) mediate prolactin's diverse actions. Short form S1b inhibits the LF function through heterodimerization. Reduced S1b/LF-ratio in breast cancer could contribute to tumor development/progression. Current work defines the structural and functional relevance of the D1 domain of S1b on its inhibitory function on prolactin-induced LF function.
Studies were conducted using mutagenesis, promoter/signaling analyses, bioluminescence resonance energy transfer (BRET) and molecular modeling approaches. Mutation of E69 in D1 S1b or adjacent residues at the receptor surface near to the binding pocket (S) causes loss of its inhibitory effect while mutations away from this region (A) or in the D2 domain display inhibitory action as the wild-type. All S1b mutants preserved prolactin-induced Jak2 activation. BRET reveals an increased affinity in D1 mutated S1b (S) homodimers in transfected cells stably expressing LF. In contrast, affinity in S1b homodimers with either D1 (A) or D2 mutations remained unchanged. This favors LF mediated signaling induced by prolactin. Molecular dynamics simulations show that mutations (S) elicit major conformational changes that propagate downward to the D1/D2 interface and change their relative orientation in the dimers.
These findings demonstrate the essential role of D1 on the S1b structure and its inhibitory action on prolactin-induced LF-mediated function. Major changes in receptor conformation and dimerization affinity are triggered by single mutations in critical regions of D1. Our structure-function/simulation studies provide a basis for modeling and design of small molecules to enhance inhibition of LF activation for potential use in breast cancer treatment.
Published by Elsevier B.V.
JF - Biochimica et biophysica acta
AU - Kang, J-H
AU - Hassan, S A
AU - Zhao, P
AU - Tsai-Morris, C H
AU - Dufau, M L
AD - Section on Molecular Endocrinology, Program on Developmental Endocrinology and Genetics, Eunice Kennedy Shriver National Institutes of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892-4510, USA. ; Center for Molecular Modeling, Division of Computational Bioscience, Center for Information Technology, National Institutes of Health, Bethesda, MD 20892-4510, USA. ; Section on Molecular Endocrinology, Program on Developmental Endocrinology and Genetics, Eunice Kennedy Shriver National Institutes of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892-4510, USA. Electronic address: dufaum@mail.nih.gov.
Y1 - 2014/07//
PY - 2014
DA - July 2014
SP - 2272
EP - 2280
VL - 1840
IS - 7
SN - 0006-3002, 0006-3002
KW - Protein Isoforms
KW - 0
KW - Receptors, Prolactin
KW - Prolactin
KW - 9002-62-4
KW - JAK2 protein, human
KW - EC 2.7.10.2
KW - Janus Kinase 2
KW - Index Medicus
KW - Structure/function
KW - Subdomain D1
KW - Human prolactin receptor
KW - Short and long form
KW - HEK293 Cells
KW - Humans
KW - Janus Kinase 2 -- chemistry
KW - Protein Binding
KW - Structure-Activity Relationship
KW - Promoter Regions, Genetic
KW - Signal Transduction -- genetics
KW - Janus Kinase 2 -- metabolism
KW - Protein Structure, Tertiary
KW - Mutation
KW - Cell Line
KW - Female
KW - Protein Conformation
KW - Breast Neoplasms -- genetics
KW - Receptors, Prolactin -- metabolism
KW - Prolactin -- chemistry
KW - Breast Neoplasms -- pathology
KW - Receptors, Prolactin -- chemistry
KW - Dimerization
KW - Breast Neoplasms -- therapy
KW - Prolactin -- genetics
KW - Receptors, Prolactin -- genetics
KW - Prolactin -- metabolism
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochimica+et+biophysica+acta&rft.atitle=Impact+of+subdomain+D1+of+the+short+form+S1b+of+the+human+prolactin+receptor+on+its+inhibitory+action+on+the+function+of+the+long+form+of+the+receptor+induced+by+prolactin.&rft.au=Kang%2C+J-H%3BHassan%2C+S+A%3BZhao%2C+P%3BTsai-Morris%2C+C+H%3BDufau%2C+M+L&rft.aulast=Kang&rft.aufirst=J-H&rft.date=2014-07-01&rft.volume=1840&rft.issue=7&rft.spage=2272&rft.isbn=&rft.btitle=&rft.title=Biochimica+et+biophysica+acta&rft.issn=00063002&rft_id=info:doi/10.1016%2Fj.bbagen.2014.04.006
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-08-18
N1 - Date created - 2014-06-16
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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Endocr Rev. 1998 Jun;19(3):225-68 [9626554]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.bbagen.2014.04.006
ER -
TY - JOUR
T1 - Persistent organochlorines and hypertensive disorders of pregnancy.
AN - 1536683829; 24742720
AB - Although there is indirect evidence to suggest that persistent organochlorines might increase risk of hypertensive disorders of pregnancy, there are no epidemiologic studies directly addressing this question. In this cohort study, sampled from the Collaborative Perinatal Project, 1933 women had complete data on organochlorine measurements, covariates, and pregnancy outcomes. Exposures to organochlorines were divided into quintiles, and levels were much higher in these patients recruited from 1959 to 1965 compared to levels in the general population at present. Among included women, 364 developed gestational hypertension (hypertension without proteinuria) and 131 developed preeclampsia (hypertension with proteinuria). We found essentially no association between serum DDE and total PCBs and risk of either gestational hypertension or preeclampsia. Results for other organochlorines showed varying patterns of results: DDT was inversely associated with risk of gestational hypertension (p for trend <0.001), B-Hexachlorocyclohexane and heptachlor epoxide were inversely related to gestational hypertension (p trend <0.01 and 0.10, respectively), dieldrin had a modestly positive association with gestational hypertension (p for trend=0.12), and hexachlorobenzene, trans-nonachlor, and oxychlordane yielded results close to the null. Hexachlorobenzene showed an inverse association with preeclampsia (p for trend <0.001). The study suggests that persistent organochlorines present at historically high level are not likely to increase the risk of hypertensive disorders of pregnancy, suggesting that other toxicants that have similar biologic effects are also unlikely to do so.
Copyright © 2014 Elsevier Inc. All rights reserved.
JF - Environmental research
AU - Savitz, David A
AU - Klebanoff, Mark A
AU - Wellenius, Gregory A
AU - Jensen, Elizabeth T
AU - Longnecker, Matthew P
AD - Department of Epidemiology, Brown University School of Public Health, Providence, Rhode Island, 47 George Street, Room 302, Providence, RI 02912, USA. Electronic address: david_savitz@brown.edu. ; Nationwide Children׳s Hospital, Departments of Pediatrics and Obstetrics and Gynecology, The Ohio State University College of Medicine, Columbus, Ohio, USA. Electronic address: Mark.Klebanoff@nationwidechildrens.org. ; Department of Epidemiology, Brown University School of Public Health, Providence, Rhode Island, 47 George Street, Room 302, Providence, RI 02912, USA. Electronic address: Gregory_wellenius@brown.edu. ; Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA. Electronic address: elizabeth.jensen@nih.gov. ; Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA. Electronic address: Longnec1@niehs.nih.gov.
Y1 - 2014/07//
PY - 2014
DA - July 2014
SP - 1
EP - 5
VL - 132
KW - Hydrocarbons, Chlorinated
KW - 0
KW - Index Medicus
KW - Organochlorines
KW - DDT
KW - PCBs
KW - Gestational hypertension
KW - Preeclampsia
KW - Young Adult
KW - Humans
KW - Cohort Studies
KW - Adolescent
KW - United States -- epidemiology
KW - Female
KW - Pregnancy
KW - Hydrocarbons, Chlorinated -- blood
KW - Hypertension, Pregnancy-Induced -- epidemiology
KW - Hypertension, Pregnancy-Induced -- etiology
KW - Hydrocarbons, Chlorinated -- adverse effects
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1536683829?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+research&rft.atitle=Persistent+organochlorines+and+hypertensive+disorders+of+pregnancy.&rft.au=Savitz%2C+David+A%3BKlebanoff%2C+Mark+A%3BWellenius%2C+Gregory+A%3BJensen%2C+Elizabeth+T%3BLongnecker%2C+Matthew+P&rft.aulast=Savitz&rft.aufirst=David&rft.date=2014-07-01&rft.volume=132&rft.issue=&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Environmental+research&rft.issn=1096-0953&rft_id=info:doi/10.1016%2Fj.envres.2014.03.020
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-08-12
N1 - Date created - 2014-06-14
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
N Engl J Med. 2010 Apr 8;362(14):1282-91 [20375405]
Best Pract Res Clin Obstet Gynaecol. 2011 Jun;25(3):329-42 [21349772]
Best Pract Res Clin Obstet Gynaecol. 2011 Aug;25(4):391-403 [21333604]
Epidemiology. 2012 May;23(3):386-92 [22370857]
J Obstet Gynaecol. 2012 Aug;32(6):512-7 [22779950]
Environ Health Perspect. 2012 Aug;120(8):1201-7 [22450153]
Matern Child Health J. 2013 Apr;17(3):545-55 [22544506]
Environ Int. 2013 May;55:1-8 [23454278]
Am J Obstet Gynecol. 2013 Oct;209(4):327.e1-17 [23711667]
Matern Child Health J. 2014 May;18(4):829-38 [23793484]
Lancet. 2001 Jul 14;358(9276):110-4 [11463412]
Epidemiology. 1995 Jul;6(4):450-4 [7548361]
J Anal Toxicol. 1996 Nov-Dec;20(7):528-36 [8934301]
BMJ. 2005 Mar 12;330(7491):565 [15743856]
Epidemiology. 2005 Sep;16(5):641-7 [16135940]
Epidemiology. 2007 Jul;18(4):461-8 [17568219]
Environ Health Perspect. 2009 Apr;117(4):568-73 [19440495]
Environ Health Perspect. 2009 Nov;117(11):1773-9 [20049131]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.envres.2014.03.020
ER -
TY - JOUR
T1 - A phase II study of dose-dense and dose-intense ABVD (ABVDDD-DI ) without consolidation radiotherapy in patients with advanced Hodgkin lymphoma.
AN - 1535632396; 24673727
AB - We explored activity and safety of a dose-dense/dose-intense adriamycin, bleomycin, vinblastine and dacarbazine regimen (ABVDDD-DI ) in 82 patients with advanced Hodgkin Lymphoma. Patients entered a two-stage Bryant-Day Phase II study to receive six cycles of ABVDDD-DI without consolidation radiotherapy. Cycles were supported with granulocyte colony-stimulating factor and delivered every 21 d; drugs were administered on days 1 and 11 at the same doses of standard ABVD except for doxorubicin (35 mg/m2; first four cycles only). Co-primary endpoints were complete response (CR) rate and severe acute cardiopulmonary toxicity; secondary endpoints were event-free (EFS) and disease-free survival (DFS). All patients received the four doxorubicin-intensified courses and 96% concluded all six cycles (82.3% within the intended 18 weeks). This translated into a 66.9% increase of received dose-intensity for doxorubicin and 31.8% for the other agents over standard ABVD. The CR rate was 95.1% (78/82) and 87.8% (72/82) achieved a metabolic CR after two cycles. Cardiopulmonary toxicity never exceeded grade 2 and affected 14.6% of patients. Most frequent toxicities were grade 4 neutropenia (10%) and anaemia (9%), grade 3 infection (17%) and grade 2 mucocutaneous changes (30%). Five-year EFS and DFS was 88.3% and 93.7%, respectively. ABVDDD-DI regimen was well-tolerated and ensured substantial CR and EFS rates without radiotherapy.
© 2014 John Wiley & Sons Ltd.
JF - British journal of haematology
AU - Russo, Filippo
AU - Corazzelli, Gaetano
AU - Frigeri, Ferdinando
AU - Capobianco, Gaetana
AU - Aloj, Luigi
AU - Volzone, Francesco
AU - De Chiara, Annarosaria
AU - Bonelli, Annamaria
AU - Gatani, Tindaro
AU - Marcacci, Gianpaolo
AU - Donnarumma, Daniela
AU - Becchimanzi, Cristina
AU - de Lutio, Elisabetta
AU - Ionna, Franco
AU - De Filippi, Rosaria
AU - Lastoria, Secondo
AU - Pinto, Antonello
AD - Haematology-Oncology and Stem Cell Transplantation Unit, National Cancer Institute, Fondazione 'G. Pascale', IRCCS, Naples, Italy.
Y1 - 2014/07//
PY - 2014
DA - July 2014
SP - 118
EP - 129
VL - 166
IS - 1
KW - Bleomycin
KW - 11056-06-7
KW - Vinblastine
KW - 5V9KLZ54CY
KW - Dacarbazine
KW - 7GR28W0FJI
KW - Doxorubicin
KW - 80168379AG
KW - Index Medicus
KW - doxorubicin
KW - dose intensity
KW - Hodgkin lymphoma
KW - radiotherapy
KW - ABVD
KW - Young Adult
KW - Humans
KW - Vinblastine -- therapeutic use
KW - Adult
KW - Treatment Outcome
KW - Vinblastine -- administration & dosage
KW - Dacarbazine -- administration & dosage
KW - Adolescent
KW - Bleomycin -- therapeutic use
KW - Male
KW - Doxorubicin -- adverse effects
KW - Drug Administration Schedule
KW - Neoplasm Staging
KW - Dose-Response Relationship, Drug
KW - Bleomycin -- administration & dosage
KW - Doxorubicin -- administration & dosage
KW - Dacarbazine -- adverse effects
KW - Bleomycin -- adverse effects
KW - Kaplan-Meier Estimate
KW - Dacarbazine -- therapeutic use
KW - Radiotherapy, Adjuvant
KW - Doxorubicin -- therapeutic use
KW - Follow-Up Studies
KW - Middle Aged
KW - Vinblastine -- adverse effects
KW - Female
KW - Hodgkin Disease -- pathology
KW - Hodgkin Disease -- drug therapy
KW - Antineoplastic Combined Chemotherapy Protocols -- administration & dosage
KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects
KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1535632396?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+journal+of+haematology&rft.atitle=A+phase+II+study+of+dose-dense+and+dose-intense+ABVD+%28ABVDDD-DI+%29+without+consolidation+radiotherapy+in+patients+with+advanced+Hodgkin+lymphoma.&rft.au=Russo%2C+Filippo%3BCorazzelli%2C+Gaetano%3BFrigeri%2C+Ferdinando%3BCapobianco%2C+Gaetana%3BAloj%2C+Luigi%3BVolzone%2C+Francesco%3BDe+Chiara%2C+Annarosaria%3BBonelli%2C+Annamaria%3BGatani%2C+Tindaro%3BMarcacci%2C+Gianpaolo%3BDonnarumma%2C+Daniela%3BBecchimanzi%2C+Cristina%3Bde+Lutio%2C+Elisabetta%3BIonna%2C+Franco%3BDe+Filippi%2C+Rosaria%3BLastoria%2C+Secondo%3BPinto%2C+Antonello&rft.aulast=Russo&rft.aufirst=Filippo&rft.date=2014-07-01&rft.volume=166&rft.issue=1&rft.spage=118&rft.isbn=&rft.btitle=&rft.title=British+journal+of+haematology&rft.issn=1365-2141&rft_id=info:doi/10.1111%2Fbjh.12862
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-08-10
N1 - Date created - 2014-06-13
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1111/bjh.12862
ER -
TY - JOUR
T1 - As a novel p53 direct target, bidirectional gene HspB2/αB-crystallin regulates the ROS level and Warburg effect.
AN - 1535631909; 24859470
AB - Many mammalian genes are composed of bidirectional gene pairs with the two genes separated by less than 1.0kb. The transcriptional regulation and function of these bidirectional genes remain largely unclear. Here, we report that bidirectional gene pair HspB2/αB-crystallin, both of which are members of the small heat shock protein gene family, is a novel direct target gene of p53. Two potential binding sites of p53 are present in the intergenic region of HspB2/αB-crystallin. p53 up-regulated the bidirectional promoter activities of HspB2/αB-crystallin. Actinomycin D (ActD), an activator of p53, induces the promoter and protein activities of HspB2/αB-crystallin. p53 binds to two p53 binding sites in the intergenic region of HspB2/αB-crystallin in vitro and in vivo. Moreover, the products of bidirectional gene pair HspB2/αB-crystallin regulate glucose metabolism, intracellular reactive oxygen species (ROS) level and the Warburg effect by affecting metabolic genes, including the synthesis of cytochrome c oxidase 2 (SCO2), hexokinase II (HK2), and TP53-induced glycolysis and apoptosis regulator (TIGAR). The ROS level and the Warburg effect are affected after the depletion of p53, HspB2 and αB-crystallin respectively. Finally, we show that both HspB2 and αB-crystallin are linked with human renal carcinogenesis. These findings provide novel insights into the role of p53 as a regulator of bidirectional gene pair HspB2/αB-crystallin-mediated ROS and the Warburg effect.
Copyright © 2014 Elsevier B.V. All rights reserved.
JF - Biochimica et biophysica acta
AU - Liu, Shuang
AU - Yan, Bin
AU - Lai, Weiwei
AU - Chen, Ling
AU - Xiao, Desheng
AU - Xi, Sichuan
AU - Jiang, Yiqun
AU - Dong, Xin
AU - An, Jing
AU - Chen, Xiang
AU - Cao, Ya
AU - Tao, Yongguang
AD - Center for Medicine Research, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China; Cancer Research Institute, Central South University, Changsha, Hunan 410078, China; Department of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China. ; Cancer Research Institute, Central South University, Changsha, Hunan 410078, China; Center for Molecular Imaging, Central South University, Changsha, Hunan 410078, China; Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Hunan 410078, China; Key Laboratory of Carcinogenesis, Ministry of Health, Hunan 410078, China. ; Department of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan 410078, China. ; Thoracic Oncology Section, Surgery Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, 20892 USA. ; State Key Laboratory of Medical Genetics, Central South University, Changsha, Hunan 4010078, China. ; Department of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China. ; Cancer Research Institute, Central South University, Changsha, Hunan 410078, China; Center for Molecular Imaging, Central South University, Changsha, Hunan 410078, China; Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Hunan 410078, China; Key Laboratory of Carcinogenesis, Ministry of Health, Hunan 410078, China. Electronic address: taoyong@csu.edu.cn.
Y1 - 2014/07//
PY - 2014
DA - July 2014
SP - 592
EP - 603
VL - 1839
IS - 7
SN - 0006-3002, 0006-3002
KW - HSP27 Heat-Shock Proteins
KW - 0
KW - HSPB2 protein, human
KW - Reactive Oxygen Species
KW - Tumor Suppressor Protein p53
KW - alpha-Crystallin B Chain
KW - Index Medicus
KW - Renal cell carcinoma
KW - p53
KW - HspB2
KW - αB-crystallin
KW - Bidirectional promoter
KW - Warburg effect
KW - Gene Expression Regulation, Neoplastic
KW - Reactive Oxygen Species -- metabolism
KW - Promoter Regions, Genetic
KW - Humans
KW - Protein Binding -- genetics
KW - Cell Line, Tumor
KW - Binding Sites -- genetics
KW - Transcriptional Activation
KW - Carcinoma, Renal Cell -- pathology
KW - HSP27 Heat-Shock Proteins -- metabolism
KW - Carcinoma, Renal Cell -- metabolism
KW - alpha-Crystallin B Chain -- metabolism
KW - HSP27 Heat-Shock Proteins -- genetics
KW - alpha-Crystallin B Chain -- genetics
KW - Tumor Suppressor Protein p53 -- genetics
KW - Tumor Suppressor Protein p53 -- metabolism
KW - Carcinoma, Renal Cell -- genetics
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-09-11
N1 - Date created - 2014-06-13
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.bbagrm.2014.05.017
ER -
TY - JOUR
T1 - Effects of Helicobacter pylori treatment on gastric cancer incidence and mortality in subgroups.
AN - 1535627557; 24925350
AB - Among 2258 Helicobacter pylori-seropositive subjects randomly assigned to receive one-time H. pylori treatment with amoxicillin-omeprazole or its placebo, we evaluated the 15-year effect of treatment on gastric cancer incidence and mortality in subgroups defined by age, baseline gastric histopathology, and post-treatment infection status. We used conditional logistic and Cox regressions for covariable adjustments in incidence and mortality analyses, respectively. Treatment was associated with a statistically significant decrease in gastric cancer incidence (odds ratio = 0.36; 95% confidence interval [CI] = 0.17 to 0.79) and mortality (hazard ratio = 0.26; 95% CI = 0.09 to 0.79) at ages 55 years and older and a statistically significant decrease in incidence among those with intestinal metaplasia or dysplasia at baseline (odds ratio = 0.56; 95% CI = 0.34 to 0.91). Treatment benefits for incidence and mortality among those with and without post-treatment infection were similar. Thus H. pylori treatment can benefit older members and those with advanced baseline histopathology, and benefits are present even with post-treatment infection, suggesting treatment can benefit an entire population, not just the young or those with mild histopathology. Published by Oxford University Press 2014.
JF - Journal of the National Cancer Institute
AU - Li, Wen-Qing
AU - Ma, Jun-Ling
AU - Zhang, Lian
AU - Brown, Linda M
AU - Li, Ji-You
AU - Shen, Lin
AU - Pan, Kai-Feng
AU - Liu, Wei-Dong
AU - Hu, Yuanreng
AU - Han, Zhong-Xiang
AU - Crystal-Mansour, Susan
AU - Pee, David
AU - Blot, William J
AU - Fraumeni, Joseph F
AU - You, Wei-Cheng
AU - Gail, Mitchell H
AD - Affiliations of authors: Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD (W-QL, JFF, MHG); Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Cancer Epidemiology, Peking University Cancer Hospital and Institute, Beijing, China (W-QL, J-LM, LZ, J-YL, LS, K-FP, W-CY); RTI International, Rockville, MD (LMB); Linqu County Public Health Bureau, Shandong, China (W-DL, Z-XH); Westat, Rockville, MD (SC-M); Information Management Services, Rockville, MD (DP); International Epidemiology Institute, Rockville, MD (WJB); Department of Medicine (Epidemiology), Vanderbilt University, Nashville, TN (WJB). ; Affiliations of authors: Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD (W-QL, JFF, MHG); Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Cancer Epidemiology, Peking University Cancer Hospital and Institute, Beijing, China (W-QL, J-LM, LZ, J-YL, LS, K-FP, W-CY); RTI International, Rockville, MD (LMB); Linqu County Public Health Bureau, Shandong, China (W-DL, Z-XH); Westat, Rockville, MD (SC-M); Information Management Services, Rockville, MD (DP); International Epidemiology Institute, Rockville, MD (WJB); Department of Medicine (Epidemiology), Vanderbilt University, Nashville, TN (WJB). gailm@mail.nih.gov weichengyou@yahoo.com.
Y1 - 2014/07//
PY - 2014
DA - July 2014
VL - 106
IS - 7
KW - Anti-Bacterial Agents
KW - 0
KW - Amoxicillin
KW - 804826J2HU
KW - Omeprazole
KW - KG60484QX9
KW - Index Medicus
KW - Randomized Controlled Trials as Topic
KW - Odds Ratio
KW - Age Factors
KW - Humans
KW - Aged
KW - Drug Therapy, Combination
KW - Amoxicillin -- therapeutic use
KW - Logistic Models
KW - Adult
KW - Treatment Outcome
KW - Omeprazole -- therapeutic use
KW - Incidence
KW - Follow-Up Studies
KW - Middle Aged
KW - Female
KW - Male
KW - Proportional Hazards Models
KW - Stomach Neoplasms -- microbiology
KW - Anti-Bacterial Agents -- therapeutic use
KW - Precancerous Conditions -- microbiology
KW - Stomach Neoplasms -- mortality
KW - Helicobacter Infections -- drug therapy
KW - Helicobacter Infections -- complications
KW - Helicobacter pylori -- drug effects
KW - Precancerous Conditions -- drug therapy
KW - Stomach Neoplasms -- prevention & control
KW - Stomach Neoplasms -- epidemiology
KW - Precancerous Conditions -- pathology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=Effects+of+Helicobacter+pylori+treatment+on+gastric+cancer+incidence+and+mortality+in+subgroups.&rft.au=Li%2C+Wen-Qing%3BMa%2C+Jun-Ling%3BZhang%2C+Lian%3BBrown%2C+Linda+M%3BLi%2C+Ji-You%3BShen%2C+Lin%3BPan%2C+Kai-Feng%3BLiu%2C+Wei-Dong%3BHu%2C+Yuanreng%3BHan%2C+Zhong-Xiang%3BCrystal-Mansour%2C+Susan%3BPee%2C+David%3BBlot%2C+William+J%3BFraumeni%2C+Joseph+F%3BYou%2C+Wei-Cheng%3BGail%2C+Mitchell+H&rft.aulast=Li&rft.aufirst=Wen-Qing&rft.date=2014-07-01&rft.volume=106&rft.issue=7&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=1460-2105&rft_id=info:doi/10.1093%2Fjnci%2Fdju116
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-08-11
N1 - Date created - 2014-06-13
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Int J Cancer. 1999 Nov 26;83(5):615-9 [10521796]
Gut. 2013 May;62(5):676-82 [22698649]
JAMA. 2013 Feb 13;309(6):578-86 [23403682]
Biometrics. 2002 Mar;58(1):21-9 [11890317]
JAMA. 2004 Jan 14;291(2):187-94 [14722144]
JAMA. 1991 Jul 3;266(1):93-8 [2046134]
Cancer Res. 1993 Mar 15;53(6):1317-21 [8443811]
Lancet. 1994 Jan 22;343(8891):243-4 [7904707]
Control Clin Trials. 1998 Aug;19(4):352-69 [9683311]
Aliment Pharmacol Ther. 2013 May;37(10):969-78 [23550594]
J Natl Cancer Inst. 2006 Jul 19;98(14):974-83 [16849680]
Gut. 2007 May;56(5):631-6 [17142647]
Helicobacter. 2007 Oct;12(5):575-8 [17760729]
Lancet. 2008 Aug 2;372(9636):392-7 [18675689]
World J Gastroenterol. 2011 Nov 7;17(41):4596-601 [22147965]
J Natl Cancer Inst. 2012 Mar 21;104(6):488-92 [22271764]
Comment In:
J Natl Cancer Inst. 2014 Nov;106(11). pii: dju352. doi: 10.1093/jnci/dju352 [25381392]
J Natl Cancer Inst. 2014 Nov;106(11). pii: dju348. doi: 10.1093/jnci/dju348 [25381391]
J Natl Cancer Inst. 2014 Jul;106(7). pii: dju148. doi: 10.1093/jnci/dju148 [24925352]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/jnci/dju116
ER -
TY - JOUR
T1 - Physical activity and cancer-specific mortality in the NIH-AARP Diet and Health Study cohort
AN - 1534817168; 19846980
AB - Higher physical activity levels have been associated with a lower risk of developing various cancers and all-cancer mortality, but the impact of pre-diagnosis physical activity on cancer-specific death has not been fully characterized. In the prospective National Institutes of Health-AARP Diet and Health Study with 293,511 men and women, we studied prediagnosis moderate to vigorous intensity leisure time physical activity (MVPA) in the past 10 years and cancer-specific mortality. Over a median 12.1 years, we observed 15,001 cancer deaths. Using Cox proportional hazards regression, we estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for MVPA with cancer mortality overall and by 20 specific cancer sites, adjusting for relevant risk factors. Compared to participants reporting never/rare MVPA, those reporting >7 hr/week MVPA had a lower risk of total cancer mortality (HR=0.89, 95% CI 0.84-0.94; p-trend 7 hr/week of MVPA to those reporting never/rare MVPA, we observed a lower risk of death from colon (HR=0.70; 95% CI 0.57-0.85; p-trend <0.001), liver (0.71; 0.52-0.98; p-trend=0.012) and lung cancer (0.84; 0.77-0.92; p-trend <0.001) and a significant p-trend for non-Hodgkins lymphoma (0.80; 0.62-1.04; p-trend=0.017). An unexpected increased mortality p-trend with increasing MVPA was observed for death from kidney cancer (1.42; 0.98-2.03; p-trend=0.016). Our findings suggest that higher prediagnosis leisure time physical activity is associated with lower risk of overall cancer mortality and mortality from multiple cancer sites. Future studies should confirm observed associations and further explore timing of physical activity and underlying biological mechanisms. What's new? Despite evidence that physical activity reduces risk of multiple chronic diseases, including cancer, as much as one-third of the U.S. population is inactive. In this study, the authors explored associations between pre-diagnosis physical activity and cancer mortality. They found that higher pre-diagnosis leisure-time physical activity is associated with a decreased risk of overall cancer mortality, and particularly mortality from cancers of the colon, liver, lung, and non-Hodgkin's lymphoma.
JF - International Journal of Cancer
AU - Arem, Hannah
AU - Moore, Steve C
AU - Park, Yikyung
AU - Ballard-Barbash, Rachel
AU - Hollenbeck, Albert
AU - Leitzmann, Michael
AU - Matthews, Charles E
AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD.
Y1 - 2014/07//
PY - 2014
DA - Jul 2014
SP - 423
EP - 431
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 135
IS - 2
SN - 0020-7136, 0020-7136
KW - Health & Safety Science Abstracts; Risk Abstracts
KW - Diets
KW - Mortality
KW - Health risks
KW - Non-Hodgkin's lymphoma
KW - USA
KW - Physical activity
KW - Risk factors
KW - Liver
KW - Kidney
KW - Risk reduction
KW - Lung cancer
KW - H 11000:Diseases/Injuries/Trauma
KW - R2 23060:Medical and environmental health
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534817168?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Cancer&rft.atitle=Physical+activity+and+cancer-specific+mortality+in+the+NIH-AARP+Diet+and+Health+Study+cohort&rft.au=Arem%2C+Hannah%3BMoore%2C+Steve+C%3BPark%2C+Yikyung%3BBallard-Barbash%2C+Rachel%3BHollenbeck%2C+Albert%3BLeitzmann%2C+Michael%3BMatthews%2C+Charles+E&rft.aulast=Arem&rft.aufirst=Hannah&rft.date=2014-07-01&rft.volume=135&rft.issue=2&rft.spage=423&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.28659
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-01
N1 - Last updated - 2014-06-26
N1 - SubjectsTermNotLitGenreText - Diets; Non-Hodgkin's lymphoma; Health risks; Mortality; Risk factors; Physical activity; Kidney; Liver; Risk reduction; Lung cancer; USA
DO - http://dx.doi.org/10.1002/ijc.28659
ER -
TY - JOUR
T1 - Mitochondrial genome maintenance in health and disease.
AN - 1534471332; 24780559
AB - Human mitochondria harbor an essential, high copy number, 16,569 base pair, circular DNA genome that encodes 13 gene products required for electron transport and oxidative phosphorylation. Mutation of this genome can compromise cellular respiration, ultimately resulting in a variety of progressive metabolic diseases collectively known as 'mitochondrial diseases'. Mutagenesis of mtDNA and the persistence of mtDNA mutations in cells and tissues is a complex topic, involving the interplay of DNA replication, DNA damage and repair, purifying selection, organelle dynamics, mitophagy, and aging. We briefly review these general elements that affect maintenance of mtDNA, and we focus on nuclear genes encoding the mtDNA replication machinery that can perturb the genetic integrity of the mitochondrial genome.
Published by Elsevier B.V.
JF - DNA repair
AU - Copeland, William C
AU - Longley, Matthew J
AD - Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, Durham, NC 27709, USA. Electronic address: copelan1@niehs.nih.gov. ; Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, Durham, NC 27709, USA.
Y1 - 2014/07//
PY - 2014
DA - July 2014
SP - 190
EP - 198
VL - 19
KW - DNA, Mitochondrial
KW - 0
KW - Index Medicus
KW - Mitochondrial DNA replication
KW - POLG
KW - mtDNA
KW - Mutagenesis
KW - Mitochondrial disease
KW - Humans
KW - Oxidative Phosphorylation
KW - Mutation
KW - DNA, Mitochondrial -- genetics
KW - Mitochondrial Diseases -- pathology
KW - Mitochondrial Diseases -- genetics
KW - DNA Replication -- genetics
KW - Genome, Mitochondrial
KW - DNA Damage -- genetics
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-02-12
N1 - Date created - 2014-06-09
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.dnarep.2014.03.010
ER -
TY - JOUR
T1 - The clinical and financial burden of pre-emptive management of cytomegalovirus disease after allogeneic stem cell transplantation-implications for preventative treatment approaches.
AN - 1534468888; 24831837
AB - Although cytomegalovirus (CMV) infection after allogeneic stem cell transplantation (SCT) is rarely fatal, the management of CMV by pre-emptive medication for viral reactivation has toxicity and carries a financial burden. New strategies to prevent CMV reactivation with vaccines and antiviral T cells may represent an advance over pre-emptive strategies but have yet to be justified in terms of transplantation outcome and cost.
We compared outcomes and post-transplantation treatment cost in 44 patients who never required pre-emptive CMV treatment with 90 treated patients undergoing SCT at our institute between 2006 and 2012. Eighty-one subjects received CD34+ selected myeloablative SCT, 12 umbilical cord blood transplants, and 41 T-replete non-myeloablative SCT. One hundred nineteen patients (89%) were at risk for CMV because either the donor or recipient was seropositive. Of these, 90 patients (75.6%) reactivated CMV at a median of 30 (range 8-105) days after transplantation and received antivirals. There was no difference in standard transplantation risk factors between the two groups. In multivariate modeling, CMV reactivation >250 copies/mL (odds ratio = 3, P < 0.048), total duration of inpatient IV antiviral therapy (odds ratio = 1.04, P < 0.001), type of transplantation (T-deplete vs. T-replete; odds ratio = 4.65, P < 0.017) were found to be significantly associated with increased non-relapse mortality. The treated group incurred an additional cost of antiviral medication and longer hospitalization within the first 6 months after SCT of $58,000 to $74,000 per patient.
Our findings suggest that to prevent CMV reactivation, treatment should be given within 1 week of SCT. Preventative treatment may improve outcome and have significant cost savings. Published by Elsevier Inc.
JF - Cytotherapy
AU - Jain, Natasha A
AU - Lu, Kit
AU - Ito, Sawa
AU - Muranski, Pawel
AU - Hourigan, Christopher S
AU - Haggerty, Janice
AU - Chokshi, Puja D
AU - Ramos, Catalina
AU - Cho, Elena
AU - Cook, Lisa
AU - Childs, Richard
AU - Battiwalla, Minoo
AU - Barrett, A John
AD - Hematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA. ; Hematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA. Electronic address: minoo.battiwalla@nih.gov.
Y1 - 2014/07//
PY - 2014
DA - July 2014
SP - 927
EP - 933
VL - 16
IS - 7
KW - Index Medicus
KW - pre-emptive therapy
KW - antiviral cellular therapy
KW - economic cost
KW - CMV reactivation
KW - Humans
KW - Aged
KW - Child
KW - T-Lymphocytes -- pathology
KW - Tissue Donors
KW - Cost of Illness
KW - Risk Factors
KW - Adult
KW - Virus Activation -- genetics
KW - Middle Aged
KW - Adolescent
KW - T-Lymphocytes -- virology
KW - Female
KW - Male
KW - T-Lymphocytes -- immunology
KW - Hematologic Neoplasms -- therapy
KW - Hematologic Neoplasms -- pathology
KW - Cytomegalovirus Infections -- economics
KW - Hematopoietic Stem Cell Transplantation -- economics
KW - Cytomegalovirus -- pathogenicity
KW - Transplantation, Homologous -- adverse effects
KW - Cytomegalovirus -- genetics
KW - Cytomegalovirus Infections -- virology
KW - Cytomegalovirus Infections -- pathology
KW - Transplantation, Homologous -- economics
KW - Hematopoietic Stem Cell Transplantation -- adverse effects
KW - Hematologic Neoplasms -- mortality
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-02-12
N1 - Date created - 2014-06-09
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Blood. 2012 Aug 23;120(8):1545-51 [22700725]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.jcyt.2014.02.010
ER -
TY - JOUR
T1 - Prevalence of suicide attempters in emergency departments in Japan: a systematic review and meta-analysis.
AN - 1526128857; 24836085
AB - The number of hospital admissions related to suicide attempts is increasing worldwide. The Emergency Department (ED) is recognized in Japan as an opportunity to intervene with suicide attempters however, the prevalence of suicide attempters in the ED is unknown. Therefore, a meta-analysis was conducted to provide this information.
We conducted searches of databases (PubMed, PsycINFO, CINAHL, ICHUSHI, CiNii) to identify studies about suicide attempters in the ED in Japan. A meta-analysis was used to calculate the pooled prevalence proportion of suicide attempters in the ED, and their prevalence proportion of psychiatric disorder and method of suicide in suicide attempters. The search of Japanese studies identified 3338 records, of which 70 were included in the meta-analysis. A total of 25 studies reported the psychiatric diagnosis and 62 studies reported the method of suicide. The pooled prevalence proportion of suicide attempters was 4.7%. Mood disorders were the most frequent psychiatric disorders (ICD: 30%, DSM: 35%), and poisoning was the most frequent method of attempting suicide (52%).
There might be a publication bias because only published studies were included. There also might be an information bias, such as reporting bias or misclassification, because most of studies included in the analysis used retrospective designs. The results provide clear evidence of the prevalence of suicide attempters in the ED in Japan. The results indicate that suicide attempters in the ED have a higher proportion of mood disorders, and that the most common method of suicide is poisoning.
Copyright © 2014 Elsevier B.V. All rights reserved.
JF - Journal of affective disorders
AU - Kawashima, Yoshitaka
AU - Yonemoto, Naohiro
AU - Inagaki, Masatoshi
AU - Yamada, Mitsuhiko
AD - Department of Neuropsychopharmacology, National Institute of Mental Health, National Center of Neurology and Psychiatry, 4-1-1, Ogawahigashimachi, Kodaira, Tokyo 187-8553, Japan. Electronic address: kawashima@ncnp.go.jp. ; Department of Epidemiology and Biostatistics, Translational Medical Center, National Centre of Neurology and Psychiatry, Kodaira, Tokyo, Japan. Electronic address: nyonemoto@gmail.com. ; Department of Neuropsychiatry, Okayama University Hospital, Kita-ku, Okayama, Japan. Electronic address: masatoshiinagaki@okayama-u.ac.jp. ; Department of Neuropsychopharmacology, National Institute of Mental Health, National Center of Neurology and Psychiatry, 4-1-1, Ogawahigashimachi, Kodaira, Tokyo 187-8553, Japan. Electronic address: mitsu@ncnp.go.jp.
Y1 - 2014/07//
PY - 2014
DA - July 2014
SP - 33
EP - 39
VL - 163
KW - Index Medicus
KW - Meta-analysis
KW - Suicide
KW - Self-harm
KW - Systematic review
KW - Emergency medicine
KW - Japan -- epidemiology
KW - Hospitalization
KW - Mental Disorders -- epidemiology
KW - Humans
KW - Retrospective Studies
KW - Emergency Service, Hospital
KW - Drug Overdose -- epidemiology
KW - Prevalence
KW - Suicide, Attempted -- statistics & numerical data
KW - Suicide, Attempted -- psychology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+affective+disorders&rft.atitle=Prevalence+of+suicide+attempters+in+emergency+departments+in+Japan%3A+a+systematic+review+and+meta-analysis.&rft.au=Kawashima%2C+Yoshitaka%3BYonemoto%2C+Naohiro%3BInagaki%2C+Masatoshi%3BYamada%2C+Mitsuhiko&rft.aulast=Kawashima&rft.aufirst=Yoshitaka&rft.date=2014-07-01&rft.volume=163&rft.issue=&rft.spage=33&rft.isbn=&rft.btitle=&rft.title=Journal+of+affective+disorders&rft.issn=1573-2517&rft_id=info:doi/10.1016%2Fj.jad.2014.03.025
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-10-14
N1 - Date created - 2014-05-19
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.jad.2014.03.025
ER -
TY - JOUR
T1 - FGFR3 induces degradation of BMP type I receptor to regulate skeletal development.
AN - 1522680006; 24657641
AB - Fibroblast growth factors (FGFs) and their receptors (FGFRs) play significant roles in vertebrate organogenesis and morphogenesis. FGFR3 is a negative regulator of chondrogenesis and multiple mutations with constitutive activity of FGFR3 result in achondroplasia, one of the most common dwarfisms in humans, but the molecular mechanism remains elusive. In this study, we found that chondrocyte-specific deletion of BMP type I receptor a (Bmpr1a) rescued the bone overgrowth phenotype observed in Fgfr3 deficient mice by reducing chondrocyte differentiation. Consistently, using in vitro chondrogenic differentiation assay system, we demonstrated that FGFR3 inhibited BMPR1a-mediated chondrogenic differentiation. Furthermore, we showed that FGFR3 hyper-activation resulted in impaired BMP signaling in chondrocytes of mouse growth plates. We also found that FGFR3 inhibited BMP-2- or constitutively activated BMPR1-induced phosphorylation of Smads through a mechanism independent of its tyrosine kinase activity. We found that FGFR3 facilitates BMPR1a to degradation through Smurf1-mediated ubiquitination pathway. We demonstrated that down-regulation of BMP signaling by BMPR1 inhibitor dorsomorphin led to the retardation of chondrogenic differentiation, which mimics the effect of FGF-2 on chondrocytes and BMP-2 treatment partially rescued the retarded growth of cultured bone rudiments from thanatophoric dysplasia type II mice. Our findings reveal that FGFR3 promotes the degradation of BMPR1a, which plays an important role in the pathogenesis of FGFR3-related skeletal dysplasia. Copyright © 2014 Elsevier B.V. All rights reserved.
JF - Biochimica et biophysica acta
AU - Qi, Huabing
AU - Jin, Min
AU - Duan, Yaqi
AU - Du, Xiaolan
AU - Zhang, Yuanquan
AU - Ren, Fangli
AU - Wang, Yinyin
AU - Tian, Qingyun
AU - Wang, Xiaofeng
AU - Wang, Quan
AU - Zhu, Ying
AU - Xie, Yangli
AU - Liu, Chuanju
AU - Cao, Xu
AU - Mishina, Yuji
AU - Chen, Di
AU - Deng, Chu-xia
AU - Chang, Zhijie
AU - Chen, Lin
AD - Center of Bone Metabolism and Repair (CBMR), Trauma Center, Institute of Surgery Research, Daping Hospital, Third Military Medical University, Chongqing 400042, China. ; Center of Bone Metabolism and Repair (CBMR), Trauma Center, Institute of Surgery Research, Daping Hospital, Third Military Medical University, Chongqing 400042, China; State Key Laboratory of Trauma, Burns and Combined Injury, Third Military Medical University, Chongqing 400042, China. ; State Key Laboratory of Biomembrane and Membrane Biotechnology, School of Medicine, Tsinghua University, Beijing 100084, China. ; Department of Cell Biology, New York University School of Medicine, New York, NY 10016, USA; Department of Orthopaedic Surgery, New York University School of Medicine and NYU Hospital for Joint Diseases, New York, NY 10003, USA. ; Department of Orthopaedic Surgery, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. ; Department of Biologic & Materials Sciences, University of Michigan School of Dentistry, Ann Arbor, MI 48109, USA. ; Department of Biochemistry, Rush University, Chicago, IL 60612, USA. ; Genetics of Development and Disease Branch, National Institute of Diabetes and Digestive and Kidney Diseases, 10/9N105, National Institutes of Health, Bethesda, MD 20892, USA. ; State Key Laboratory of Biomembrane and Membrane Biotechnology, School of Medicine, Tsinghua University, Beijing 100084, China. Electronic address: zhijiec@tsinghua.edu.cn. ; Center of Bone Metabolism and Repair (CBMR), Trauma Center, Institute of Surgery Research, Daping Hospital, Third Military Medical University, Chongqing 400042, China; State Key Laboratory of Trauma, Burns and Combined Injury, Third Military Medical University, Chongqing 400042, China; Department of Rehabilitation Medicine, Institute of Surgery Research, Daping Hospital, Third Military Medical University, Chongqing 400042, China. Electronic address: linchen70@163.com.
Y1 - 2014/07//
PY - 2014
DA - July 2014
SP - 1237
EP - 1247
VL - 1843
IS - 7
SN - 0006-3002, 0006-3002
KW - (6-(4-(2-piperidin-1-ylethoxy)phenyl))-3-pyridin-4-ylpyrazolo(1,5-a)pyrimidine
KW - 0
KW - Bmp2 protein, mouse
KW - Bone Morphogenetic Protein 2
KW - Pyrazoles
KW - Pyrimidines
KW - Smad Proteins
KW - Fibroblast Growth Factor 2
KW - 103107-01-3
KW - Smurf1 protein, mouse
KW - EC 2.3.2.26
KW - Ubiquitin-Protein Ligases
KW - EC 2.3.2.27
KW - Fgfr3 protein, mouse
KW - EC 2.7.10.1
KW - Receptor, Fibroblast Growth Factor, Type 3
KW - Bmpr1a protein, mouse
KW - EC 2.7.11.30
KW - Bone Morphogenetic Protein Receptors, Type I
KW - Index Medicus
KW - Achondroplasia
KW - Smurf1
KW - FGFR3
KW - Chondrocyte
KW - BMPR1
KW - Smad Proteins -- genetics
KW - Fibroblast Growth Factor 2 -- metabolism
KW - Fibroblast Growth Factor 2 -- pharmacology
KW - Animals
KW - Morphogenesis -- genetics
KW - Humans
KW - Pyrimidines -- pharmacology
KW - Cell Differentiation
KW - Mice
KW - Phosphorylation -- drug effects
KW - Bone Morphogenetic Protein 2 -- pharmacology
KW - Mice, Knockout
KW - Smad Proteins -- metabolism
KW - Pyrazoles -- pharmacology
KW - Bone Morphogenetic Protein 2 -- metabolism
KW - Ubiquitination -- drug effects
KW - Ubiquitin-Protein Ligases -- genetics
KW - Ubiquitin-Protein Ligases -- metabolism
KW - Embryo, Mammalian
KW - Signal Transduction
KW - Gene Expression Regulation, Developmental
KW - Receptor, Fibroblast Growth Factor, Type 3 -- deficiency
KW - Growth Plate -- cytology
KW - Receptor, Fibroblast Growth Factor, Type 3 -- genetics
KW - Chondrocytes -- drug effects
KW - Chondrocytes -- cytology
KW - Bone Morphogenetic Protein Receptors, Type I -- genetics
KW - Achondroplasia -- metabolism
KW - Growth Plate -- metabolism
KW - Bone Morphogenetic Protein Receptors, Type I -- metabolism
KW - Chondrocytes -- metabolism
KW - Achondroplasia -- genetics
KW - Growth Plate -- growth & development
KW - Achondroplasia -- pathology
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-06-30
N1 - Date created - 2014-05-07
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.bbamcr.2014.03.011
ER -
TY - JOUR
T1 - Menopausal hormone therapy and risk of endometrial cancer.
AN - 1521912978; 23680641
AB - Endometrial cancer is clearly a hormonally responsive tumor, with a critical role played by estrogens unopposed by progestins. Numerous epidemiologic studies have shown substantial risk increases associated with use of unopposed estrogens, especially among thin women. This risk, however, can be reduced if progestins are added to the therapy. The manner in which progestins are prescribed is a critical determinant of risk. Most studies show that women who have ever used progestins continuously (>25 days/months) are at somewhat reduced risk relative to non-users (meta-analysis relative risk, RR, based on observational studies=0.78, 95 confidence intervals, CI, 0.72-0.86). The reduced risk in greatest among heavy women. In contrast, women who have ever used progestins sequentially for <10 days each month are at increased risk, with meta-analysis results showing on overall RR of 1.76 (1.51-2.05); in contrast, progestins given for 10-24 days/month appear unrelated to risk (RR=1.07, 0.92-1.24). These risks were based on varying patterns of usage, with little information available regarding how endometrial cancer risk is affected by duration of use, type and/or dose of estrogen or progestin, or mode of administration. Effects may also vary by clinical characteristics (e.g., differences for Type I vs. II tumors). Further resolution of many of these relationships may be dependent on pooling data from multiple studies to derive sufficient power for subgroups of users. With changing clinical practices, it will be important for future studies to monitor a wide range of exposures and to account for divergent effects of different usage patterns. This article is part of a Special Issue entitled 'Menopause'.
Published by Elsevier Ltd.
JF - The Journal of steroid biochemistry and molecular biology
AU - Brinton, Louise A
AU - Felix, Ashley S
AD - Hormonal and Reproductive Epidemiology Branch, National Cancer Institute, Rockville, MD 20852-7234, United States. Electronic address: brinton@nih.gov. ; Hormonal and Reproductive Epidemiology Branch, National Cancer Institute, Rockville, MD 20852-7234, United States.
Y1 - 2014/07//
PY - 2014
DA - July 2014
SP - 83
EP - 89
VL - 142
KW - Progestins
KW - 0
KW - Index Medicus
KW - Risk
KW - Epidemiology
KW - Endometrial cancer
KW - Menopausal hormone therapy
KW - Humans
KW - Progestins -- administration & dosage
KW - Menopause
KW - Female
KW - Endometrial Neoplasms -- chemically induced
KW - Estrogen Replacement Therapy -- adverse effects
KW - Estrogen Replacement Therapy -- methods
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+steroid+biochemistry+and+molecular+biology&rft.atitle=Menopausal+hormone+therapy+and+risk+of+endometrial+cancer.&rft.au=Brinton%2C+Louise+A%3BFelix%2C+Ashley+S&rft.aulast=Brinton&rft.aufirst=Louise&rft.date=2014-07-01&rft.volume=142&rft.issue=&rft.spage=83&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+steroid+biochemistry+and+molecular+biology&rft.issn=1879-1220&rft_id=info:doi/10.1016%2Fj.jsbmb.2013.05.001
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-06-19
N1 - Date created - 2014-05-06
N1 - Date revised - 2017-01-13
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.jsbmb.2013.05.001
ER -
TY - JOUR
T1 - miR-126 contributes to Parkinson's disease by dysregulating the insulin-like growth factor/phosphoinositide 3-kinase signaling.
AN - 1514433929; 24559646
AB - Dopamine (DA) neurons in sporadic Parkinson's disease (PD) display dysregulated gene expression networks and signaling pathways that are implicated in PD pathogenesis. Micro (mi)RNAs are regulators of gene expression, which could be involved in neurodegenerative diseases. We determined the miRNA profiles in laser microdissected DA neurons from postmortem sporadic PD patients' brains and age-matched controls. DA neurons had a distinctive miRNA signature and a set of miRNAs was dysregulated in PD. Bioinformatics analysis provided evidence for correlations of miRNAs with signaling pathways relevant to PD, including an association of miR-126 with insulin/IGF-1/PI3K signaling. In DA neuronal cell systems, enhanced expression of miR-126 impaired IGF-1 signaling and increased vulnerability to the neurotoxin 6-OHDA by downregulating factors in IGF-1/PI3K signaling, including its targets p85β, IRS-1, and SPRED1. Blocking of miR-126 function increased IGF-1 trophism and neuroprotection to 6-OHDA. Our data imply that elevated levels of miR-126 may play a functional role in DA neurons and in PD pathogenesis by downregulating IGF-1/PI3K/AKT signaling and that its inhibition could be a mechanism of neuroprotection.
Copyright © 2014 Elsevier Inc. All rights reserved.
JF - Neurobiology of aging
AU - Kim, Woori
AU - Lee, Yenarae
AU - McKenna, Noah D
AU - Yi, Ming
AU - Simunovic, Filip
AU - Wang, Yulei
AU - Kong, Benjamin
AU - Rooney, Robert J
AU - Seo, Hyemyung
AU - Stephens, Robert M
AU - Sonntag, Kai C
AD - Department of Psychiatry, McLean Hospital, Harvard Medical School, Belmont, MA, USA; Department of Psychiatry, McLean Hospital, Harvard Medical School, Belmont, MA, USA. ; Department of Psychiatry, McLean Hospital, Harvard Medical School, Belmont, MA, USA. ; Bioinformatics Support Group, Advanced Biomedical Computing Center, NCI-Frederick, Frederick, MD, USA. ; Life Technologies, Foster City, CA, USA. ; Genome Explorations Inc, Memphis, TN, USA. ; Division of Molecular & Life Sciences, College of Science & Technology, Hanyang University, Seoul, Korea. ; Department of Psychiatry, McLean Hospital, Harvard Medical School, Belmont, MA, USA. Electronic address: ksonntag@mclean.harvard.edu.
Y1 - 2014/07//
PY - 2014
DA - July 2014
SP - 1712
EP - 1721
VL - 35
IS - 7
KW - MIRN126 microRNA, human
KW - 0
KW - MicroRNAs
KW - Insulin-Like Growth Factor I
KW - 67763-96-6
KW - Oxidopamine
KW - 8HW4YBZ748
KW - Phosphatidylinositol 3-Kinases
KW - EC 2.7.1.-
KW - Index Medicus
KW - Dopamine neurons
KW - 6-OHDA neurotoxicity
KW - Postmortem
KW - Laser capture microdissection
KW - Cell systems
KW - Parkinson's disease
KW - IGF-1 signaling
KW - PI3K
KW - miR-126
KW - miRNAs
KW - Insulin
KW - Oxidopamine -- toxicity
KW - Cells, Cultured
KW - Humans
KW - Brain -- metabolism
KW - Down-Regulation -- drug effects
KW - Signal Transduction -- physiology
KW - Phosphatidylinositol 3-Kinases -- metabolism
KW - Signal Transduction -- drug effects
KW - Parkinson Disease -- metabolism
KW - Signal Transduction -- genetics
KW - Insulin-Like Growth Factor I -- metabolism
KW - Dopaminergic Neurons -- metabolism
KW - MicroRNAs -- physiology
KW - Parkinson Disease -- genetics
KW - Gene Expression Regulation -- genetics
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1514433929?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurobiology+of+aging&rft.atitle=miR-126+contributes+to+Parkinson%27s+disease+by+dysregulating+the+insulin-like+growth+factor%2Fphosphoinositide+3-kinase+signaling.&rft.au=Kim%2C+Woori%3BLee%2C+Yenarae%3BMcKenna%2C+Noah+D%3BYi%2C+Ming%3BSimunovic%2C+Filip%3BWang%2C+Yulei%3BKong%2C+Benjamin%3BRooney%2C+Robert+J%3BSeo%2C+Hyemyung%3BStephens%2C+Robert+M%3BSonntag%2C+Kai+C&rft.aulast=Kim&rft.aufirst=Woori&rft.date=2014-07-01&rft.volume=35&rft.issue=7&rft.spage=1712&rft.isbn=&rft.btitle=&rft.title=Neurobiology+of+aging&rft.issn=1558-1497&rft_id=info:doi/10.1016%2Fj.neurobiolaging.2014.01.021
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-11-17
N1 - Date created - 2014-04-07
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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Lancet Neurol. 2004 Mar;3(3):169-78 [14980532]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.neurobiolaging.2014.01.021
ER -
TY - JOUR
T1 - Mapping topoisomerase sites in mitochondrial DNA with a poisonous mitochondrial topoisomerase I (Top1mt).
AN - 1549631722; 24798329
AB - Mitochondrial topoisomerase I (Top1mt) is a type IB topoisomerase present in vertebrates and exclusively targeted to mitochondria. Top1mt relaxes mitochondrial DNA (mtDNA) supercoiling by introducing transient cleavage complexes wherein the broken DNA strand swivels around the intact strand. Top1mt cleavage complexes (Top1mtcc) can be stabilized in vitro by camptothecin (CPT). However, CPT does not trap Top1mtcc efficiently in cells and is highly cytotoxic due to nuclear Top1 targeting. To map Top1mtcc on mtDNA in vivo and to overcome the limitations of CPT, we designed two substitutions (T546A and N550H) in Top1mt to stabilize Top1mtcc. We refer to the double-mutant enzyme as Top1mt*. Using retroviral transduction and ChIP-on-chip assays with Top1mt* in Top1mt knock-out murine embryonic fibroblasts, we demonstrate that Top1mt* forms high levels of cleavage complexes preferentially in the noncoding regulatory region of mtDNA, accumulating especially at the heavy strand replication origin OH, in the ribosomal genes (12S and 16S) and at the light strand replication origin OL. Expression of Top1mt* also caused rapid mtDNA depletion without affecting mitochondria mass, suggesting the existence of specific mitochondrial pathways for the removal of damaged mtDNA.
© 2014 by The American Society for Biochemistry and Molecular Biology, Inc.
JF - The Journal of biological chemistry
AU - Dalla Rosa, Ilaria
AU - Huang, Shar-Yin N
AU - Agama, Keli
AU - Khiati, Salim
AU - Zhang, Hongliang
AU - Pommier, Yves
AD - From the Laboratory of Molecular Pharmacology, Developmental Therapeutics Branch, Center for Cancer Research, NCI, National Institutes of Health, Bethesda, Maryland 20892. ; From the Laboratory of Molecular Pharmacology, Developmental Therapeutics Branch, Center for Cancer Research, NCI, National Institutes of Health, Bethesda, Maryland 20892 pommier@nih.gov.
Y1 - 2014/06/27/
PY - 2014
DA - 2014 Jun 27
SP - 18595
EP - 18602
VL - 289
IS - 26
KW - DNA, Mitochondrial
KW - 0
KW - DNA Topoisomerases, Type I
KW - EC 5.99.1.2
KW - Index Medicus
KW - DNA Topoisomerase
KW - Mitochondrial DNA (mtDNA)
KW - Mitochondrial Metabolism
KW - DNA Topology
KW - Chromatin Immunoprecipitation (ChiP)
KW - mtDNA Transcription
KW - Top1mt
KW - Regulatory Sequences, Nucleic Acid
KW - Animals
KW - DNA Damage
KW - Mice
KW - Mice, Knockout
KW - Mitochondria -- enzymology
KW - DNA, Mitochondrial -- metabolism
KW - DNA, Mitochondrial -- chemistry
KW - DNA Topoisomerases, Type I -- genetics
KW - Mitochondria -- genetics
KW - DNA Topoisomerases, Type I -- metabolism
KW - DNA, Mitochondrial -- genetics
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1549631722?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Mapping+topoisomerase+sites+in+mitochondrial+DNA+with+a+poisonous+mitochondrial+topoisomerase+I+%28Top1mt%29.&rft.au=Dalla+Rosa%2C+Ilaria%3BHuang%2C+Shar-Yin+N%3BAgama%2C+Keli%3BKhiati%2C+Salim%3BZhang%2C+Hongliang%3BPommier%2C+Yves&rft.aulast=Dalla+Rosa&rft.aufirst=Ilaria&rft.date=2014-06-27&rft.volume=289&rft.issue=26&rft.spage=18595&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M114.555367
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-10-16
N1 - Date created - 2014-07-29
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
J Biol Chem. 1985 Nov 25;260(27):14873-8 [2997227]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1074/jbc.M114.555367
ER -
TY - JOUR
T1 - 4-amino-1-hydroxy-2-oxo-1,8-naphthyridine-containing compounds having high potency against raltegravir-resistant integrase mutants of HIV-1.
AN - 1541371201; 24901667
AB - There are currently three HIV-1 integrase (IN) strand transfer inhibitors (INSTIs) approved by the FDA for the treatment of AIDS. However, the emergence of drug-resistant mutants emphasizes the need to develop additional agents that have improved efficacies against the existent resistant mutants. As reported herein, we modified our recently disclosed 1-hydroxy-2-oxo-1,2-dihydro-1,8-naphthyridine-3-carboxamides IN inhibitors to develop compounds that have improved efficacies against recombinant IN in biochemical assays. These new compounds show single-digit nanomolar antiviral potencies against HIV vectors that carry wild-type (WT) IN in a single round replication assay and have improved potency against vectors harboring the major forms of drug resistant IN mutants. These compounds also have low toxicity for cultured cells, which in several cases, results in selectivity indices (CC50/EC50) of greater than 10000. The compounds have the potential, with additional structural modifications, to yield clinical agents that are effective against the known strains of resistant viruses.
JF - Journal of medicinal chemistry
AU - Zhao, Xue Zhi
AU - Smith, Steven J
AU - Métifiot, Mathieu
AU - Marchand, Christophe
AU - Boyer, Paul L
AU - Pommier, Yves
AU - Hughes, Stephen H
AU - Burke, Terrence R
AD - Chemical Biology Laboratory, and ‡HIV Drug Resistance Program, Center for Cancer Research, NCI at Frederick, National Institutes of Health , Building 376, Boyles Street, P.O. Box B, Frederick, Maryland 21702, United States.
Y1 - 2014/06/26/
PY - 2014
DA - 2014 Jun 26
SP - 5190
EP - 5202
VL - 57
IS - 12
KW - HIV Integrase Inhibitors
KW - 0
KW - Naphthyridines
KW - Pyrrolidinones
KW - Recombinant Proteins
KW - Raltegravir Potassium
KW - 43Y000U234
KW - HIV Integrase
KW - EC 2.7.7.-
KW - Index Medicus
KW - Stereoisomerism
KW - Drug Resistance, Viral
KW - Virus Replication -- drug effects
KW - Humans
KW - HEK293 Cells
KW - Cell Line, Tumor
KW - Recombinant Proteins -- chemistry
KW - Mutation
KW - Structure-Activity Relationship
KW - HIV-1 -- genetics
KW - HIV Integrase Inhibitors -- chemical synthesis
KW - Naphthyridines -- pharmacology
KW - HIV Integrase Inhibitors -- chemistry
KW - HIV Integrase -- genetics
KW - HIV Integrase Inhibitors -- pharmacology
KW - HIV-1 -- enzymology
KW - Naphthyridines -- chemical synthesis
KW - Pyrrolidinones -- pharmacology
KW - HIV-1 -- drug effects
KW - Naphthyridines -- chemistry
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541371201?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+medicinal+chemistry&rft.atitle=4-amino-1-hydroxy-2-oxo-1%2C8-naphthyridine-containing+compounds+having+high+potency+against+raltegravir-resistant+integrase+mutants+of+HIV-1.&rft.au=Zhao%2C+Xue+Zhi%3BSmith%2C+Steven+J%3BM%C3%A9tifiot%2C+Mathieu%3BMarchand%2C+Christophe%3BBoyer%2C+Paul+L%3BPommier%2C+Yves%3BHughes%2C+Stephen+H%3BBurke%2C+Terrence+R&rft.aulast=Zhao&rft.aufirst=Xue&rft.date=2014-06-26&rft.volume=57&rft.issue=12&rft.spage=5190&rft.isbn=&rft.btitle=&rft.title=Journal+of+medicinal+chemistry&rft.issn=1520-4804&rft_id=info:doi/10.1021%2Fjm5001908
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-09-05
N1 - Date created - 2014-06-26
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Mol Genet Genomics. 2004 Sep;272(2):216-26 [15316769]
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Antimicrob Agents Chemother. 2008 Apr;52(4):1351-8 [18227187]
Bioorg Med Chem Lett. 2009 May 15;19(10):2714-7 [19364649]
Curr Top Med Chem. 2009;9(11):1016-37 [19747122]
Antimicrob Agents Chemother. 2010 Jan;54(1):491-501 [19901095]
Drugs. 2010 Mar 26;70(5):631-42 [20329808]
Biochemistry. 2010 May 4;49(17):3715-22 [20334344]
J Virol. 2010 Aug;84(15):7625-33 [20484498]
Bioorg Med Chem Lett. 2010 Nov 15;20(22):6754-7 [20869872]
Curr Opin Struct Biol. 2011 Apr;21(2):249-56 [21277766]
Chem Biol Drug Des. 2012 Feb;79(2):157-65 [22107736]
Expert Opin Investig Drugs. 2012 Mar;21(3):395-401 [22321026]
Expert Opin Investig Drugs. 2012 Apr;21(4):523-30 [22380682]
Curr Opin HIV AIDS. 2012 Sep;7(5):401-8 [22789986]
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Drugs. 2013 Sep;73(14):1627-37 [24052331]
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J Med Chem. 2013 Nov 14;56(21):8588-98 [24124919]
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Erratum In:
J Med Chem. 2014 Aug 14;57(15):6885
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1021/jm5001908
ER -
TY - JOUR
T1 - Chloroquine synergizes sunitinib cytotoxicity via modulating autophagic, apoptotic and angiogenic machineries.
AN - 1526129822; 24751611
AB - Tyrosine kinases play a pivotal role in oncogenesis. Although tyrosine kinase inhibitors as sunitinib malate are used in cancer therapy, emerging studies report compromised cytotoxicity when used as monotherapy and thus combinations with other anti-cancer agents is recommended. Chloroquine is a clinically available anti-malarial agent which has been shown to exhibit anti-cancer activity. In the current study, we questioned whether chloroquine can modulate sunitinib cytotoxicity. We found that chloroquine synergistically augmented sunitinib cytotoxicity on human breast (MCF-7 and T-47D), cervical (Hela), colorectal (Caco-2 and HCT116), hepatocellular (HepG2), laryngeal (HEp-2) and prostate (PC3) cancer cell lines as indicated by combination and concentration reduction indices. These results were also consistent with that of Ehrlich ascites carcinoma (EAC) Swiss albino mice models as confirmed by tumor volume, weight, histopathological examination and PCNA expression. Sunitinib induced autophagy via upregulating beclin-1 expression which was blocked by chloroquine as evidenced by accumulated SQTSM1/p62 level. Furthermore, chloroquine augmented sunitinib-induced apoptosis by decreasing survivin level and increasing caspase 3 activity. Chloroquine also enhanced the antiangiogenic capacity of sunitinib as indicated by decreased CD34 expression and peritoneal/skin angiogenesis. Sunitinib when combined with chloroquine also increased reactive nitrogen species production via increasing inducible nitric oxide synthase expression and nitric oxide level whilst reduced reactive oxygen species production by increasing GSH level, activities of glutathione peroxidase and catalase and reducing lipid peroxides compared to sunitinib-only treated group. Taken together, these findings suggest that chloroquine enhanced sunitinib cytotoxicity in a synergistic manner via inducing apoptosis while switching off autophagic and angiogenic machineries. Nevertheless, further studies are required to elucidate the efficacy and safety profile of such combination. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.
JF - Chemico-biological interactions
AU - Abdel-Aziz, Amal Kamal
AU - Shouman, Samia
AU - El-Demerdash, Ebtehal
AU - Elgendy, Mohamed
AU - Abdel-Naim, Ashraf B
AD - Pharmacology and Toxicology Department, Faculty of Pharmacy, Ain Shams University, Cairo, Egypt; Department of Experimental Oncology, European Institute of Oncology, Milan, Italy. ; Cancer Biology Department, National Cancer Institute, Cairo University, Cairo, Egypt. ; Pharmacology and Toxicology Department, Faculty of Pharmacy, Ain Shams University, Cairo, Egypt. ; Department of Experimental Oncology, European Institute of Oncology, Milan, Italy. ; Pharmacology and Toxicology Department, Faculty of Pharmacy, Ain Shams University, Cairo, Egypt. Electronic address: abnaim@pharma.asu.edu.eg.
Y1 - 2014/06/25/
PY - 2014
DA - 2014 Jun 25
SP - 28
EP - 40
VL - 217
KW - Antineoplastic Agents
KW - 0
KW - Indoles
KW - Pyrroles
KW - Chloroquine
KW - 886U3H6UFF
KW - sunitinib
KW - V99T50803M
KW - Index Medicus
KW - Apoptosis
KW - Sunitinib
KW - Oxidative stress
KW - Autophagy
KW - Angiogenesis
KW - Animals
KW - HeLa Cells
KW - Humans
KW - Mice
KW - Caco-2 Cells
KW - Cell Line, Tumor
KW - HCT116 Cells
KW - Blotting, Western
KW - Neovascularization, Pathologic -- drug therapy
KW - Cell Survival -- drug effects
KW - Hep G2 Cells
KW - Apoptosis -- drug effects
KW - MCF-7 Cells
KW - Drug Synergism
KW - Immunohistochemistry
KW - Female
KW - Carcinoma, Ehrlich Tumor -- blood supply
KW - Chloroquine -- pharmacology
KW - Carcinoma, Ehrlich Tumor -- pathology
KW - Carcinoma, Ehrlich Tumor -- drug therapy
KW - Indoles -- pharmacology
KW - Pyrroles -- pharmacology
KW - Antineoplastic Agents -- pharmacology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemico-biological+interactions&rft.atitle=Chloroquine+synergizes+sunitinib+cytotoxicity+via+modulating+autophagic%2C+apoptotic+and+angiogenic+machineries.&rft.au=Abdel-Aziz%2C+Amal+Kamal%3BShouman%2C+Samia%3BEl-Demerdash%2C+Ebtehal%3BElgendy%2C+Mohamed%3BAbdel-Naim%2C+Ashraf+B&rft.aulast=Abdel-Aziz&rft.aufirst=Amal&rft.date=2014-06-25&rft.volume=217&rft.issue=&rft.spage=28&rft.isbn=&rft.btitle=&rft.title=Chemico-biological+interactions&rft.issn=1872-7786&rft_id=info:doi/10.1016%2Fj.cbi.2014.04.007
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-07-01
N1 - Date created - 2014-05-19
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.cbi.2014.04.007
ER -
TY - JOUR
T1 - IP6K structure and the molecular determinants of catalytic specificity in an inositol phosphate kinase family.
AN - 1540112972; 24956979
AB - Inositol trisphosphate kinases (IP3Ks) and inositol hexakisphosphate kinases (IP6Ks) each regulate specialized signalling activities by phosphorylating either InsP3 or InsP6 respectively. The molecular basis for these different kinase activities can be illuminated by a structural description of IP6K. Here we describe the crystal structure of an Entamoeba histolytica hybrid IP6K/IP3K, an enzymatic parallel to a 'living fossil'. Through molecular modelling and mutagenesis, we extrapolated our findings to human IP6K2, which retains vestigial IP3K activity. Two structural elements, an α-helical pair and a rare, two-turn 310 helix, together forge a substrate-binding pocket with an open clamshell geometry. InsP6 forms substantial contacts with both structural elements. Relative to InsP6, enzyme-bound InsP3 rotates 55° closer to the α-helices, which provide most of the protein's interactions with InsP3. These data reveal the molecular determinants of IP6K activity, and suggest an unusual evolutionary trajectory for a primordial kinase that could have favored efficient bifunctionality, before propagation of separate IP3Ks and IP6Ks.
JF - Nature communications
AU - Wang, Huanchen
AU - DeRose, Eugene F
AU - London, Robert E
AU - Shears, Stephen B
AD - Inositol Signaling Group, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, NC 27709, USA. ; Nuclear Magnetic Resonance Group, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, NC 27709, USA.
Y1 - 2014/06/24/
PY - 2014
DA - 2014 Jun 24
SP - 4178
VL - 5
KW - Inositol Phosphates
KW - 0
KW - Protozoan Proteins
KW - Adenosine Triphosphate
KW - 8L70Q75FXE
KW - Phosphotransferases (Phosphate Group Acceptor)
KW - EC 2.7.4.-
KW - inositol hexakisphosphate kinase
KW - EC 2.7.4.21
KW - Index Medicus
KW - Sensitivity and Specificity
KW - Multigene Family
KW - Humans
KW - Adenosine Triphosphate -- metabolism
KW - Crystallography, X-Ray
KW - Evolution, Molecular
KW - Catalysis
KW - Binding Sites
KW - Adenosine Triphosphate -- chemistry
KW - Protozoan Proteins -- chemistry
KW - Phosphotransferases (Phosphate Group Acceptor) -- chemistry
KW - Protozoan Proteins -- metabolism
KW - Inositol Phosphates -- metabolism
KW - Protozoan Proteins -- genetics
KW - Phosphotransferases (Phosphate Group Acceptor) -- metabolism
KW - Entamoeba histolytica -- enzymology
KW - Phosphotransferases (Phosphate Group Acceptor) -- genetics
KW - Entamoeba histolytica -- chemistry
KW - Inositol Phosphates -- chemistry
KW - Entamoeba histolytica -- genetics
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+communications&rft.atitle=IP6K+structure+and+the+molecular+determinants+of+catalytic+specificity+in+an+inositol+phosphate+kinase+family.&rft.au=Wang%2C+Huanchen%3BDeRose%2C+Eugene+F%3BLondon%2C+Robert+E%3BShears%2C+Stephen+B&rft.aulast=Wang&rft.aufirst=Huanchen&rft.date=2014-06-24&rft.volume=5&rft.issue=&rft.spage=4178&rft.isbn=&rft.btitle=&rft.title=Nature+communications&rft.issn=2041-1723&rft_id=info:doi/10.1038%2Fncomms5178
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-11-16
N1 - Date created - 2014-06-24
N1 - Date revised - 2017-01-14
N1 - Genetic sequence - 4O4F; PDB; 4O4E; 4O4B; 4O4D; 4O4C
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1038/ncomms5178
ER -
TY - CPAPER
T1 - The Adventures of an NIH Program Officer
T2 - 33rd Annual Meeting of the American Society for Virology (ASV2014)
AN - 1562647230; 6301780
JF - 33rd Annual Meeting of the American Society for Virology (ASV2014)
AU - Post, Diane
Y1 - 2014/06/21/
PY - 2014
DA - 2014 Jun 21
KW - Virology
KW - Microbiology
KW - Public health
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1562647230?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=33rd+Annual+Meeting+of+the+American+Society+for+Virology+%28ASV2014%29&rft.atitle=The+Adventures+of+an+NIH+Program+Officer&rft.au=Post%2C+Diane&rft.aulast=Post&rft.aufirst=Diane&rft.date=2014-06-21&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=33rd+Annual+Meeting+of+the+American+Society+for+Virology+%28ASV2014%29&rft.issn=&rft_id=info:doi/
L2 - http://asv2014.colostate.edu/meeting-details/
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-08-31
N1 - Last updated - 2014-09-18
ER -
TY - CPAPER
T1 - Perspectives and current status of poliovirus vaccines
T2 - 33rd Annual Meeting of the American Society for Virology (ASV2014)
AN - 1562647065; 6301763
JF - 33rd Annual Meeting of the American Society for Virology (ASV2014)
AU - Ehrenfeld, Ellie
Y1 - 2014/06/21/
PY - 2014
DA - 2014 Jun 21
KW - Poliovirus
KW - Disease control
KW - Vaccines
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1562647065?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=33rd+Annual+Meeting+of+the+American+Society+for+Virology+%28ASV2014%29&rft.atitle=Perspectives+and+current+status+of+poliovirus+vaccines&rft.au=Ehrenfeld%2C+Ellie&rft.aulast=Ehrenfeld&rft.aufirst=Ellie&rft.date=2014-06-21&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=33rd+Annual+Meeting+of+the+American+Society+for+Virology+%28ASV2014%29&rft.issn=&rft_id=info:doi/
L2 - http://asv2014.colostate.edu/meeting-details/
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-08-31
N1 - Last updated - 2014-09-18
ER -
TY - CPAPER
T1 - A gammaretrovirus isolated from koalas in US zoos with malignant neoplasias
T2 - 33rd Annual Meeting of the American Society for Virology (ASV2014)
AN - 1562644670; 6301789
JF - 33rd Annual Meeting of the American Society for Virology (ASV2014)
AU - Eiden, Maribeth
Y1 - 2014/06/21/
PY - 2014
DA - 2014 Jun 21
KW - Neoplasia
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1562644670?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=33rd+Annual+Meeting+of+the+American+Society+for+Virology+%28ASV2014%29&rft.atitle=A+gammaretrovirus+isolated+from+koalas+in+US+zoos+with+malignant+neoplasias&rft.au=Eiden%2C+Maribeth&rft.aulast=Eiden&rft.aufirst=Maribeth&rft.date=2014-06-21&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=33rd+Annual+Meeting+of+the+American+Society+for+Virology+%28ASV2014%29&rft.issn=&rft_id=info:doi/
L2 - http://asv2014.colostate.edu/scientific-program/
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-08-31
N1 - Last updated - 2014-09-18
ER -
TY - JOUR
T1 - Identification of drivers from cancer genome diversity in hepatocellular carcinoma.
AN - 1540130046; 24955791
AB - Hepatocellular carcinoma (HCC) is one of the most common cancers with a dismal outcome. The complicated molecular pathogenesis of HCC caused by tumor heterogeneity makes it difficult to identify druggable targets useful for treating HCC patients. One approach that has a potential for the improvement of patient prognosis is the identification of cancer driver genes that play a critical role in the development of HCC. Recent technological advances of high-throughput methods, such as gene expression profiles, DNA copy number alterations and somatic mutations, have expanded our understanding of the comprehensive genetic profiles of HCC. Integrative analysis of these omics profiles enables us to classify the molecular subgroups of HCC patients. As each subgroup classified according to genetic profiles has different clinical features, such as recurrence rate and prognosis, the tumor subclassification tools are useful in clinical practice. Furthermore, a global genetic analysis, including genome-wide RNAi functional screening, makes it possible to identify cancer vulnerable genes. Identification of common cancer driver genes in HCC leads to the development of an effective molecular target therapy.
JF - International journal of molecular sciences
AU - Takai, Atsushi
AU - Dang, Hien T
AU - Wang, Xin W
AD - Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. atsushi.takai@nih.gov. ; Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. hien.dang@nih.gov. ; Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. xw3u@nih.gov.
Y1 - 2014/06/20/
PY - 2014
DA - 2014 Jun 20
SP - 11142
EP - 11160
VL - 15
IS - 6
KW - Biomarkers, Tumor
KW - 0
KW - RNA, Small Interfering
KW - Index Medicus
KW - Biomarkers, Tumor -- metabolism
KW - Animals
KW - Polymorphism, Single Nucleotide
KW - Humans
KW - Transcriptome
KW - RNA, Small Interfering -- metabolism
KW - Genetic Variation
KW - Liver Neoplasms -- pathology
KW - Carcinoma, Hepatocellular -- metabolism
KW - Carcinoma, Hepatocellular -- genetics
KW - Carcinoma, Hepatocellular -- pathology
KW - Liver Neoplasms -- genetics
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+molecular+sciences&rft.atitle=Identification+of+drivers+from+cancer+genome+diversity+in+hepatocellular+carcinoma.&rft.au=Takai%2C+Atsushi%3BDang%2C+Hien+T%3BWang%2C+Xin+W&rft.aulast=Takai&rft.aufirst=Atsushi&rft.date=2014-06-20&rft.volume=15&rft.issue=6&rft.spage=11142&rft.isbn=&rft.btitle=&rft.title=International+journal+of+molecular+sciences&rft.issn=1422-0067&rft_id=info:doi/10.3390%2Fijms150611142
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-02-04
N1 - Date created - 2014-06-24
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.3390/ijms150611142
ER -
TY - JOUR
T1 - New strategies in ewing sarcoma: lost in translation?
AN - 1535622225; 24756371
AB - Ewing sarcoma is the second most common pediatric malignant bone tumor. Aggressive multimodality therapy has led to an improvement in outcomes, particularly in patients with localized disease. However, therapy-related toxicities are not trivial, and the prognosis for patients with relapsed and/or metastatic disease continues to be poor. In this article, we outline some of the promising therapies that have the potential to change the Ewing sarcoma therapeutic paradigm in the not-too-distant future: insulin-like growth factor receptor inhibitors, targeting of the fusion protein, epigenetic manipulation, PARP inhibitors, and immunotherapy.
©2014 American Association for Cancer Research.
JF - Clinical cancer research : an official journal of the American Association for Cancer Research
AU - Arnaldez, Fernanda I
AU - Helman, Lee J
AD - Authors' Affiliation: Pediatric Oncology Branch, National Cancer Institute, NIH, Bethesda, Maryland arnaldezf@mail.nih.gov. ; Authors' Affiliation: Pediatric Oncology Branch, National Cancer Institute, NIH, Bethesda, Maryland.
Y1 - 2014/06/15/
PY - 2014
DA - 2014 Jun 15
SP - 3050
EP - 3056
VL - 20
IS - 12
SN - 1078-0432, 1078-0432
KW - Antineoplastic Agents
KW - 0
KW - Enzyme Inhibitors
KW - Poly(ADP-ribose) Polymerase Inhibitors
KW - Receptors, Somatomedin
KW - PARP1 protein, human
KW - EC 2.4.2.30
KW - Poly (ADP-Ribose) Polymerase-1
KW - Index Medicus
KW - Receptors, Somatomedin -- antagonists & inhibitors
KW - Humans
KW - Sarcoma, Ewing -- immunology
KW - Enzyme Inhibitors -- therapeutic use
KW - Bone Neoplasms -- immunology
KW - Immunotherapy
KW - Bone Neoplasms -- metabolism
KW - Sarcoma, Ewing -- metabolism
KW - Molecular Targeted Therapy
KW - Bone Neoplasms -- therapy
KW - Antineoplastic Agents -- therapeutic use
KW - Sarcoma, Ewing -- therapy
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1535622225?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+cancer+research+%3A+an+official+journal+of+the+American+Association+for+Cancer+Research&rft.atitle=New+strategies+in+ewing+sarcoma%3A+lost+in+translation%3F&rft.au=Arnaldez%2C+Fernanda+I%3BHelman%2C+Lee+J&rft.aulast=Arnaldez&rft.aufirst=Fernanda&rft.date=2014-06-15&rft.volume=20&rft.issue=12&rft.spage=3050&rft.isbn=&rft.btitle=&rft.title=Clinical+cancer+research+%3A+an+official+journal+of+the+American+Association+for+Cancer+Research&rft.issn=10780432&rft_id=info:doi/10.1158%2F1078-0432.CCR-13-0633
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-10-15
N1 - Date created - 2014-06-14
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1158/1078-0432.CCR-13-0633
ER -
TY - JOUR
T1 - Noninvasive urinary metabolomic profiling identifies diagnostic and prognostic markers in lung cancer.
AN - 1535621967; 24736543
AB - Lung cancer remains the most common cause of cancer deaths worldwide, yet there is currently a lack of diagnostic noninvasive biomarkers that could guide treatment decisions. Small molecules (<1,500 Da) were measured in urine collected from 469 patients with lung cancer and 536 population controls using unbiased liquid chromatography/mass spectrometry. Clinical putative diagnostic and prognostic biomarkers were validated by quantitation and normalized to creatinine levels at two different time points and further confirmed in an independent sample set, which comprises 80 cases and 78 population controls, with similar demographic and clinical characteristics when compared with the training set. Creatine riboside (IUPAC name: 2-{2-[(2R,3R,4S,5R)-3,4-dihydroxy-5-(hydroxymethyl)-oxolan-2-yl]-1-methylcarbamimidamido}acetic acid), a novel molecule identified in this study, and N-acetylneuraminic acid (NANA) were each significantly (P < 0.00001) elevated in non-small cell lung cancer and associated with worse prognosis [HR = 1.81 (P = 0.0002), and 1.54 (P = 0.025), respectively]. Creatine riboside was the strongest classifier of lung cancer status in all and stage I-II cases, important for early detection, and also associated with worse prognosis in stage I-II lung cancer (HR = 1.71, P = 0.048). All measurements were highly reproducible with intraclass correlation coefficients ranging from 0.82 to 0.99. Both metabolites were significantly (P < 0.03) enriched in tumor tissue compared with adjacent nontumor tissue (N = 48), thus revealing their direct association with tumor metabolism. Creatine riboside and NANA may be robust urinary clinical metabolomic markers that are elevated in tumor tissue and associated with early lung cancer diagnosis and worse prognosis.
©2014 American Association for Cancer Research.
JF - Cancer research
AU - Mathé, Ewy A
AU - Patterson, Andrew D
AU - Haznadar, Majda
AU - Manna, Soumen K
AU - Krausz, Kristopher W
AU - Bowman, Elise D
AU - Shields, Peter G
AU - Idle, Jeffrey R
AU - Smith, Philip B
AU - Anami, Katsuhiro
AU - Kazandjian, Dickran G
AU - Hatzakis, Emmanuel
AU - Gonzalez, Frank J
AU - Harris, Curtis C
AD - Authors' Affiliations: Laboratory of Molecular Immunogenomics, Genomic and Immunity Section, NIAMS/NIH; Laboratories of Human Carcinogenesis, and Metabolism, National Cancer Institute, NIH, Bethesda, Maryland; Department of Veterinary and Biomedical Sciences and Center for Molecular Toxicology and Carcinogenesis; Metabolomics Core Facility; Nuclear Magnetic Resonance Spectroscopy, The Pennsylvania State University, University Park, Pennsylvania; Ohio State University Comprehensive Cancer Center, Columbus, Ohio; and Department of Clinical Research, University of Bern, Bern, SwitzerlandAuthors' Affiliations: Laboratory of Molecular Immunogenomics, Genomic and Immunity Section, NIAMS/NIH; Laboratories of Human Carcinogenesis, and Metabolism, National Cancer Institute, NIH, Bethesda, Maryland; Department of Veterinary and Biomedical Sciences and Center for Molecular Toxicology and Carcinogenesis; Metabolomics Core Facility; Nuclear Magnetic Resonance Spectroscopy, The Pennsylvania State University, University Park, Pennsylvania; Ohio State University Comprehensive Cancer Center, Columbus, Ohio; and Department of Clinical Research, University of Bern, Bern, Switzerland. ; Authors' Affiliations: Laboratory of Molecular Immunogenomics, Genomic and Immunity Section, NIAMS/NIH; Laboratories of Human Carcinogenesis, and Metabolism, National Cancer Institute, NIH, Bethesda, Maryland; Department of Veterinary and Biomedical Sciences and Center for Molecular Toxicology and Carcinogenesis; Metabolomics Core Facility; Nuclear Magnetic Resonance Spectroscopy, The Pennsylvania State University, University Park, Pennsylvania; Ohio State University Comprehensive Cancer Center, Columbus, Ohio; and Department of Clinical Research, University of Bern, Bern, Switzerland. ; Authors' Affiliations: Laboratory of Molecular Immunogenomics, Genomic and Immunity Section, NIAMS/NIH; Laboratories of Human Carcinogenesis, and Metabolism, National Cancer Institute, NIH, Bethesda, Maryland; Department of Veterinary and Biomedical Sciences and Center for Molecular Toxicology and Carcinogenesis; Metabolomics Core Facility; Nuclear Magnetic Resonance Spectroscopy, The Pennsylvania State University, University Park, Pennsylvania; Ohio State University Comprehensive Cancer Center, Columbus, Ohio; and Department of Clinical Research, University of Bern, Bern, Switzerland Curtis_Harris@nih.gov.
Y1 - 2014/06/15/
PY - 2014
DA - 2014 Jun 15
SP - 3259
EP - 3270
VL - 74
IS - 12
KW - 2-(2-(3,4-dihydroxy-5-(hydroxymethyl)oxolan-2-yl)-1-methylcarbamimidamido)acetic acid
KW - 0
KW - Biomarkers, Tumor
KW - Ribonucleosides
KW - N-Acetylneuraminic Acid
KW - GZP2782OP0
KW - Creatine
KW - MU72812GK0
KW - Index Medicus
KW - Kaplan-Meier Estimate
KW - Smoking -- urine
KW - Metabolome
KW - ROC Curve
KW - Humans
KW - Prognosis
KW - Case-Control Studies
KW - Aged
KW - Middle Aged
KW - Male
KW - Female
KW - Proportional Hazards Models
KW - Ribonucleosides -- urine
KW - Lung Neoplasms -- diagnosis
KW - Lung Neoplasms -- urine
KW - Carcinoma, Non-Small-Cell Lung -- mortality
KW - Creatine -- analogs & derivatives
KW - Biomarkers, Tumor -- urine
KW - Lung Neoplasms -- mortality
KW - Creatine -- urine
KW - Carcinoma, Non-Small-Cell Lung -- urine
KW - Carcinoma, Non-Small-Cell Lung -- diagnosis
KW - N-Acetylneuraminic Acid -- urine
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1535621967?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Noninvasive+urinary+metabolomic+profiling+identifies+diagnostic+and+prognostic+markers+in+lung+cancer.&rft.au=Math%C3%A9%2C+Ewy+A%3BPatterson%2C+Andrew+D%3BHaznadar%2C+Majda%3BManna%2C+Soumen+K%3BKrausz%2C+Kristopher+W%3BBowman%2C+Elise+D%3BShields%2C+Peter+G%3BIdle%2C+Jeffrey+R%3BSmith%2C+Philip+B%3BAnami%2C+Katsuhiro%3BKazandjian%2C+Dickran+G%3BHatzakis%2C+Emmanuel%3BGonzalez%2C+Frank+J%3BHarris%2C+Curtis+C&rft.aulast=Math%C3%A9&rft.aufirst=Ewy&rft.date=2014-06-15&rft.volume=74&rft.issue=12&rft.spage=3259&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=1538-7445&rft_id=info:doi/10.1158%2F0008-5472.CAN-14-0109
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-08-08
N1 - Date created - 2014-06-14
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Rapid Commun Mass Spectrom. 2009 Jun;23(11):1543-9 [19399767]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1158/0008-5472.CAN-14-0109
ER -
TY - JOUR
T1 - Druggable oncogene fusions in invasive mucinous lung adenocarcinoma.
AN - 1535621629; 24727320
AB - To identify druggable oncogenic fusions in invasive mucinous adenocarcinoma (IMA) of the lung, a malignant type of lung adenocarcinoma in which KRAS mutations frequently occur.
From an IMA cohort of 90 cases, consisting of 56 cases (62%) with KRAS mutations and 34 cases without (38%), we conducted whole-transcriptome sequencing of 32 IMAs, including 27 cases without KRAS mutations. We used the sequencing data to identify gene fusions, and then performed functional analyses of the fusion gene products. We identified oncogenic fusions that occurred mutually exclusively with KRAS mutations: CD74-NRG1, SLC3A2-NRG1, EZR-ERBB4, TRIM24-BRAF, and KIAA1468-RET. NRG1 fusions were present in 17.6% (6/34) of KRAS-negative IMAs. The CD74-NRG1 fusion activated HER2:HER3 signaling, whereas the EZR-ERBB4 and TRIM24-BRAF fusions constitutively activated the ERBB4 and BRAF kinases, respectively. Signaling pathway activation and fusion-induced anchorage-independent growth/tumorigenicity of NIH3T3 cells expressing these fusions were suppressed by tyrosine kinase inhibitors approved for clinical use.
Oncogenic fusions act as driver mutations in IMAs without KRAS mutations, and thus represent promising therapeutic targets for the treatment of such IMAs. ©2014 American Association for Cancer Research.
JF - Clinical cancer research : an official journal of the American Association for Cancer Research
AU - Nakaoku, Takashi
AU - Tsuta, Koji
AU - Ichikawa, Hitoshi
AU - Shiraishi, Kouya
AU - Sakamoto, Hiromi
AU - Enari, Masato
AU - Furuta, Koh
AU - Shimada, Yoko
AU - Ogiwara, Hideaki
AU - Watanabe, Shun-ichi
AU - Nokihara, Hiroshi
AU - Yasuda, Kazuki
AU - Hiramoto, Masaki
AU - Nammo, Takao
AU - Ishigame, Teruhide
AU - Schetter, Aaron J
AU - Okayama, Hirokazu
AU - Harris, Curtis C
AU - Kim, Young Hak
AU - Mishima, Michiaki
AU - Yokota, Jun
AU - Yoshida, Teruhiko
AU - Kohno, Takashi
AD - Authors' Affiliations: Divisions of Genome Biology, Genetics, and Refractory Cancer Research, National Cancer Center Research Institute, Divisions of Pathology and Clinical Laboratories, Thoracic Surgery, and Thoracic Oncology, National Cancer Center Hospital, Chuo-ku; Department of Metabolic Disorder, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Shinjuku-ku, Tokyo; Department of Respiratory Medicine, Graduate School of Medicine, Kyoto University, Yoshida-Konoe-cho, Sakyo-ku, Kyoto, Japan; Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland; and The Institute of Predictive and Personalized Medicine of Cancer (IMPPC), Barcelona, SpainAuthors' Affiliations: Divisions of Genome Biology, Genetics, and Refractory Cancer Research, National Cancer Center Research Institute, Divisions of Pathology and Clinical Laboratories, Thoracic Surgery, and Thoracic Oncology, National Cancer Center Hospital, Chuo-ku; Department of Metabolic Disorder, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Shinjuku-ku, Tokyo; Department of Respiratory Medicine, Graduate School of Medicine, Kyoto University, Yoshida-Konoe-cho, Sakyo-ku, Kyoto, Japan; Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland; and The Institute of Predictive and Personalized Medicine of Cancer (IMPPC), Barcelona, Spain. ; Authors' Affiliations: Divisions of Genome Biology, Genetics, and Refractory Cancer Research, National Cancer Center Research Institute, Divisions of Pathology and Clinical Laboratories, Thoracic Surgery, and Thoracic Oncology, National Cancer Center Hospital, Chuo-ku; Department of Metabolic Disorder, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Shinjuku-ku, Tokyo; Department of Respiratory Medicine, Graduate School of Medicine, Kyoto University, Yoshida-Konoe-cho, Sakyo-ku, Kyoto, Japan; Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland; and The Institute of Predictive and Personalized Medicine of Cancer (IMPPC), Barcelona, Spain. ; Authors' Affiliations: Divisions of Genome Biology, Genetics, and Refractory Cancer Research, National Cancer Center Research Institute, Divisions of Pathology and Clinical Laboratories, Thoracic Surgery, and Thoracic Oncology, National Cancer Center Hospital, Chuo-ku; Department of Metabolic Disorder, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Shinjuku-ku, Tokyo; Department of Respiratory Medicine, Graduate School of Medicine, Kyoto University, Yoshida-Konoe-cho, Sakyo-ku, Kyoto, Japan; Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland; and The Institute of Predictive and Personalized Medicine of Cancer (IMPPC), Barcelona, Spain tkkohno@ncc.go.jp.
Y1 - 2014/06/15/
PY - 2014
DA - 2014 Jun 15
SP - 3087
EP - 3093
VL - 20
IS - 12
SN - 1078-0432, 1078-0432
KW - KRAS protein, human
KW - 0
KW - Oncogene Proteins, Fusion
KW - Protein Kinase Inhibitors
KW - Proto-Oncogene Proteins
KW - Proto-Oncogene Proteins p21(ras)
KW - EC 3.6.5.2
KW - ras Proteins
KW - Index Medicus
KW - Neoplasm Invasiveness
KW - Animals
KW - Cell Transformation, Neoplastic -- pathology
KW - Neoplasm Staging
KW - Humans
KW - Prognosis
KW - Aged
KW - Cell Transformation, Neoplastic -- drug effects
KW - Mice
KW - Mice, Nude
KW - NIH 3T3 Cells
KW - Signal Transduction -- drug effects
KW - Follow-Up Studies
KW - Middle Aged
KW - Female
KW - Male
KW - ras Proteins -- genetics
KW - Adenocarcinoma, Mucinous -- genetics
KW - Protein Kinase Inhibitors -- therapeutic use
KW - Oncogene Proteins, Fusion -- genetics
KW - Lung Neoplasms -- drug therapy
KW - Mutation -- genetics
KW - Lung Neoplasms -- genetics
KW - Adenocarcinoma, Mucinous -- drug therapy
KW - Proto-Oncogene Proteins -- genetics
KW - Adenocarcinoma, Mucinous -- pathology
KW - Oncogene Proteins, Fusion -- antagonists & inhibitors
KW - Lung Neoplasms -- pathology
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1535621629?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+cancer+research+%3A+an+official+journal+of+the+American+Association+for+Cancer+Research&rft.atitle=Druggable+oncogene+fusions+in+invasive+mucinous+lung+adenocarcinoma.&rft.au=Nakaoku%2C+Takashi%3BTsuta%2C+Koji%3BIchikawa%2C+Hitoshi%3BShiraishi%2C+Kouya%3BSakamoto%2C+Hiromi%3BEnari%2C+Masato%3BFuruta%2C+Koh%3BShimada%2C+Yoko%3BOgiwara%2C+Hideaki%3BWatanabe%2C+Shun-ichi%3BNokihara%2C+Hiroshi%3BYasuda%2C+Kazuki%3BHiramoto%2C+Masaki%3BNammo%2C+Takao%3BIshigame%2C+Teruhide%3BSchetter%2C+Aaron+J%3BOkayama%2C+Hirokazu%3BHarris%2C+Curtis+C%3BKim%2C+Young+Hak%3BMishima%2C+Michiaki%3BYokota%2C+Jun%3BYoshida%2C+Teruhiko%3BKohno%2C+Takashi&rft.aulast=Nakaoku&rft.aufirst=Takashi&rft.date=2014-06-15&rft.volume=20&rft.issue=12&rft.spage=3087&rft.isbn=&rft.btitle=&rft.title=Clinical+cancer+research+%3A+an+official+journal+of+the+American+Association+for+Cancer+Research&rft.issn=10780432&rft_id=info:doi/10.1158%2F1078-0432.CCR-14-0107
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-10-15
N1 - Date created - 2014-06-14
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1158/1078-0432.CCR-14-0107
ER -
TY - JOUR
T1 - Voriconazole metabolism, toxicity, and the effect of cytochrome P450 2C19 genotype.
AN - 1530953712; 24403552
AB - Prospective evaluation of the antifungal drug, voriconazole, is needed to determine whether drug toxicity correlates with CYP2C19 genotype or serum concentrations of voriconazole or its metabolites.
We conducted a prospective study of 95 patients to determine voriconazole toxicity and its relationship to genotype and serum levels of voriconazole and its two metabolites. Efficacy was not evaluated because, in most cases, the drug was given for empirical or prophylactic therapy. Hallucinations occurred in 16 patients (16.8%), visual changes in 17 (17.9%), photosensitivity in 10 (10.5%), and hepatotoxicity in 6 (6.3%). There was no correlation between photosensitivity or hepatotoxicity and levels of voriconazole or metabolites. Patients with hallucinations had higher average voriconazole levels (4.5 vs 2.5 μg/mL) but with extensive overlap. The recommended oral dose of 200 mg did not provide consistently detectable serum voriconazole levels in adults. CYP2C19 and CYP2C9 genotypes had a minor influence over levels, though the 4 patients homozygous for the 2C19*2 genotype had higher average levels for voriconazole (4.3 vs 2.5 μg/mL) and lower N-oxide levels (1.6 vs 2.5 μg/mL).
CYP2C19 and 2C9 genotypes were not major determinants of voriconazole metabolism. No toxic serum level of voriconazole or its metabolites could be identified. Published by Oxford University Press on behalf of the Infectious Diseases Society of America 2014. This work is written by (a) US Government employee(s) and is in the public domain in the US.
JF - The Journal of infectious diseases
AU - Zonios, Dimitrios
AU - Yamazaki, Hiroshi
AU - Murayama, Norie
AU - Natarajan, Ven
AU - Palmore, Tara
AU - Childs, Richard
AU - Skinner, Jeff
AU - Bennett, John E
AD - National Institute of Allergy and Infectious Diseases, National Institutes of Health (NIH), Bethesda, Maryland. ; Showa Pharmaceutical University, Machida, Tokyo 194-8543, Japan. ; SAIC-Frederick Inc, National Cancer Institute at Frederick, Maryland. ; National Heart, Lung, and Blood Institute, NIH, Bethesda, Maryland.
Y1 - 2014/06/15/
PY - 2014
DA - 2014 Jun 15
SP - 1941
EP - 1948
VL - 209
IS - 12
KW - Antifungal Agents
KW - 0
KW - Pyrimidines
KW - Triazoles
KW - CYP2C9 protein, human
KW - EC 1.14.13.-
KW - Cytochrome P-450 CYP2C9
KW - Aryl Hydrocarbon Hydroxylases
KW - EC 1.14.14.1
KW - CYP2C19 protein, human
KW - Cytochrome P-450 CYP2C19
KW - Voriconazole
KW - JFU09I87TR
KW - Abridged Index Medicus
KW - Index Medicus
KW - metabolites
KW - toxicity
KW - CYP2C19
KW - voriconazole
KW - Young Adult
KW - Homozygote
KW - Dose-Response Relationship, Drug
KW - Humans
KW - Aged
KW - Liver -- metabolism
KW - Prospective Studies
KW - Liver -- drug effects
KW - Adult
KW - Middle Aged
KW - Adolescent
KW - Female
KW - Male
KW - Antifungal Agents -- toxicity
KW - Triazoles -- toxicity
KW - Hallucinations -- chemically induced
KW - Pyrimidines -- toxicity
KW - Triazoles -- blood
KW - Pyrimidines -- blood
KW - Antifungal Agents -- administration & dosage
KW - Aryl Hydrocarbon Hydroxylases -- genetics
KW - Pyrimidines -- administration & dosage
KW - Antifungal Agents -- blood
KW - Triazoles -- administration & dosage
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+infectious+diseases&rft.atitle=Voriconazole+metabolism%2C+toxicity%2C+and+the+effect+of+cytochrome+P450+2C19+genotype.&rft.au=Zonios%2C+Dimitrios%3BYamazaki%2C+Hiroshi%3BMurayama%2C+Norie%3BNatarajan%2C+Ven%3BPalmore%2C+Tara%3BChilds%2C+Richard%3BSkinner%2C+Jeff%3BBennett%2C+John+E&rft.aulast=Zonios&rft.aufirst=Dimitrios&rft.date=2014-06-15&rft.volume=209&rft.issue=12&rft.spage=1941&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+infectious+diseases&rft.issn=1537-6613&rft_id=info:doi/10.1093%2Finfdis%2Fjiu017
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-07-14
N1 - Date created - 2014-05-30
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/infdis/jiu017
ER -
TY - JOUR
T1 - Medial vascular calcification revisited: review and perspectives.
AN - 1548630094; 24740885
AB - Vascular calcifications (VCs) are actively regulated biological processes associated with crystallization of hydroxyapatite in the extracellular matrix and in cells of the media (VCm) or intima (VCi) of the arterial wall. Both patterns of VC often coincide and occur in patients with type II diabetes, chronic kidney disease, and other less frequent disorders; VCs are also typical in senile degeneration. In this article, we review the current state of knowledge about the pathology, molecular biology, and nosology of VCm, expand on potential mechanisms responsible for poor prognosis, and expose some of the directions for future research in this area. Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2014. For permissions please email: journals.permissions@oup.com.
JF - European heart journal
AU - Lanzer, Peter
AU - Boehm, Manfred
AU - Sorribas, Victor
AU - Thiriet, Marc
AU - Janzen, Jan
AU - Zeller, Thomas
AU - St Hilaire, Cynthia
AU - Shanahan, Catherine
AD - Division of Cardiovascular Disease, Department of Internal Medicine, Health Care Center Bitterfeld, Bitterfeld-Wolfen gGmbH, Friedrich-Ludwig-Jahn-Straße 2, D-06749 Bitterfeld-Wolfen, Germany planzer@gzbiwo.de. ; Center for Molecular Medicine, National Institutes of Health, Bethesda, MD, USA. ; Laboratory of Molecular Toxicology, University of Zaragoza, Zaragoza, Spain. ; National Institute for Research in Computer Science and Control, Paris, France. ; VascPath, Bern, Switzerland. ; University Heart Center Freiburg, Bad Krozingen, Germany. ; Cardiovascular Division, King's College London, London, UK.
Y1 - 2014/06/14/
PY - 2014
DA - 2014 Jun 14
SP - 1515
EP - 1525
VL - 35
IS - 23
KW - Biomarkers
KW - 0
KW - Calcium-Binding Proteins
KW - Phosphates
KW - Index Medicus
KW - Vascular function
KW - Vascular molecular biology and genetics
KW - Mönckeberg's media sclerosis
KW - Vascular calcifications
KW - Monckeberg Medial Calcific Sclerosis -- therapy
KW - Renal Insufficiency, Chronic -- physiopathology
KW - Hyperphosphatemia -- physiopathology
KW - Tunica Media -- physiopathology
KW - Phosphates -- physiology
KW - Humans
KW - Tunica Intima -- physiopathology
KW - Prognosis
KW - Monckeberg Medial Calcific Sclerosis -- pathology
KW - Terminology as Topic
KW - Diabetes Mellitus, Type 2 -- physiopathology
KW - Tunica Media -- pathology
KW - Arteriosclerosis -- pathology
KW - Arteriosclerosis -- physiopathology
KW - Monckeberg Medial Calcific Sclerosis -- physiopathology
KW - Diabetes Mellitus, Type 2 -- pathology
KW - Adult
KW - Diabetic Angiopathies -- physiopathology
KW - Biomarkers -- metabolism
KW - Calcium-Binding Proteins -- physiology
KW - Tunica Intima -- pathology
KW - Male
KW - Female
KW - Diabetic Angiopathies -- pathology
KW - Vascular Calcification -- therapy
KW - Vascular Calcification -- physiopathology
KW - Vascular Calcification -- pathology
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1548630094?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+heart+journal&rft.atitle=Medial+vascular+calcification+revisited%3A+review+and+perspectives.&rft.au=Lanzer%2C+Peter%3BBoehm%2C+Manfred%3BSorribas%2C+Victor%3BThiriet%2C+Marc%3BJanzen%2C+Jan%3BZeller%2C+Thomas%3BSt+Hilaire%2C+Cynthia%3BShanahan%2C+Catherine&rft.aulast=Lanzer&rft.aufirst=Peter&rft.date=2014-06-14&rft.volume=35&rft.issue=23&rft.spage=1515&rft.isbn=&rft.btitle=&rft.title=European+heart+journal&rft.issn=1522-9645&rft_id=info:doi/10.1093%2Feurheartj%2Fehu163
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-02-02
N1 - Date created - 2014-06-16
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/eurheartj/ehu163
ER -
TY - JOUR
T1 - Simplagrin, a Platelet Aggregation Inhibitor from Simulium nigrimanum Salivary Glands Specifically Binds to the Von Willebrand Factor Receptor in Collagen and Inhibits Carotid Thrombus Formation In Vivo
AN - 1611613031; 20168513
AB - Blood feeding arthropods-like mosquitoes and black flies-have evolved salivary secretions rich in molecules that affect hemostasis, including vasodilators and inhibitors of blood clotting and platelet aggregation. Among the platelet inhibitors, antagonists of collagen-induced platelet aggregation and adhesion have been found in salivary glands of blood feeders. Here we report the first collagen-binding protein from salivary glands of a black fly. This molecule prevents thrombosis in mice without causing significant bleeding, making it an attractive candidate as an antithrombotic agent. Because blackflies and mosquitoes shared a common blood feeding ancestor approximately 250 million years ago, it appears that collagen-binding activity in salivary glands was an evolutionary innovation present in an ancient dipteran ancestor. Our work highlights the central role of inhibition of platelet aggregation as a vital salivary function in blood feeding arthropods.
JF - PLoS Neglected Tropical Diseases
AU - Chagas, Andrezza C
AU - McPhie, Peter
AU - San, Hong
AU - Narum, David
AU - Reiter, Karine
AU - Tokomasu, Fuyuki
AU - Brayner, Fabio A
AU - Alves, Luiz C
AU - Ribeiro, Jose MC
AU - Calvo, Eric
AD - Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Rockville, Maryland, United States of America
Y1 - 2014/06/12/
PY - 2014
DA - 2014 Jun 12
PB - Public Library of Science, 185 Berry Street San Francisco CA 94107 United States
VL - 8
IS - 6
SN - 1935-2727, 1935-2727
KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources
KW - Simulium
KW - Arthropoda
KW - Glands
KW - Secretion
KW - Receptors
KW - Inhibitors
KW - Aggregation
KW - Aquatic insects
KW - Adhesion
KW - Public health
KW - Collagen
KW - Q1 08484:Species interactions: parasites and diseases
KW - Q5 08524:Public health, medicines, dangerous organisms
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1611613031?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PLoS+Neglected+Tropical+Diseases&rft.atitle=Simplagrin%2C+a+Platelet+Aggregation+Inhibitor+from+Simulium+nigrimanum+Salivary+Glands+Specifically+Binds+to+the+Von+Willebrand+Factor+Receptor+in+Collagen+and+Inhibits+Carotid+Thrombus+Formation+In+Vivo&rft.au=Chagas%2C+Andrezza+C%3BMcPhie%2C+Peter%3BSan%2C+Hong%3BNarum%2C+David%3BReiter%2C+Karine%3BTokomasu%2C+Fuyuki%3BBrayner%2C+Fabio+A%3BAlves%2C+Luiz+C%3BRibeiro%2C+Jose+MC%3BCalvo%2C+Eric&rft.aulast=Chagas&rft.aufirst=Andrezza&rft.date=2014-06-12&rft.volume=8&rft.issue=6&rft.spage=&rft.isbn=&rft.btitle=&rft.title=PLoS+Neglected+Tropical+Diseases&rft.issn=19352727&rft_id=info:doi/10.1371%2Fjournal.pntd.0002947
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-10-01
N1 - Last updated - 2015-06-26
N1 - SubjectsTermNotLitGenreText - Secretion; Glands; Receptors; Aggregation; Inhibitors; Adhesion; Aquatic insects; Collagen; Public health; Simulium; Arthropoda
DO - http://dx.doi.org/10.1371/journal.pntd.0002947
ER -
TY - JOUR
T1 - Macrophage Models of Gaucher Disease for Evaluating Disease Pathogenesis and Candidate Drugs
AN - 1823946437; PQ0001725961
AB - Gaucher disease is caused by an inherited deficiency of glucocerebrosidase that manifests with storage of glycolipids in lysosomes, particularly in macrophages. Available cell lines modeling Gaucher disease do not demonstrate lysosomal storage of glycolipids; therefore, we set out to develop two macrophage models of Gaucher disease that exhibit appropriate substrate accumulation. We used these cellular models both to investigate altered macrophage biology in Gaucher disease and to evaluate candidate drugs for its treatment. We generated and characterized monocyte-derived macrophages from 20 patients carrying different Gaucher disease mutations. In addition, we created induced pluripotent stem cell (iPSC)-derived macrophages from five fibroblast lines taken from patients with type 1 or type 2 Gaucher disease. Macrophages derived from patient monocytes or iPSCs showed reduced glucocerebrosidase activity and increased storage of glucocerebroside and glucosylsphingosine in lysosomes. These macrophages showed efficient phagocytosis of bacteria but reduced production of intracellular reactive oxygen species and impaired chemotaxis. The disease phenotype was reversed with a noninhibitory small-molecule chaperone drug that enhanced glucocerebrosidase activity in the macrophages, reduced glycolipid storage, and normalized chemotaxis and production of reactive oxygen species. Macrophages differentiated from patient monocytes or patient-derived iPSCs provide cellular models that can be used to investigate disease pathogenesis and facilitate drug development.
JF - Science Translational Medicine
AU - Aflaki, Elma
AU - Stubblefield, Barbara K
AU - Maniwang, Emerson
AU - Lopez, Grisel
AU - Moaven, Nima
AU - Goldin, Ehud
AU - Marugan, Juan
AU - Patnaik, Samarjit
AU - Dutra, Amalia
AU - Southall, Noel
AU - Zheng, Wei
AU - Tayebi, Nahid
AU - Sidransky, Ellen
AD - Section on Molecular Neurogenetics, Medical Genetics Branch, National Institutes of Health, Bethesda, MD 20892, USA, sidranse@mail.nih.gov
Y1 - 2014/06/11/
PY - 2014
DA - 2014 Jun 11
PB - American Association for the Advancement of Science, 1200 New York Avenue, NW Washington DC 20005 United States
VL - 6
IS - 240
SN - 1946-6234, 1946-6234
KW - Biotechnology and Bioengineering Abstracts
KW - Macrophages
KW - Translation
KW - Inhibitory postsynaptic potentials
KW - Drug development
KW - Glucosylceramidase
KW - Chemotaxis
KW - Fibroblasts
KW - Glycolipids
KW - Stem cells
KW - Reactive oxygen species
KW - Gaucher's disease
KW - Chaperones
KW - Monocytes
KW - Phagocytosis
KW - Drugs
KW - Mutation
KW - Lysosomes
KW - W 30965:Miscellaneous, Reviews
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1823946437?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Science+Translational+Medicine&rft.atitle=Macrophage+Models+of+Gaucher+Disease+for+Evaluating+Disease+Pathogenesis+and+Candidate+Drugs&rft.au=Aflaki%2C+Elma%3BStubblefield%2C+Barbara+K%3BManiwang%2C+Emerson%3BLopez%2C+Grisel%3BMoaven%2C+Nima%3BGoldin%2C+Ehud%3BMarugan%2C+Juan%3BPatnaik%2C+Samarjit%3BDutra%2C+Amalia%3BSouthall%2C+Noel%3BZheng%2C+Wei%3BTayebi%2C+Nahid%3BSidransky%2C+Ellen&rft.aulast=Aflaki&rft.aufirst=Elma&rft.date=2014-06-11&rft.volume=6&rft.issue=240&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Science+Translational+Medicine&rft.issn=19466234&rft_id=info:doi/10.1126%2Fscitranslmed.3008659
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2016-09-01
N1 - Last updated - 2016-09-29
N1 - SubjectsTermNotLitGenreText - Macrophages; Translation; Inhibitory postsynaptic potentials; Drug development; Glucosylceramidase; Chemotaxis; Fibroblasts; Glycolipids; Stem cells; Reactive oxygen species; Gaucher's disease; Chaperones; Monocytes; Phagocytosis; Mutation; Drugs; Lysosomes
DO - http://dx.doi.org/10.1126/scitranslmed.3008659
ER -
TY - JOUR
T1 - Removing T-cell epitopes with computational protein design.
AN - 1535630293; 24843166
AB - Immune responses can make protein therapeutics ineffective or even dangerous. We describe a general computational protein design method for reducing immunogenicity by eliminating known and predicted T-cell epitopes and maximizing the content of human peptide sequences without disrupting protein structure and function. We show that the method recapitulates previous experimental results on immunogenicity reduction, and we use it to disrupt T-cell epitopes in GFP and Pseudomonas exotoxin A without disrupting function.
JF - Proceedings of the National Academy of Sciences of the United States of America
AU - King, Chris
AU - Garza, Esteban N
AU - Mazor, Ronit
AU - Linehan, Jonathan L
AU - Pastan, Ira
AU - Pepper, Marion
AU - Baker, David
AD - Institute for Protein Design, Department of Biochemistry and chrisk1@uw.edu. ; Department of Immunology, University of Washington, Seattle, WA 98195; and. ; National Cancer Institute and. ; National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD 20892. ; Institute for Protein Design, Department of Biochemistry and.
Y1 - 2014/06/10/
PY - 2014
DA - 2014 Jun 10
SP - 8577
EP - 8582
VL - 111
IS - 23
KW - Bacterial Toxins
KW - 0
KW - Epitopes, T-Lymphocyte
KW - Exotoxins
KW - HLA Antigens
KW - Immunotoxins
KW - Proteins
KW - Virulence Factors
KW - Green Fluorescent Proteins
KW - 147336-22-9
KW - ADP Ribose Transferases
KW - EC 2.4.2.-
KW - toxA protein, Pseudomonas aeruginosa
KW - EC 2.4.2.31
KW - Index Medicus
KW - Rosetta
KW - machine learning
KW - biotherapeutics
KW - immunotoxin
KW - deimmunization
KW - Animals
KW - Spectrometry, Fluorescence
KW - Virulence Factors -- chemistry
KW - Humans
KW - ADP Ribose Transferases -- genetics
KW - Green Fluorescent Proteins -- genetics
KW - Bacterial Toxins -- genetics
KW - ADP Ribose Transferases -- chemistry
KW - Support Vector Machine
KW - Green Fluorescent Proteins -- immunology
KW - Molecular Sequence Data
KW - Computer-Aided Design
KW - Flow Cytometry
KW - Sequence Homology, Amino Acid
KW - Exotoxins -- genetics
KW - HLA Antigens -- genetics
KW - Green Fluorescent Proteins -- chemistry
KW - ADP Ribose Transferases -- immunology
KW - Models, Molecular
KW - Virulence Factors -- genetics
KW - Exotoxins -- chemistry
KW - Cell Line, Tumor
KW - Mice
KW - Exotoxins -- immunology
KW - Bacterial Toxins -- immunology
KW - Virulence Factors -- immunology
KW - Immunization
KW - HLA Antigens -- immunology
KW - Mice, Inbred C57BL
KW - Bacterial Toxins -- chemistry
KW - Protein Structure, Tertiary
KW - Immunotoxins -- chemistry
KW - Proteins -- chemistry
KW - Immunotoxins -- immunology
KW - Protein Engineering -- methods
KW - Immunotoxins -- genetics
KW - Epitopes, T-Lymphocyte -- immunology
KW - Proteins -- genetics
KW - Proteins -- immunology
KW - Epitopes, T-Lymphocyte -- genetics
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Removing+T-cell+epitopes+with+computational+protein+design.&rft.au=King%2C+Chris%3BGarza%2C+Esteban+N%3BMazor%2C+Ronit%3BLinehan%2C+Jonathan+L%3BPastan%2C+Ira%3BPepper%2C+Marion%3BBaker%2C+David&rft.aulast=King&rft.aufirst=Chris&rft.date=2014-06-10&rft.volume=111&rft.issue=23&rft.spage=8577&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=1091-6490&rft_id=info:doi/10.1073%2Fpnas.1321126111
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-09-30
N1 - Date created - 2014-06-14
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Bioinformatics. 2001 Dec;17(12):1236-7 [11751237]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1073/pnas.1321126111
ER -
TY - JOUR
T1 - NADPH oxidases: a perspective on reactive oxygen species production in tumor biology.
AN - 1526730787; 24156355
AB - Reactive oxygen species (ROS) promote genomic instability, altered signal transduction, and an environment that can sustain tumor formation and growth. The NOX family of NADPH oxidases, membrane-bound epithelial superoxide and hydrogen peroxide producers, plays a critical role in the maintenance of immune function, cell growth, and apoptosis. The impact of NOX enzymes in carcinogenesis is currently being defined and may directly link chronic inflammation and NOX ROS-mediated tumor formation.
Increased interest in the function of NOX enzymes in tumor biology has spurred a surge of investigative effort to understand the variability of NOX expression levels in tumors and the effect of NOX activity on tumor cell proliferation. These initial efforts have demonstrated a wide variance in NOX distribution and expression levels across numerous cancers as well as in common tumor cell lines, suggesting that much remains to be discovered about the unique role of NOX-related ROS production within each system. Progression from in vitro cell line studies toward in vivo tumor tissue screening and xenograft models has begun to provide evidence supporting the importance of NOX expression in carcinogenesis. A lack of universally available, isoform-specific antibodies and animal tumor models of inducible knockout or over-expression of NOX isoforms has hindered progress toward the completion of in vivo studies.
In vivo validation experiments and the use of large, existing gene expression data sets should help define the best model systems for studying the NOX homologues in the context of cancer.
JF - Antioxidants & redox signaling
AU - Meitzler, Jennifer L
AU - Antony, Smitha
AU - Wu, Yongzhong
AU - Juhasz, Agnes
AU - Liu, Han
AU - Jiang, Guojian
AU - Lu, Jiamo
AU - Roy, Krishnendu
AU - Doroshow, James H
AD - 1 Laboratory of Molecular Pharmacology of the Center for Cancer Research, National Cancer Institute, National Institutes of Health , Bethesda, Maryland.
Y1 - 2014/06/10/
PY - 2014
DA - 2014 Jun 10
SP - 2873
EP - 2889
VL - 20
IS - 17
KW - Reactive Oxygen Species
KW - 0
KW - Superoxides
KW - 11062-77-4
KW - Hydrogen Peroxide
KW - BBX060AN9V
KW - NADPH Oxidase
KW - EC 1.6.3.1
KW - Index Medicus
KW - Oxidation-Reduction
KW - Reactive Oxygen Species -- metabolism
KW - Superoxides -- metabolism
KW - Apoptosis -- genetics
KW - Hydrogen Peroxide -- metabolism
KW - Humans
KW - Cell Cycle -- genetics
KW - NADPH Oxidase -- metabolism
KW - Signal Transduction -- genetics
KW - Neoplasms -- physiopathology
KW - Cell Proliferation -- genetics
KW - Neoplasms -- therapy
KW - NADPH Oxidase -- genetics
KW - Neoplasms -- genetics
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Antioxidants+%26+redox+signaling&rft.atitle=NADPH+oxidases%3A+a+perspective+on+reactive+oxygen+species+production+in+tumor+biology.&rft.au=Meitzler%2C+Jennifer+L%3BAntony%2C+Smitha%3BWu%2C+Yongzhong%3BJuhasz%2C+Agnes%3BLiu%2C+Han%3BJiang%2C+Guojian%3BLu%2C+Jiamo%3BRoy%2C+Krishnendu%3BDoroshow%2C+James+H&rft.aulast=Meitzler&rft.aufirst=Jennifer&rft.date=2014-06-10&rft.volume=20&rft.issue=17&rft.spage=2873&rft.isbn=&rft.btitle=&rft.title=Antioxidants+%26+redox+signaling&rft.issn=1557-7716&rft_id=info:doi/10.1089%2Fars.2013.5603
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-12-30
N1 - Date created - 2014-05-20
N1 - Date revised - 2017-01-13
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1089/ars.2013.5603
ER -
TY - CPAPER
T1 - Public Health Researcher's Perspective on CECs, Public Health and Inter-Disciplinary
T2 - 2014 Annual Conference of the American Water Works Association (ACE 2014)
AN - 1548628240; 6290475
JF - 2014 Annual Conference of the American Water Works Association (ACE 2014)
AU - Weis, Christopher
Y1 - 2014/06/08/
PY - 2014
DA - 2014 Jun 08
KW - Public health
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1548628240?accountid=14244
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L2 - http://www.awwa.org/conferences-education/conferences/annual-conference/program/ace14-online-program.aspx#
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-30
N1 - Last updated - 2014-07-28
ER -
TY - JOUR
T1 - Allosteric inhibitors of the Eya2 phosphatase are selective and inhibit Eya2-mediated cell migration.
AN - 1549631473; 24755226
AB - Eya proteins are essential co-activators of the Six family of transcription factors and contain a unique tyrosine phosphatase domain belonging to the haloacid dehalogenase family of phosphatases. The phosphatase activity of Eya is important for the transcription of a subset of Six1-target genes, and also directs cells to the repair rather than apoptosis pathway upon DNA damage. Furthermore, Eya phosphatase activity has been shown to mediate transformation, invasion, migration, and metastasis of breast cancer cells, making it a potential new drug target for breast cancer. We have previously identified a class of N-arylidenebenzohydrazide compounds that specifically inhibit the Eya2 phosphatase. Herein, we demonstrate that these compounds are reversible inhibitors that selectively inhibit the phosphatase activity of Eya2, but not Eya3. Our mutagenesis results suggest that this class of compounds does not bind to the active site and the binding does not require the coordination with Mg(2+). Moreover, these compounds likely bind within a site on the opposite face of the active site, and function as allosteric inhibitors. We also demonstrate that this class of compounds inhibits Eya2 phosphatase-mediated cell migration, setting the foundation for these molecules to be developed into chemical probes for understanding the specific function of the Eya2 phosphatase and to serve as a prototype for the development of Eya2 phosphatase specific anti-cancer drugs.
© 2014 by The American Society for Biochemistry and Molecular Biology, Inc.
JF - The Journal of biological chemistry
AU - Krueger, Aaron B
AU - Drasin, David J
AU - Lea, Wendy A
AU - Patrick, Aaron N
AU - Patnaik, Samarjit
AU - Backos, Donald S
AU - Matheson, Christopher J
AU - Hu, Xin
AU - Barnaeva, Elena
AU - Holliday, Michael J
AU - Blevins, Melanie A
AU - Robin, Tyler P
AU - Eisenmesser, Elan Z
AU - Ferrer, Marc
AU - Simeonov, Anton
AU - Southall, Noel
AU - Reigan, Philip
AU - Marugan, Juan
AU - Ford, Heide L
AU - Zhao, Rui
AD - From the Department of Biochemistry and Molecular Genetics, University of Colorado School of Medicine, Aurora, Colorado 80045. ; the Department of Pharmacology, University of Colorado School of Medicine, Aurora, Colorado 80045. ; the National Center for Advancing Translational Sciences, National Institutes of Health, Bethesda, Maryland 20892, and. ; the Department of Pharmaceutical Sciences, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado School of Pharmacy, Aurora, Colorado 80045. ; the National Center for Advancing Translational Sciences, National Institutes of Health, Bethesda, Maryland 20892, and maruganj@mail.nih.gov. ; the Department of Pharmacology, University of Colorado School of Medicine, Aurora, Colorado 80045, heide.ford@ucdenver.edu. ; From the Department of Biochemistry and Molecular Genetics, University of Colorado School of Medicine, Aurora, Colorado 80045, rui.zhao@ucdenver.edu.
Y1 - 2014/06/06/
PY - 2014
DA - 2014 Jun 06
SP - 16349
EP - 16361
VL - 289
IS - 23
KW - Enzyme Inhibitors
KW - 0
KW - Intracellular Signaling Peptides and Proteins
KW - Nuclear Proteins
KW - EYA2 protein, human
KW - EC 3.1.3.48
KW - Protein Tyrosine Phosphatases
KW - Magnesium
KW - I38ZP9992A
KW - Index Medicus
KW - Transcription Coactivator
KW - Enzyme Inhibitor
KW - Phosphatase
KW - Migration
KW - Anticancer Drug
KW - Humans
KW - Spectrophotometry, Ultraviolet
KW - Amino Acid Sequence
KW - Protein Binding
KW - Magnesium -- metabolism
KW - Molecular Docking Simulation
KW - Nuclear Magnetic Resonance, Biomolecular
KW - Molecular Sequence Data
KW - Calorimetry
KW - Enzyme Inhibitors -- pharmacology
KW - Allosteric Regulation
KW - Crystallography, X-Ray
KW - Sequence Homology, Amino Acid
KW - Cell Line
KW - Intracellular Signaling Peptides and Proteins -- chemistry
KW - Protein Tyrosine Phosphatases -- metabolism
KW - Protein Tyrosine Phosphatases -- physiology
KW - Nuclear Proteins -- antagonists & inhibitors
KW - Intracellular Signaling Peptides and Proteins -- antagonists & inhibitors
KW - Intracellular Signaling Peptides and Proteins -- metabolism
KW - Cell Movement -- physiology
KW - Nuclear Proteins -- chemistry
KW - Intracellular Signaling Peptides and Proteins -- physiology
KW - Nuclear Proteins -- metabolism
KW - Nuclear Proteins -- physiology
KW - Protein Tyrosine Phosphatases -- chemistry
KW - Protein Tyrosine Phosphatases -- antagonists & inhibitors
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Allosteric+inhibitors+of+the+Eya2+phosphatase+are+selective+and+inhibit+Eya2-mediated+cell+migration.&rft.au=Krueger%2C+Aaron+B%3BDrasin%2C+David+J%3BLea%2C+Wendy+A%3BPatrick%2C+Aaron+N%3BPatnaik%2C+Samarjit%3BBackos%2C+Donald+S%3BMatheson%2C+Christopher+J%3BHu%2C+Xin%3BBarnaeva%2C+Elena%3BHolliday%2C+Michael+J%3BBlevins%2C+Melanie+A%3BRobin%2C+Tyler+P%3BEisenmesser%2C+Elan+Z%3BFerrer%2C+Marc%3BSimeonov%2C+Anton%3BSouthall%2C+Noel%3BReigan%2C+Philip%3BMarugan%2C+Juan%3BFord%2C+Heide+L%3BZhao%2C+Rui&rft.aulast=Krueger&rft.aufirst=Aaron&rft.date=2014-06-06&rft.volume=289&rft.issue=23&rft.spage=16349&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M114.566729
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-10-07
N1 - Date created - 2014-07-29
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1074/jbc.M114.566729
ER -
TY - JOUR
T1 - Dopamine D(3) receptors contribute to methamphetamine-induced alterations in dopaminergic neuronal function: role of hyperthermia.
AN - 1521333684; 24685638
AB - Methamphetamine administration causes long-term deficits to dopaminergic systems that, in humans, are thought to be associated with motor slowing and memory impairment. Methamphetamine interacts with the dopamine transporter (DAT) and increases extracellular concentrations of dopamine that, in turn, binds to a number of dopamine receptor subtypes. Although the relative contribution of each receptor subtype to the effects of methamphetamine is not fully known, non-selective dopamine D2/D3 receptor antagonists can attenuate methamphetamine-induced changes to dopamine systems. The present study extended these findings by testing the role of the dopamine D3 receptor subtype in mediating the long-term dopaminergic, and for comparison serotonergic, deficits caused by methamphetamine. Results indicate that the dopamine D3 receptor selective antagonist, PG01037, attenuated methamphetamine-induced decreases in striatal DAT, but not hippocampal serotonin (5HT) transporter (SERT), function, as assessed 7 days after treatment. However, PG01037 also attenuated methamphetamine-induced hyperthermia. When methamphetamine-induced hyperthermia was maintained by treating rats in a warm ambient environment, PG01037 failed to attenuate the effects of methamphetamine on DAT uptake. Furthermore, PG01037 did not attenuate methamphetamine-induced decreases in dopamine and 5HT content. Taken together, the present study demonstrates that dopamine D3 receptors mediate, in part, the long-term deficits in DAT function caused by methamphetamine, and that this effect likely involves an attenuation of methamphetamine-induced hyperthermia.
Copyright © 2014 Elsevier B.V. All rights reserved.
JF - European journal of pharmacology
AU - Baladi, Michelle G
AU - Newman, Amy H
AU - Nielsen, Shannon M
AU - Hanson, Glen R
AU - Fleckenstein, Annette E
AD - Department of Pharmacology and Toxicology, University of Utah, Salt Lake City, Utah, USA. ; Medicinal Chemistry Section, National Institute on Drug Abuse, Intramural Research Program, National Institutes of Health, Baltimore, MD, USA. ; Department of Pharmacology and Toxicology, University of Utah, Salt Lake City, Utah, USA; School of Dentistry, University of Utah, Salt Lake City, Utah, USA. ; Department of Pharmacology and Toxicology, University of Utah, Salt Lake City, Utah, USA. Electronic address: fleckenstein@hsc.utah.edu.
Y1 - 2014/06/05/
PY - 2014
DA - 2014 Jun 05
SP - 105
EP - 110
VL - 732
KW - Central Nervous System Stimulants
KW - 0
KW - Dopamine Antagonists
KW - Receptors, Dopamine D3
KW - Serotonin
KW - 333DO1RDJY
KW - Methamphetamine
KW - 44RAL3456C
KW - Dopamine
KW - VTD58H1Z2X
KW - Index Medicus
KW - Dopamine transporter
KW - Dopamine D(3) receptors
KW - PG01037
KW - Serotonin transporter
KW - D(3) antagonist
KW - Rats
KW - Animals
KW - Rats, Sprague-Dawley
KW - Synaptosomes -- drug effects
KW - Serotonin -- physiology
KW - Dopamine Antagonists -- pharmacology
KW - Hippocampus -- metabolism
KW - Dopamine -- metabolism
KW - Synaptosomes -- metabolism
KW - Male
KW - Hippocampus -- drug effects
KW - Dopaminergic Neurons -- drug effects
KW - Central Nervous System Stimulants -- toxicity
KW - Receptors, Dopamine D3 -- drug effects
KW - Fever -- physiopathology
KW - Methamphetamine -- toxicity
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-12-09
N1 - Date created - 2014-05-05
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.ejphar.2014.03.023
ER -
TY - JOUR
T1 - Residential Levels of Polybrominated Diphenyl Ethers and Risk of Childhood Acute Lymphoblastic Leukemia in California
AN - 1622604891; 20889827
AB - Background: House dust is a major source of exposure to polybrominated diphenyl ethers (PBDEs), which are found at high levels in U.S. homes. Methods: We studied 167 acute lymphoblastic leukemia (ALL) cases 0-7 years of age and 214 birth certificate controls matched on date of birth, sex, and race/ethnicity from the Northern California Childhood Leukemia Study. In 2001-2007, we sampled carpets in the room where the child spent the most time while awake; we used a high-volume small-surface sampler or we took dust from the home vacuum. We measured concentrations of 14 PBDE congeners including penta (28, 47, 99, 100, 153, 154), octa (183, 196, 197, 203), and decaBDEs (206-209). Odds ratios (ORs) were calculated using logistic regression, adjusting for demographics, income, year of dust collection, and sampling method. Results: BDE-47, BDE-99, and BDE-209 were found at the highest concentrations (medians, 1,173, 1,579, and 938 ng/g, respectively). Comparing the highest to lowest quartile, we found no association with ALL for summed pentaBDEs (OR = 0.7; 95% CI: 0.4, 1.3), octaBDEs (OR = 1.3; 95% CI: 0.7, 2.3), or decaBDEs (OR = 1.0; 95% CI: 0.6, 1.8). Comparing homes in the highest concentration (nanograms per gram) tertile to those with no detections, we observed significantly increased ALL risk for BDE-196 (OR = 2.1; 95% CI: 1.1, 3.8), BDE-203 (OR = 2.0; 95% CI: 1.1, 3.6), BDE-206 (OR = 2.1; 95% CI: 1.1, 3.9), and BDE-207 (OR = 2.0; 95% CI: 1.03, 3.8). Conclusion: We found no association with ALL for common PBDEs, but we observed positive associations for specific octa and nonaBDEs. Additional studies with repeated sampling and biological measures would be informative. Citation: Ward MH, Colt JS, Deziel NC, Whitehead TP, Reynolds P, Gunier RB, Nishioka M, Dahl GV, Rappaport SM, Buffler PA, Metayer C. 2014. Residential levels of polybrominated diphenyl ethers and risk of childhood acute lymphoblastic leukemia in California. Environ Health Perspect 122:1110-1116; http://dx.doi.org/10.1289/ehp.1307602
JF - Environmental Health Perspectives
AU - Ward, Mary H
AU - Colt, Joanne S
AU - Deziel, Nicole C
AU - Whitehead, Todd P
AU - Reynolds, Peggy
AU - Gunier, Robert B
AU - Nishioka, Marcia
AU - Dahl, Gary V
AU - Rappaport, Stephen M
AU - Buffler, Patricia A
AU - Metayer, Catherine
AD - Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland, USA
Y1 - 2014/06/03/
PY - 2014
DA - 2014 Jun 03
SP - 1110
EP - 1116
PB - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States
VL - 122
IS - 10
SN - 0091-6765, 0091-6765
KW - Toxicology Abstracts; Risk Abstracts; Health & Safety Science Abstracts
KW - Age
KW - Retinoblastoma protein
KW - Dust
KW - Income
KW - Polybrominated diphenyl ethers
KW - Demography
KW - Leukemia
KW - Carpets
KW - Acute lymphatic leukemia
KW - Congeners
KW - USA, California
KW - Sampling
KW - Ethnic groups
KW - Races
KW - Sex
KW - Vacuum
KW - Children
KW - Samplers
KW - Birth
KW - polybrominated diphenyl ethers
KW - House dust
KW - Sampling methods
KW - H 12000:Epidemiology and Public Health
KW - R2 23060:Medical and environmental health
KW - X 24350:Industrial Chemicals
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-11-01
N1 - Last updated - 2015-05-13
N1 - SubjectsTermNotLitGenreText - Retinoblastoma protein; Vacuum; Children; Samplers; Dust; Birth; Demography; polybrominated diphenyl ethers; House dust; Carpets; Acute lymphatic leukemia; Congeners; Sampling; Races; Ethnic groups; Sex; Polybrominated diphenyl ethers; Leukemia; Age; Sampling methods; Income; USA, California
DO - http://dx.doi.org/10.1289/ehp.1307602
ER -
TY - JOUR
T1 - Virus World as an Evolutionary Network of Viruses and Capsidless Selfish Elements
AN - 1753468656; 19990207
JF - Microbiology and Molecular Biology Reviews
AU - Koonin, Eugene V
AU - Dolja, Valerian V
AD - National Center for Biotechnology Information, National Library of Medicine, Bethesda, Maryland, USA, koonin@ncbi.nlm.nih.gov.
Y1 - 2014/06//
PY - 2014
DA - June 2014
SP - 278
EP - 303
PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL - 78
IS - 2
SN - 1092-2172, 1092-2172
KW - Microbiology Abstracts B: Bacteriology
KW - Evolution
KW - J 02310:Genetics & Taxonomy
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2016-01-01
N1 - Number of references - 202
N1 - Last updated - 2016-09-14
N1 - SubjectsTermNotLitGenreText - Evolution
DO - http://dx.doi.org/10.1128/MMBR.00049-13
ER -
TY - JOUR
T1 - Central nervous system norcardiosis with granulomatous pachymeningitis and osteomyelitis of skull vault
AN - 1722170056; PQ0002098617
AB - A 34-year-old immunocompetent man weighing 95 kg was operated for a small left parietal scalp swelling in the year 2002. He was well until 2008, when he developed chronic diffuse headache, vomiting and drowsiness. The left parietal dura and overlying vault biopsy showed evidence of granulomatous pachymeningitis with osteomyelitis secondary to nocardiosis. He had responded well to inadequate antibiotic therapy. After a dormant period of 3 years, there was recrudescence of severe raised intracranial tension symptoms in 2011. Magnetic resonance imaging showed diffuse pachymeningeal thickening mainly involving the occipital dura, posterior falx, and tentorium cerebelli. In addition, well-defined small nodules with hypointense signals on both Tl- and T2-weighted images were seen in occipital lobes. Patient was treated with three drug regime with good recovery at 3 months follow-up. This is a rare case of central nervous system nocardiosis with skull vault osteomyelitis and a protracted clinical course.
JF - Indian Journal of Pathology and Microbiology
AU - Nalini, Atchayaram
AU - Saini, Jitender
AU - Mahadevan, Anita
AD - Department of Neurology, National Institute of Mental Health and Neurosciences, Bengaluru, Karnataka, India
Y1 - 2014/06//
PY - 2014
DA - June 2014
SP - 332
EP - 334
PB - Medknow Publications and Media Pvt. Ltd., B-9, Kanara Business Ctr, Off Link Rd, Ghatkopar (E) Mumbai, Maharastra 400 075 India
VL - 57
IS - 2
SN - 0377-4929, 0377-4929
KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Calcium & Calcified Tissue Abstracts; CSA Neurosciences Abstracts
KW - Central nervous system
KW - Nocardiosis
KW - Vomiting
KW - Scalp
KW - Magnetic resonance imaging
KW - Antibiotics
KW - Drowsiness
KW - Biopsy
KW - Nodules
KW - Skull
KW - Headache
KW - Occipital lobe
KW - Drugs
KW - Osteomyelitis
KW - N3 11027:Neurology & neuropathology
KW - T 2025:Bone and Bone Diseases
KW - A 01400:Soil Microbes
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Indian+Journal+of+Pathology+and+Microbiology&rft.atitle=Central+nervous+system+norcardiosis+with+granulomatous+pachymeningitis+and+osteomyelitis+of+skull+vault&rft.au=Nalini%2C+Atchayaram%3BSaini%2C+Jitender%3BMahadevan%2C+Anita&rft.aulast=Nalini&rft.aufirst=Atchayaram&rft.date=2014-06-01&rft.volume=57&rft.issue=2&rft.spage=332&rft.isbn=&rft.btitle=&rft.title=Indian+Journal+of+Pathology+and+Microbiology&rft.issn=03774929&rft_id=info:doi/10.4103%2F0377-4929.134735
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-10-01
N1 - Last updated - 2016-02-18
N1 - SubjectsTermNotLitGenreText - Central nervous system; Vomiting; Nocardiosis; Scalp; Magnetic resonance imaging; Biopsy; Drowsiness; Antibiotics; Nodules; Skull; Headache; Occipital lobe; Drugs; Osteomyelitis
DO - http://dx.doi.org/10.4103/0377-4929.134735
ER -
TY - JOUR
T1 - Modelling batched Gaussian longitudinal weight data in mice subject to informative dropout
AN - 1683508521
AB - Modelling longitudinal data subject to informative dropout is an active area in statistical research. This article focuses on modelling such longitudinal data when the outcome at each follow-up time is collected in batches rather than individually collected. The problem occurred in a study that compared the weight of mice over time between a control and a treatment group, where animal weight was measured in batches of five animals per cage. We develop both a shared parameter and a pattern mixture modelling approach for accounting for potentially informative dropout due to an animalʼs death. Our methodology suggests that animals receiving the treatment have a lower weight in mid-life, and have a slower decline in weight in the later period of life. Our simulations suggest that both the shared random parameter and pattern mixture modelling approaches work well under a correctly specified model. However, the pattern mixture model is more robust against model misspecification than the shared random parameter model, but the shared random parameter model parameters have a more direct interpretation than those of the pattern mixture modelling approach.
JF - Statistical Methods in Medical Research
AU - Albert, Paul S
AU - Shih, Joanna H
AD - Biostatistics and Bioinformatics Branch, Division of Epidemiology, Statistics, and Prevention Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD, USA ; Biometrics Research Branch, Division of Cancer Treatment and Diagnosis, National Cancer Institute, Bethesda, MD, USA ; Biostatistics and Bioinformatics Branch, Division of Epidemiology, Statistics, and Prevention Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD, USA
Y1 - 2014/06//
PY - 2014
DA - Jun 2014
SP - 203
EP - 217
CY - London
PB - Sage Publications Ltd.
VL - 23
IS - 3
SN - 0962-2802
KW - Medical Sciences
KW - Missing data
KW - pattern mixture models
KW - repeated measures
KW - shared random parameter models
KW - Animals
KW - Approaches
KW - Death
KW - Dropping out
KW - Methodology
KW - Modelling
KW - Parameters
KW - Weight
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1683508521?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Statistical+Methods+in+Medical+Research&rft.atitle=Modelling+batched+Gaussian+longitudinal+weight+data+in+mice+subject+to+informative+dropout&rft.au=Albert%2C+Paul+S%3BShih%2C+Joanna+H&rft.aulast=Albert&rft.aufirst=Paul&rft.date=2014-06-01&rft.volume=23&rft.issue=3&rft.spage=203&rft.isbn=&rft.btitle=&rft.title=Statistical+Methods+in+Medical+Research&rft.issn=09622802&rft_id=info:doi/10.1177%2F0962280210397886
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Date revised - 2015-05-12
N1 - Last updated - 2016-05-12
DO - http://dx.doi.org/10.1177/0962280210397886
ER -
TY - JOUR
T1 - Mental Health of HIV-Seropositive Women During Pregnancy and Postpartum Period: A Comprehensive Literature Review
AN - 1680149897; 201502965
AB - With growing numbers of HIV-seropositive (HIV+) women of child-bearing age and increased access to effective clinical protocols for preventing mother-to-child transmission (MTCT) of HIV, mental health-related factors have become increasingly relevant due to their potential to affect the women's quality of life, obstetric outcomes and risk of MTCT. This review synthesizes evidence from 53 peer-reviewed publications examining mental health-related variables in pregnant and postpartum HIV+ women. The presentation of results is organized by the level of socioeconomic resources in the countries where studies were conducted (i.e., high-, middle-, and low-income countries). It is concluded that psychiatric symptoms, particularly depression, and mental health vulnerabilities (e.g., inadequate coping skills) are widespread among pregnant HIV+ women globally and have a potential to affect psychological well-being, quality of life and salient clinical outcomes. The current body of evidence provides rationale for developing and evaluating clinical and structural interventions aimed at improving mental health outcomes and their clinical correlates in pregnant HIV+ women. Adapted from the source document.
JF - AIDS and Behavior
AU - Kapetanovic, Suad
AU - Dass-Brailsford, Priscilla
AU - Nora, Diana
AU - Talisman, Nicholas
AD - National Institutes of Health, National Institute of Mental Health, Bethesda, MD, USA suad.kapetanovic@nih.gov
Y1 - 2014/06//
PY - 2014
DA - June 2014
SP - 1152
EP - 1173
PB - Springer, Dordrecht, The Netherlands
VL - 18
IS - 6
SN - 1090-7165, 1090-7165
KW - Treatment Outcomes
KW - Depression (Psychology)
KW - Well Being
KW - Acquired Immune Deficiency Syndrome
KW - Quality of Life
KW - Mental Health
KW - Females
KW - Literature Reviews
KW - Pregnancy
KW - article
KW - 6126: acquired immune deficiency syndrome (AIDS)
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1680149897?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Asocialservices&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS+and+Behavior&rft.atitle=Mental+Health+of+HIV-Seropositive+Women+During+Pregnancy+and+Postpartum+Period%3A+A+Comprehensive+Literature+Review&rft.au=Kapetanovic%2C+Suad%3BDass-Brailsford%2C+Priscilla%3BNora%2C+Diana%3BTalisman%2C+Nicholas&rft.aulast=Kapetanovic&rft.aufirst=Suad&rft.date=2014-06-01&rft.volume=18&rft.issue=6&rft.spage=1152&rft.isbn=&rft.btitle=&rft.title=AIDS+and+Behavior&rft.issn=10907165&rft_id=info:doi/10.1007%2Fs10461-014-0728-9
LA - English
DB - Social Services Abstracts
N1 - Date revised - 2015-05-01
N1 - Number of references - 73
N1 - Last updated - 2016-09-28
N1 - CODEN - AIBEFC
N1 - SubjectsTermNotLitGenreText - Females; Acquired Immune Deficiency Syndrome; Pregnancy; Treatment Outcomes; Quality of Life; Depression (Psychology); Well Being; Mental Health; Literature Reviews
DO - http://dx.doi.org/10.1007/s10461-014-0728-9
ER -
TY - JOUR
T1 - Challenges in diagnosing a metabolic disorder: error of pyruvate metabolism or drug induced?
AN - 1671215324; 23439713
AB - Certain drugs are known to cause metabolic changes resulting in altered metabolic profiles. We report here a case where a combination of antiepileptic drugs resulted in a profile that mimicked a metabolic disorder. A 16month-old female child on antiepileptic drugs (valproate and topiramate) was suspected to have the inherited metabolic disorder, dihydrolipoamide dehydrogenase deficiency, based on clinical symptoms and metabolic profile showing hyperalaninemia, elevated branched-chain amino acids, and lactate-pyruvate ratio. Suspecting that the observed metabolic changes could have also arised from medication, current medication was weaned off and replaced with levetiracetam, clonazepam, and levocarnitine (supportive therapy). Metabolic profiling conducted after 47 days showed normal alanine, branched-chain amino acids, ornithine, and lactate-pyruvate ratio, suggesting that the earlier abnormalities could have been medication induced. We stress that metabolic changes resulting from chronic medication should be considered while interpreting a positive result when investigating an inherited metabolic disorder.
© The Author(s) 2013.
JF - Journal of child neurology
AU - Mampilly, George Tomy
AU - Mampilly, Tomy Kochuvareed
AU - Christopher, Rita
AU - Chandramohan, Neeradha
AU - Janaki, Vijayalakshmy
AD - Department of Physical Medicine and Rehabilitation, National Institute for Empowerment of Persons with Multiple Disabilities, Muttukadu, Chennai, India. ; Department of Physical Medicine and Rehabilitation, National Institute for Empowerment of Persons with Multiple Disabilities, Muttukadu, Chennai, India tomymampilly@gmail.com. ; Department of Neurochemistry, National Institute of Mental Health and Neurosciences, Bangalore, India. ; Department of Clinical Psychology, National Institute for Empowerment of Persons with Multiple Disabilities, Muttukadu, Chennai, India.
Y1 - 2014/06//
PY - 2014
DA - June 2014
SP - 833
EP - 836
VL - 29
IS - 6
KW - Anticonvulsants
KW - 0
KW - topiramate
KW - 0H73WJJ391
KW - Fructose
KW - 30237-26-4
KW - Valproic Acid
KW - 614OI1Z5WI
KW - Pyruvic Acid
KW - 8558G7RUTR
KW - Index Medicus
KW - valproate
KW - metabolic disorder
KW - false positives
KW - Infant
KW - Fructose -- analogs & derivatives
KW - Humans
KW - Fructose -- adverse effects
KW - Valproic Acid -- adverse effects
KW - Female
KW - Metabolic Diseases -- chemically induced
KW - Anticonvulsants -- adverse effects
KW - Pyruvic Acid -- metabolism
KW - Metabolic Diseases -- diagnosis
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1671215324?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+child+neurology&rft.atitle=Challenges+in+diagnosing+a+metabolic+disorder%3A+error+of+pyruvate+metabolism+or+drug+induced%3F&rft.au=Mampilly%2C+George+Tomy%3BMampilly%2C+Tomy+Kochuvareed%3BChristopher%2C+Rita%3BChandramohan%2C+Neeradha%3BJanaki%2C+Vijayalakshmy&rft.aulast=Mampilly&rft.aufirst=George&rft.date=2014-06-01&rft.volume=29&rft.issue=6&rft.spage=833&rft.isbn=&rft.btitle=&rft.title=Journal+of+child+neurology&rft.issn=1708-8283&rft_id=info:doi/10.1177%2F0883073813477201
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-11-02
N1 - Date created - 2015-04-07
N1 - Date revised - 2017-01-13
N1 - Last updated - 2017-01-18
DO - http://dx.doi.org/10.1177/0883073813477201
ER -
TY - JOUR
T1 - Infectivity of urogenital Chlamydia trachomatis plasmid-deficient, CT135-null, and double-deficient strains in female mice
AN - 1654666334; 21296995
AB - Chlamydia trachomatis is the most common cause of human bacterial sexually transmitted infections and is the world's leading cause of infectious preventable blindness. The chlamydial 7.5-kb plasmid and chromosomal gene CT135 have been shown to be important virulence factors in both nonhuman primate and mouse infection models. Chlamydia trachomatis plasmid-deficient urogenital isolates and a predicted CT135 null mutant have been evaluated independently in the female mouse genital tract model and both have been shown to reduce infectivity and virulence. However, these attenuating phenotypes have not been evaluated collectively in the murine model. Here, we test the infectivity of C. trachomatis serovar D strains in the mouse model that are plasmid-deficient, CT135 disrupted, or possess a combination of these attenuating genotypes. We find that the presence of the plasmid results in infections with higher infectious burdens, whereas CT135 facilitates a more protracted or chronic infection. Not unexpectedly, a combination of these genetic deficiencies resulted in a strain with enhanced infection attenuation characteristics. A composite figure showing scanning (left) and transmission (right-center) electron photomicrographs of Chlamydia trachomatis infected epithelial cells. The biosynthesis of glycogen (gold granules among blue developmental forms) is dependent on the chlamydial plasmid which is thought to be an important virulence factor.
JF - Pathogens and Disease
AU - Sturdevant, Gail L
AU - Zhou, Bing
AU - Carlson, John H
AU - Whitmire, William M
AU - Song, Lihua
AU - Caldwell, Harlan D
AD - Laboratory of Intracellular Parasites, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT, USA.
Y1 - 2014/06//
PY - 2014
DA - Jun 2014
SP - 90
EP - 92
PB - Wiley Subscription Services, Inc., 1105 N Market St Wilmington DE 19801 England
VL - 71
IS - 1
SN - 2049-632X, 2049-632X
KW - Microbiology Abstracts B: Bacteriology
KW - Granules
KW - Epithelial cells
KW - virulence factors
KW - Animal models
KW - Chlamydia trachomatis
KW - Genotypes
KW - Blindness
KW - Pathogens
KW - Plasmids
KW - Glycogen
KW - Infectivity
KW - Scanning
KW - Chronic infection
KW - Gold
KW - Genital tract
KW - J 02410:Animal Diseases
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1654666334?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pathogens+and+Disease&rft.atitle=Infectivity+of+urogenital+Chlamydia+trachomatis+plasmid-deficient%2C+CT135-null%2C+and+double-deficient+strains+in+female+mice&rft.au=Sturdevant%2C+Gail+L%3BZhou%2C+Bing%3BCarlson%2C+John+H%3BWhitmire%2C+William+M%3BSong%2C+Lihua%3BCaldwell%2C+Harlan+D&rft.aulast=Sturdevant&rft.aufirst=Gail&rft.date=2014-06-01&rft.volume=71&rft.issue=1&rft.spage=90&rft.isbn=&rft.btitle=&rft.title=Pathogens+and+Disease&rft.issn=2049632X&rft_id=info:doi/10.1111%2F2049-632X.12121
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-02-01
N1 - Last updated - 2015-11-16
N1 - SubjectsTermNotLitGenreText - Granules; Epithelial cells; virulence factors; Animal models; Pathogens; Blindness; Genotypes; Plasmids; Glycogen; Infectivity; Scanning; Chronic infection; Gold; Genital tract; Chlamydia trachomatis
DO - http://dx.doi.org/10.1111/2049-632X.12121
ER -
TY - JOUR
T1 - Regional Variation in the Correlation of Antibody and T-Cell Responses to Trypanosoma cruzi
AN - 1647022865; 21189927
AB - Chagas disease, caused by the protozoan parasite Trypanosoma cruzi, is a major cause of morbidity and mortality in Central and South America. Geographic variations in the sensitivity of serologic diagnostic assays to T. cruzi may reflect differences in T. cruzi exposure. We measured parasite-specific T-cell responses among seropositive individuals in two populations from South America with widely varying antibody titers against T. cruzi. Antibody titers among seropositive individuals were significantly lower in Arequipa, Peru compared with Santa Cruz, Bolivia. Similarly, the proportion of seropositive individuals with positive T-cell responses was lower in Peru than Bolivia, resulting in overall lower frequencies of interferon- gamma (IFN gamma )-secreting cells from Peruvian samples. However, the magnitude of the IFN gamma response was similar among the IFN gamma responders in both locations. These data indicate that immunological discrepancies based on geographic region are reflected in T-cell responses as well as antibody responses.
JF - American Journal of Tropical Medicine and Hygiene
AU - Martin, Diana L
AU - Marks, Morgan
AU - Galdos-Cardenas, Gerson
AU - Gilman, Robert H
AU - Goodhew, Brook
AU - Ferrufino, Lisbeth
AU - Halperin, Anthony
AU - Sanchez, Gerardo
AU - Verastegui, Manuela
AU - Escalante, Patricia
AU - Naquira, Cesar
AU - Levy, Michael Z
AU - Bern, Caryn
AD - National Institutes of Health, Bethesda, Maryland; Hospital Universitario Japones, Santa Cruz, Bolivia; Asociacion Benefica PRISMA, Lima, Peru; Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland; Arequipa Ministry of Health, Arequipa, Peru; University of Pennsylvania, Philadelphia, Pennsylvania; Universidad Peruana Cayetano Heredia, Lima, Peru; Division of Parasitic Diseases and Malaria, MS D-65, 1600 Clifton Road NE, Centers for Disease Control and Prevention, Atlanta, GA 30329, hz3@cdc.gov
Y1 - 2014/06//
PY - 2014
DA - June 2014
SP - 1074
EP - 1081
PB - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States
VL - 90
IS - 6
SN - 0002-9637, 0002-9637
KW - Microbiology Abstracts B: Bacteriology; Microbiology Abstracts C: Algology, Mycology & Protozoology; ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality
KW - Trypanosoma cruzi
KW - gamma -Interferon
KW - Mortality
KW - Parasites
KW - Data processing
KW - Morbidity
KW - Bolivia
KW - Public health
KW - Antibodies
KW - Lymphocytes T
KW - Peru
KW - Geographical variations
KW - Hygiene
KW - Regional variations
KW - Mortality causes
KW - Chagas' disease
KW - K 03350:Immunology
KW - Q1 08484:Species interactions: parasites and diseases
KW - Q5 08502:Methods and instruments
KW - J 02350:Immunology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.atitle=Regional+Variation+in+the+Correlation+of+Antibody+and+T-Cell+Responses+to+Trypanosoma+cruzi&rft.au=Martin%2C+Diana+L%3BMarks%2C+Morgan%3BGaldos-Cardenas%2C+Gerson%3BGilman%2C+Robert+H%3BGoodhew%2C+Brook%3BFerrufino%2C+Lisbeth%3BHalperin%2C+Anthony%3BSanchez%2C+Gerardo%3BVerastegui%2C+Manuela%3BEscalante%2C+Patricia%3BNaquira%2C+Cesar%3BLevy%2C+Michael+Z%3BBern%2C+Caryn&rft.aulast=Martin&rft.aufirst=Diana&rft.date=2014-06-01&rft.volume=90&rft.issue=6&rft.spage=1074&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.13-0391
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-01-01
N1 - Last updated - 2016-03-17
N1 - SubjectsTermNotLitGenreText - Parasites; Antibodies; Hygiene; Regional variations; Mortality causes; Public health; Mortality; gamma -Interferon; Data processing; Lymphocytes T; Geographical variations; Morbidity; Chagas' disease; Trypanosoma cruzi; Peru; Bolivia
DO - http://dx.doi.org/10.4269/ajtmh.13-0391
ER -
TY - JOUR
T1 - Mitigating the risk of radiation-induced cancers: limitations and paradigms in drug development
AN - 1642619725; 21099727
AB - The United States radiation medical countermeasures (MCM) programme for radiological and nuclear incidents has been focusing on developing mitigators for the acute radiation syndrome (ARS) and delayed effects of acute radiation exposure (DEARE), and biodosimetry technologies to provide radiation dose assessments for guiding treatment. Because a nuclear accident or terrorist incident could potentially expose a large number of people to low to moderate doses of ionising radiation, and thus increase their excess lifetime cancer risk, there is an interest in developing mitigators for this purpose. This article discusses the current status, issues, and challenges regarding development of mitigators against radiation-induced cancers. The challenges of developing mitigators for ARS include: the long latency between exposure and cancer manifestation, limitations of animal models, potential side effects of the mitigator itself, potential need for long-term use, the complexity of human trials to demonstrate effectiveness, and statistical power constraints for measuring health risks (and reduction of health risks after mitigation) following relatively low radiation doses (<0:75 Gy). Nevertheless, progress in the understanding of the molecular mechanisms resulting in radiation injury, along with parallel progress in dose assessment technologies, make this an opportune, if not critical, time to invest in research strategies that result in the development of agents to lower the risk of radiation-induced cancers for populations that survive a significant radiation exposure incident.
JF - Journal of Radiological Protection
AU - Yoo, Stephen S
AU - Jorgensen, Timothy J
AU - Kennedy, Ann R
AU - Boice, John D, Jr
AU - Shapiro, Alla
AU - Hu, Tom C-C
AU - Moyer, Brian R
AU - Grace, Marcy B
AU - Kelloff, Gary J
AU - Fenech, Michael
AU - Prasanna, Pataje GS
AU - Coleman, C Norman
AD - Radiation Research Program, Division of Cancer Treatment and Diagnosis, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA, ccoleman@mail.nih.gov
Y1 - 2014/06//
PY - 2014
DA - Jun 2014
SP - R25
EP - r52
PB - IOP Publishing, The Public Ledger Building, Suite 929 Philadelphia PA 19106 United States
VL - 34
IS - 2
SN - 0952-4746, 0952-4746
KW - Risk Abstracts; Health & Safety Science Abstracts
KW - radiation-induced cancer
KW - radiation mitigator
KW - radioprotector
KW - radiation risk
KW - Risk assessment
KW - Mitigation
KW - Terrorism
KW - Injuries
KW - Animal models
KW - Cancer
KW - Health risks
KW - USA
KW - Accidents
KW - Radiation
KW - Ionizing radiation
KW - Drugs
KW - Research programs
KW - Side effects
KW - Technology
KW - R2 23060:Medical and environmental health
KW - H 4000:Food and Drugs
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Radiological+Protection&rft.atitle=Mitigating+the+risk+of+radiation-induced+cancers%3A+limitations+and+paradigms+in+drug+development&rft.au=Yoo%2C+Stephen+S%3BJorgensen%2C+Timothy+J%3BKennedy%2C+Ann+R%3BBoice%2C+John+D%2C+Jr%3BShapiro%2C+Alla%3BHu%2C+Tom+C-C%3BMoyer%2C+Brian+R%3BGrace%2C+Marcy+B%3BKelloff%2C+Gary+J%3BFenech%2C+Michael%3BPrasanna%2C+Pataje+GS%3BColeman%2C+C+Norman&rft.aulast=Yoo&rft.aufirst=Stephen&rft.date=2014-06-01&rft.volume=34&rft.issue=2&rft.spage=R25&rft.isbn=&rft.btitle=&rft.title=Journal+of+Radiological+Protection&rft.issn=09524746&rft_id=info:doi/10.1088%2F0952-4746%2F34%2F2%2FR25
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-01-01
N1 - Last updated - 2015-04-16
N1 - SubjectsTermNotLitGenreText - Risk assessment; Mitigation; Terrorism; Injuries; Animal models; Cancer; Health risks; Accidents; Radiation; Ionizing radiation; Drugs; Side effects; Research programs; Technology; USA
DO - http://dx.doi.org/10.1088/0952-4746/34/2/R25
ER -
TY - JOUR
T1 - Expanding rare disease drug trials based on shared molecular etiology
AN - 1554953467; 20508042
JF - Nature Biotechnology
AU - Brooks, Philip J
AU - Tagle, Danilo A
AU - Groft, Steve
AD - Office of Rare Diseases Research, National Center for Advancing Translational Sciences (NCATS), National Institutes of Health, Bethesda, Maryland, USA.
Y1 - 2014/06//
PY - 2014
DA - Jun 2014
SP - 515
EP - 518
PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL - 32
IS - 6
SN - 1087-0156, 1087-0156
KW - Biotechnology and Bioengineering Abstracts
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+Biotechnology&rft.atitle=Expanding+rare+disease+drug+trials+based+on+shared+molecular+etiology&rft.au=Brooks%2C+Philip+J%3BTagle%2C+Danilo+A%3BGroft%2C+Steve&rft.aulast=Brooks&rft.aufirst=Philip&rft.date=2014-06-01&rft.volume=32&rft.issue=6&rft.spage=515&rft.isbn=&rft.btitle=&rft.title=Nature+Biotechnology&rft.issn=10870156&rft_id=info:doi/10.1038%2Fnbt.2924
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-08-01
N1 - Last updated - 2014-08-21
DO - http://dx.doi.org/10.1038/nbt.2924
ER -
TY - JOUR
T1 - Receiving and Adhering to Lifestyle Modification Counseling for Hypertension: Disparities Between Smokers and Nonsmokers
AN - 1547864626; 20167163
AB - Hypertensive patients who smoke are in particular need of lifestyle modification counseling because they are at increased risk for poorer outcomes. The authors examined whether hypertensive smokers were more or less likely than nonsmokers to report receiving recommendations for diet, salt intake, exercise, alcohol use, and medication and whether receipt of recommendations was differentially associated with lifestyle changes among smokers vs nonsmokers. In an analysis of data from the 2011 Behavioral Risk Factor Surveillance System on a representative sample of hypertensive adults from 9 US states (N=23,093), smokers were less likely than nonsmokers to report being told by a provider to exercise (odds ratio [OR], 0.66; P<.001) and change their diet (OR, 0.83; P<.05). Receiving dietary recommendations was more strongly associated with self-reported dietary improvements among smokers (OR, 7.08; P<.001) compared with nonsmokers (OR, 4.17; P<.001) P<.01. Delivery of counseling may vary by smoking status. When provided, lifestyle counseling may be equally or more effective for smokers compared with nonsmokers.
JF - Journal of Clinical Hypertension
AU - Persoskie, Alexander
AU - Kaufman, Annette R
AU - Leyva, Bryan
AD - Basic Biobehavioral and Psychological Sciences Branch. National Cancer Institute
Y1 - 2014/06//
PY - 2014
DA - Jun 2014
SP - 429
EP - 436
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 16
IS - 6
SN - 1524-6175, 1524-6175
KW - Risk Abstracts
KW - Diets
KW - Salts
KW - Smoking
KW - Alcohol
KW - Risk factors
KW - Drugs
KW - Hypertension
KW - R2 23060:Medical and environmental health
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Clinical+Hypertension&rft.atitle=Receiving+and+Adhering+to+Lifestyle+Modification+Counseling+for+Hypertension%3A+Disparities+Between+Smokers+and+Nonsmokers&rft.au=Persoskie%2C+Alexander%3BKaufman%2C+Annette+R%3BLeyva%2C+Bryan&rft.aulast=Persoskie&rft.aufirst=Alexander&rft.date=2014-06-01&rft.volume=16&rft.issue=6&rft.spage=429&rft.isbn=&rft.btitle=&rft.title=Journal+of+Clinical+Hypertension&rft.issn=15246175&rft_id=info:doi/10.1111%2Fjch.12314
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-07-01
N1 - Last updated - 2014-08-07
N1 - SubjectsTermNotLitGenreText - Diets; Alcohol; Smoking; Salts; Risk factors; Drugs; Hypertension
DO - http://dx.doi.org/10.1111/jch.12314
ER -
TY - JOUR
T1 - Class probability estimation for medical studies
AN - 1547848057; 20215403
AB - I provide a commentary on two papers "Probability estimation with machine learning methods for dichotomous and multicategory outcome: Theory" by Jochen Kruppa, Yufeng Liu, Gerard Biau, Michael Kohler, Inke R. Konig, James D. Malley, and Andreas Ziegler; and "Probability estimation with machine learning methods for dichotomous and multicategory outcome: Applications" by Jochen Kruppa, Yufeng Liu, Hans-Christian Diener, Theresa Holste, Christian Weimar, Inke R. Konig, and Andreas Ziegler. Those papers provide an up-to-date review of some popular machine learning methods for class probability estimation and compare those methods to logistic regression modeling in real and simulated datasets.
JF - Biometrical Journal
AU - Simon, Richard
AD - Biometric Research Branch, National Cancer Institute, 9609 Medical Park Drive, Rockville, MD, 20892-9735, USA.
Y1 - 2014/06//
PY - 2014
DA - Jun 2014
SP - 597
EP - 600
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 56
IS - 4
SN - 0323-3847, 0323-3847
KW - Biotechnology and Bioengineering Abstracts
KW - Statistics
KW - Reviews
KW - Learning algorithms
KW - Biometrics
KW - W 30900:Methods
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-07-01
N1 - Last updated - 2014-08-21
N1 - SubjectsTermNotLitGenreText - Statistics; Reviews; Biometrics; Learning algorithms
DO - http://dx.doi.org/10.1002/bimj.201300296
ER -
TY - JOUR
T1 - Discovery of mesothelin and exploiting it as a target for immunotherapy.
AN - 1543995528; 24824231
AB - We have recently reported that an immunotoxin targeting mesothelin produced durable major tumor regressions in patients with extensive treatment-refractory mesothelioma. These unprecedented tumor responses have prompted us to review how mesothelin was discovered and the advances that led to these tumor responses. This review is not comprehensive but focuses on major developments over the past 20 years since mesothelin was first identified in our laboratory. Mesothelin is a cell-surface glycoprotein whose expression in normal human tissues is restricted to mesothelial cells. Because it is highly expressed by many solid tumors, it is an attractive immunotherapy target. Antibody-based therapies currently in clinical trials include an immunotoxin, a chimeric monoclonal antibody, and an antibody drug conjugate. In addition, a mesothelin tumor vaccine and a mesothelin- chimeric antigen receptor are being evaluated in the clinic. SS1P, an anti-mesothelin immunotoxin, was the first mesothelin-directed therapy to enter the clinic, and its use showed that mesothelin-targeted therapy was safe in patients. More importantly, our recent work has shown that SS1P in combination with pentostatin and cyclophosphamide can result in durable tumor regression in patients with advanced mesothelioma and opens up the possibility that such an approach can benefit patients with many common cancers.
©2014 American Association for Cancer Research.
JF - Cancer research
AU - Pastan, Ira
AU - Hassan, Raffit
AD - Authors' Affiliation: Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland pastani@mail.nih.gov hassanr@mail.nih.gov.
Y1 - 2014/06/01/
PY - 2014
DA - 2014 Jun 01
SP - 2907
EP - 2912
VL - 74
IS - 11
KW - Antibodies, Monoclonal
KW - 0
KW - Cancer Vaccines
KW - GPI-Linked Proteins
KW - Immunotoxins
KW - Membrane Glycoproteins
KW - mesothelin
KW - Index Medicus
KW - Animals
KW - Humans
KW - Molecular Targeted Therapy
KW - Cancer Vaccines -- therapeutic use
KW - Clinical Trials as Topic
KW - Antibodies, Monoclonal -- immunology
KW - Antibodies, Monoclonal -- therapeutic use
KW - Immunotherapy -- methods
KW - Cancer Vaccines -- immunology
KW - Immunotoxins -- immunology
KW - Immunotoxins -- therapeutic use
KW - Drug Evaluation, Preclinical
KW - Membrane Glycoproteins -- immunology
KW - Membrane Glycoproteins -- metabolism
KW - GPI-Linked Proteins -- metabolism
KW - GPI-Linked Proteins -- immunology
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-08-28
N1 - Date created - 2014-06-02
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1158/0008-5472.CAN-14-0337
ER -
TY - JOUR
T1 - Fronto-limbic-striatal dysfunction in pediatric and adult patients with bipolar disorder: impact of face emotion and attentional demands
AN - 1541979861; 201415508
AB - Research in bipolar disorder (BD) implicates fronto-limbic-striatal dysfunction during face emotion processing but it is unknown how such dysfunction varies by task demands, face emotion and patient age. During functional magnetic resonance imaging (fMRI), 181 participants, including 62 BD (36 children and 26 adults) and 119 healthy comparison (HC) subjects (57 children and 62 adults), engaged in constrained and unconstrained processing of emotional (angry, fearful, happy) and non-emotional (neutral) faces. During constrained processing, subjects answered questions focusing their attention on the face; this was processed either implicitly (nose width rating) or explicitly (hostility; subjective fear ratings). Unconstrained processing consisted of passive viewing. Pediatric BD rated neutral faces as more hostile than did other groups. In BD patients, family-wise error (FWE)-corrected region of interest (ROI) analyses revealed dysfunction in the amygdala, inferior frontal gyrus (IFG), anterior cingulate cortex (ACC) and putamen. Patients with BD showed amygdala hyperactivation during explicit processing (hostility ratings) of fearful faces and passive viewing of angry and neutral faces but IFG hypoactivation during implicit processing of neutral and happy faces. In the ACC and striatum, the direction of dysfunction varied by task demand: BD demonstrated hyperactivation during unconstrained processing of angry or neutral faces but hypoactivation during constrained processing (implicit or explicit) of angry, neutral or happy faces. Findings suggest amygdala hyperactivation in BD while processing negatively valenced and neutral faces, regardless of attentional condition, and BD IFG hypoactivation during implicit processing. In the cognitive control circuit involving the ACC and putamen, BD neural dysfunction was sensitive to task demands. Adapted from the source document.
JF - Psychological Medicine
AU - Brotman, M A
AU - Tseng, W.-L.
AU - Olsavsky, A K
AU - Fromm, S J
AU - Muhrer, E J
AU - Rutenberg, J G
AU - Deveney, C M
AU - Adleman, N E
AU - Zarate, C A
AU - Pine, D S
AU - Leibenluft, E
AD - Emotion and Development Branch, National Institute of Mental Health, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, USA brotmanm@mail.nih.gov
Y1 - 2014/06//
PY - 2014
DA - June 2014
SP - 1639
EP - 1651
PB - Cambridge University Press, UK
VL - 44
IS - 8
SN - 0033-2917, 0033-2917
KW - Paediatrics
KW - Emotions
KW - Hostility
KW - Facial expressions
KW - Dysfunction
KW - Anger
KW - article
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Psychological+Medicine&rft.atitle=Fronto-limbic-striatal+dysfunction+in+pediatric+and+adult+patients+with+bipolar+disorder%3A+impact+of+face+emotion+and+attentional+demands&rft.au=Brotman%2C+M+A%3BTseng%2C+W.-L.%3BOlsavsky%2C+A+K%3BFromm%2C+S+J%3BMuhrer%2C+E+J%3BRutenberg%2C+J+G%3BDeveney%2C+C+M%3BAdleman%2C+N+E%3BZarate%2C+C+A%3BPine%2C+D+S%3BLeibenluft%2C+E&rft.aulast=Brotman&rft.aufirst=M&rft.date=2014-06-01&rft.volume=44&rft.issue=8&rft.spage=1639&rft.isbn=&rft.btitle=&rft.title=Psychological+Medicine&rft.issn=00332917&rft_id=info:doi/10.1017%2FS003329171300202X
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Date revised - 2014-07-01
N1 - Number of references - 77
N1 - Last updated - 2016-09-27
N1 - CODEN - PSMDCO
N1 - SubjectsTermNotLitGenreText - Dysfunction; Facial expressions; Anger; Emotions; Paediatrics; Hostility
DO - http://dx.doi.org/10.1017/S003329171300202X
ER -
TY - JOUR
T1 - Association Between Informal Caregiving and Cellular Aging in the Survey of the Health of Wisconsin: The Role of Caregiving Characteristics, Stress, and Strain
AN - 1540232223; 20082649
AB - The pathophysiological consequences of caregiving have not been fully elucidated. We evaluated how caregiving, stress, and caregiver strain were associated with shorter relative telomere length (RTL), a marker of cellular aging. Caregivers (n = 240) and some noncaregivers (n = 98) in the 2008-2010 Survey of the Health of Wisconsin, comprising a representative sample of Wisconsin adults aged 21-74 years, reported their sociodemographic, health, and psychological characteristics. RTL was assayed from blood or saliva samples. Median T and S values were used to determine the telomere-to-single copy gene ratio (T/S) for each sample, and log(T/S) was used as the dependent variable in analyses. Multivariable generalized additive models showed that RTL did not differ between caregivers and noncaregivers (difference in log(T/S) = -0.03; P > 0.05), but moderate-to-high levels of stress versus low stress were associated with longer RTL (difference = 0.15; P = 0.04). Among caregivers, more hours per week of care, caring for a young person, and greater strain were associated with shorter RTL (P < 0.05). Caregivers with discordant levels of stress and strain (i.e., low perceived stress/high strain) compared with low stress/low strain had the shortest RTL (difference = -0.24; P = 0.02, P sub(interaction) = 0.13), corresponding to approximately 10-15 additional years of aging. Caregivers with these characteristics may be at increased risk for accelerated aging. Future work is necessary to better elucidate these relationships and develop interventions to improve the long-term health and well-being of caregivers.
JF - American Journal of Epidemiology
AU - Litzelman, Kristin
AU - Witt, Whitney P
AU - Gangnon, Ronald E
AU - Nieto, F Javier
AU - Engelman, Corinne D
AU - Mailick, Marsha R
AU - Skinner, Halcyon G
AD - Correspondence to Dr. Kristin Litzelman, National Cancer Institute, 9609 Medical Center Drive, MSC 9761, Room 3E620, Bethesda, MD 20892-9761,; kristin.litzelman@gmail.com] kristin.litzelman@nih.gov
Y1 - 2014/06/01/
PY - 2014
DA - 2014 Jun 01
SP - 1340
EP - 1352
PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL - 179
IS - 11
SN - 0002-9262, 0002-9262
KW - Health & Safety Science Abstracts; Risk Abstracts
KW - caregivers
KW - caregiver strain
KW - population-based studies
KW - stress, psychological
KW - Survey of the Health of Wisconsin
KW - Psychology
KW - Perception
KW - Aging
KW - Stress
KW - Intervention
KW - USA, Wisconsin
KW - H 12000:Epidemiology and Public Health
KW - R2 23060:Medical and environmental health
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Epidemiology&rft.atitle=Association+Between+Informal+Caregiving+and+Cellular+Aging+in+the+Survey+of+the+Health+of+Wisconsin%3A+The+Role+of+Caregiving+Characteristics%2C+Stress%2C+and+Strain&rft.au=Litzelman%2C+Kristin%3BWitt%2C+Whitney+P%3BGangnon%2C+Ronald+E%3BNieto%2C+F+Javier%3BEngelman%2C+Corinne+D%3BMailick%2C+Marsha+R%3BSkinner%2C+Halcyon+G&rft.aulast=Litzelman&rft.aufirst=Kristin&rft.date=2014-06-01&rft.volume=179&rft.issue=11&rft.spage=1340&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Epidemiology&rft.issn=00029262&rft_id=info:doi/10.1093%2Faje%2Fkwu066
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-01
N1 - Last updated - 2014-10-02
N1 - SubjectsTermNotLitGenreText - Perception; Psychology; Aging; Intervention; Stress; USA, Wisconsin
DO - http://dx.doi.org/10.1093/aje/kwu066
ER -
TY - JOUR
T1 - The Francisella O-antigen mediates survival in the macrophage cytosol via autophagy avoidance
AN - 1540221968; 19971649
AB - Autophagy is a key innate immune response to intracellular parasites that promotes their delivery to degradative lysosomes following detection in the cytosol or within damaged vacuoles. Like Listeria and Shigella, which use specific mechanisms to avoid autophagic detection and capture, the bacterial pathogen Francisella tularensis proliferates within the cytosol of macrophages without demonstrable control by autophagy. To examine how Francisella evades autophagy, we screened a library of F. tularensis subsp. tularensisSchu S4 HimarFT transposon mutants in GFP-LC3-expressing murine macrophages by microscopy for clones localized within autophagic vacuoles after phagosomal escape. Eleven clones showed autophagic capture at 6 h post-infection, whose HimarFT insertions clustered to fourgenetic loci involved in lipopolysaccharidic and capsular O-antigen biosynthesis. Consistent with the HimarFT mutants, in-frame deletion mutants of two representative loci, FTT1236 and FTT1448c (manC), lacking both LPS and capsular O-antigen, underwent phagosomal escape but were cleared from the host cytosol. Unlike wild-type Francisella, the O-antigen deletion mutants were ubiquitinated, and recruited the autophagy adaptor p62/SQSTM1 and LC3 prior to cytosolic clearance. Autophagy-deficient macrophages partially supported replication of both mutants, indicating that O-antigen-lacking Francisella are controlled by autophagy. These data demonstrate the intracellular protective role of this bacterial surface polysaccharide against autophagy.
JF - Cellular Microbiology
AU - Case, Elizabeth Di Russo
AU - Chong, Audrey
AU - Wehrly, Tara D
AU - Hansen, Bryan
AU - Child, Robert
AU - Hwang, Seungmin
AU - Virgin, Herbert W
AU - Celli, Jean
AD - Laboratory of Intracellular Parasites Rocky Mountain Laboratories. National Institute of Allergy and Infectious Diseases, National Institutes of Health
Y1 - 2014/06//
PY - 2014
DA - Jun 2014
SP - 862
EP - 877
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 16
IS - 6
SN - 1462-5814, 1462-5814
KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Microbiology Abstracts B: Bacteriology
KW - Cell survival
KW - Macrophages
KW - Parasites
KW - Avoidance reactions
KW - Survival
KW - Polysaccharides
KW - Defence mechanisms
KW - Listeria
KW - Transposons
KW - Lipopolysaccharides
KW - Phagocytosis
KW - Clones
KW - Data processing
KW - Deletion mutant
KW - Replication
KW - Francisella tularensis
KW - Shigella
KW - Pathogens
KW - Insertion
KW - Microscopy
KW - Vacuoles
KW - Microbiology
KW - Cytosol
KW - Immune response
KW - Lysosomes
KW - Q1 08484:Species interactions: parasites and diseases
KW - J 02350:Immunology
KW - Q5 08524:Public health, medicines, dangerous organisms
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cellular+Microbiology&rft.atitle=The+Francisella+O-antigen+mediates+survival+in+the+macrophage+cytosol+via+autophagy+avoidance&rft.au=Case%2C+Elizabeth+Di+Russo%3BChong%2C+Audrey%3BWehrly%2C+Tara+D%3BHansen%2C+Bryan%3BChild%2C+Robert%3BHwang%2C+Seungmin%3BVirgin%2C+Herbert+W%3BCelli%2C+Jean&rft.aulast=Case&rft.aufirst=Elizabeth+Di&rft.date=2014-06-01&rft.volume=16&rft.issue=6&rft.spage=862&rft.isbn=&rft.btitle=&rft.title=Cellular+Microbiology&rft.issn=14625814&rft_id=info:doi/10.1111%2Fcmi.12246
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-01
N1 - Last updated - 2015-06-26
N1 - SubjectsTermNotLitGenreText - Clones; Macrophages; Replication; Microbiology; Survival; Avoidance reactions; Pathogens; Defence mechanisms; Lysosomes; Cell survival; Parasites; Deletion mutant; Data processing; Polysaccharides; Transposons; Insertion; Vacuoles; Microscopy; Cytosol; Lipopolysaccharides; Immune response; Phagocytosis; Shigella; Francisella tularensis; Listeria
DO - http://dx.doi.org/10.1111/cmi.12246
ER -
TY - JOUR
T1 - Eosinophilic gastroenteritis and related eosinophilic disorders.
AN - 1535622928; 24813518
AB - Eosinophilic gastroenteritis (EGE) represents one member within the spectrum of diseases collectively referred to as eosinophilic gastrointestinal disorders, which includes eosinophilic esophagitis (EoE), gastritis, enteritis, and colitis. EGE is less common than EoE and involves a different site of disease but otherwise shares many common features with EoE. The clinical manifestations of EGE are protean and can vary from nausea and vomiting to protein-losing enteropathy or even bowel obstruction requiring surgery. Although systemic corticosteroids are an effective treatment for EGE, their use results in substantial corticosteroid toxicity. Accordingly, there is a great need for improved therapies for these patients.
Published by Elsevier Inc.
JF - Gastroenterology clinics of North America
AU - Prussin, Calman
AD - Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 10 Center Drive, MSC-1881, Bethesda, MD 20892-1881, USA. Electronic address: cprussin@niaid.nih.gov.
Y1 - 2014/06//
PY - 2014
DA - June 2014
SP - 317
EP - 327
VL - 43
IS - 2
KW - Index Medicus
KW - Food allergy
KW - Eosinophilic gastritis
KW - Eosinophilic gastroenteritis
KW - Eosinophilia
KW - EGID
KW - Humans
KW - Enteritis -- etiology
KW - Eosinophilia -- therapy
KW - Enteritis -- complications
KW - Enteritis -- therapy
KW - Enteritis -- diagnosis
KW - Gastritis -- diagnosis
KW - Eosinophilia -- diagnosis
KW - Gastritis -- therapy
KW - Gastritis -- etiology
KW - Gastritis -- complications
KW - Eosinophilia -- etiology
KW - Eosinophilia -- complications
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1535622928?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gastroenterology+clinics+of+North+America&rft.atitle=Eosinophilic+gastroenteritis+and+related+eosinophilic+disorders.&rft.au=Prussin%2C+Calman&rft.aulast=Prussin&rft.aufirst=Calman&rft.date=2014-06-01&rft.volume=43&rft.issue=2&rft.spage=317&rft.isbn=&rft.btitle=&rft.title=Gastroenterology+clinics+of+North+America&rft.issn=1558-1942&rft_id=info:doi/10.1016%2Fj.gtc.2014.02.013
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-01-15
N1 - Date created - 2014-05-12
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.gtc.2014.02.013
ER -
TY - JOUR
T1 - Establishing a Bone Marrow Stromal Cell Transplant Program at the National Institutes of Health Clinical Center
AN - 1534847262; 19986459
AB - A repository of cryopreserved bone marrow stromal cell (BMSC) products prepared from marrow aspirates of healthy subjects has been created and is being used to treat patients with inflammatory bowel disease, cardiovascular disease, and acute graft-versus-host disease following allogeneic hematopoietic stem cell transplantation. New methods of manufacturing BMSCs are being investigated including the use of an automated bioreactor for BMSC expansion and the replacement of fetal bovine serum with human platelet lysate as a media supplement. Efforts are also being made to identify markers that can be used to assess the potency of BMSCs.
JF - Tissue Engineering, Part B: Reviews
AU - Stroncek, David F
AU - Sabatino, Marianna
AU - Ren, Jiaqiang
AU - England, Lee
AU - Kuznetsov, Sergei A
AU - Klein, Harvey G
AU - Robey, Pamela G
AD - Department of Transfusion Medicine, Clinical Center, National Institutes of Health, Bethesda, Maryland.
Y1 - 2014/06//
PY - 2014
DA - Jun 2014
SP - 200
EP - 205
PB - Mary Ann Liebert, Inc., 140 Huguenot St 3rd Fl New Rochelle NY 10801 United States
VL - 20
IS - 3
SN - 1937-3368, 1937-3368
KW - Biotechnology and Bioengineering Abstracts
KW - stromal cells
KW - Inflammatory bowel diseases
KW - Reviews
KW - stem cell transplantation
KW - Bioreactors
KW - Platelets
KW - Graft-versus-host reaction
KW - Cardiovascular diseases
KW - Tissue engineering
KW - Cryopreservation
KW - Bone marrow transplantation
KW - W 30920:Tissue Engineering
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534847262?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Tissue+Engineering%2C+Part+B%3A+Reviews&rft.atitle=Establishing+a+Bone+Marrow+Stromal+Cell+Transplant+Program+at+the+National+Institutes+of+Health+Clinical+Center&rft.au=Stroncek%2C+David+F%3BSabatino%2C+Marianna%3BRen%2C+Jiaqiang%3BEngland%2C+Lee%3BKuznetsov%2C+Sergei+A%3BKlein%2C+Harvey+G%3BRobey%2C+Pamela+G&rft.aulast=Stroncek&rft.aufirst=David&rft.date=2014-06-01&rft.volume=20&rft.issue=3&rft.spage=200&rft.isbn=&rft.btitle=&rft.title=Tissue+Engineering%2C+Part+B%3A+Reviews&rft.issn=19373368&rft_id=info:doi/10.1089%2Ften.teb.2013.0529
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-01
N1 - Number of references - 37
N1 - Last updated - 2014-06-26
N1 - SubjectsTermNotLitGenreText - Inflammatory bowel diseases; stromal cells; Bioreactors; stem cell transplantation; Reviews; Platelets; Graft-versus-host reaction; Cardiovascular diseases; Tissue engineering; Cryopreservation; Bone marrow transplantation
DO - http://dx.doi.org/10.1089/ten.teb.2013.0529
ER -
TY - JOUR
T1 - Bone Marrow Mesenchymal Stromal Cells to Treat Complications Following Allogeneic Stem Cell Transplantation
AN - 1534846644; 19986460
AB - Allogeneic hematopoietic stem cell transplantation (HSCT) is a technologically complicated procedure that represents the only cure for many hematologic malignancies. However, HSCT is often complicated by life-threatening toxicities related to the chemo-radiation conditioning regimen, poor engraftment of donor HSCs, the hyperinflammatory syndrome of graft-versus-host disease (GVHD), infection risks from immunosuppression, and end-organ damage. Bone marrow stromal cells (MSCs), also known as "mesenchymal stromal cells," not only play a nurturing role in the hematopoietic microenvironment but also can differentiate into other cell types of mesenchymal origin. MSCs are poorly immunogenic, and they can modulate immunological responses through interactions with a wide range of innate and adaptive immune cells to reduce inflammation. They are easily expanded ex vivo and after infusion, home to sites of injury and inflammation to promote tissue repair. Despite promising early trial results in HSCT with significant responses that have translated into survival benefits, there have been significant barriers to successful commercialization as an off-the-shelf therapy. Current efforts with MSCs in the HSCT setting are geared toward determining the factors determining potency, understanding the precise mechanisms of action in human HSCT, knowing their kinetics and fate, optimizing dose and schedule, incorporating biomarkers as response surrogates, addressing concerns about safety, optimizing clinical trial design, and negotiating the uncharted regulatory landscape for licensable cellular therapy.
JF - Tissue Engineering, Part B: Reviews
AU - Battiwalla, Minoo
AU - Barrett, AJohn
AD - Hematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland.
Y1 - 2014/06//
PY - 2014
DA - Jun 2014
SP - 211
EP - 217
PB - Mary Ann Liebert, Inc., 140 Huguenot St 3rd Fl New Rochelle NY 10801 United States
VL - 20
IS - 3
SN - 1937-3368, 1937-3368
KW - Biotechnology and Bioengineering Abstracts
KW - Donors
KW - stromal cells
KW - Injuries
KW - stem cell transplantation
KW - Bone marrow
KW - Graft-versus-host reaction
KW - Toxicity
KW - Infection
KW - Tissue engineering
KW - biomarkers
KW - Clinical trials
KW - Inflammation
KW - Malignancy
KW - Immunogenicity
KW - Kinetics
KW - Microenvironments
KW - Mesenchyme
KW - Bone marrow transplantation
KW - Immunosuppression
KW - W 30920:Tissue Engineering
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534846644?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Tissue+Engineering%2C+Part+B%3A+Reviews&rft.atitle=Bone+Marrow+Mesenchymal+Stromal+Cells+to+Treat+Complications+Following+Allogeneic+Stem+Cell+Transplantation&rft.au=Battiwalla%2C+Minoo%3BBarrett%2C+AJohn&rft.aulast=Battiwalla&rft.aufirst=Minoo&rft.date=2014-06-01&rft.volume=20&rft.issue=3&rft.spage=211&rft.isbn=&rft.btitle=&rft.title=Tissue+Engineering%2C+Part+B%3A+Reviews&rft.issn=19373368&rft_id=info:doi/10.1089%2Ften.teb.2013.0566
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-01
N1 - Number of references - 55
N1 - Last updated - 2014-06-26
N1 - SubjectsTermNotLitGenreText - Donors; Injuries; stromal cells; stem cell transplantation; Bone marrow; Graft-versus-host reaction; Toxicity; Tissue engineering; Infection; Clinical trials; biomarkers; Inflammation; Malignancy; Immunogenicity; Kinetics; Microenvironments; Mesenchyme; Bone marrow transplantation; Immunosuppression
DO - http://dx.doi.org/10.1089/ten.teb.2013.0566
ER -
TY - JOUR
T1 - Risk of second benign brain tumors among cancer survivors in the surveillance, epidemiology, and end results program
AN - 1534830371; 19902424
AB - Purpose: To assess risk of developing a second benign brain tumor in a nationwide population of cancer survivors. Methods: We evaluated the risk of developing second benign brain tumors among 2,038,074 1-year minimum cancer survivors compared to expected risk in the general population between 1973 and 2007 in nine population-based cancer registries in the NCI's surveillance, epidemiology, and end results program. Excess risk was estimated using standardized incidence ratios (SIRs) for all second benign brain tumors and specifically for second meningiomas and acoustic neuromas diagnosed during 2004-2008. Results: 1,025 patients were diagnosed with a second primary benign brain tumor, of which second meningiomas composed the majority (n = 745). Statistically significant increases in risk of developing a second meningioma compared to the general population were observed following first cancers of the brain [SIR = 19.82; 95 % confidence interval (CI) 13.88-27.44], other central nervous system (CNS) (SIR = 9.54; CI 3.10-22.27), thyroid (SIR = 2.05; CI 1.47-2.79), prostate (SIR = 1.21; CI 1.02-1.43), and acute lymphocytic leukemia (ALL) (SIR = 42.4; CI 23.18-71.13). Statistically significant decreases in risk were observed following first cancers of the uterine corpus (SIR = 0.63; CI 0.42-0.91) and colon (SIR = 0.56; CI 0.37-0.82). Differences in risk between patients initially treated with radiotherapy versus non-irradiated patients were statistically significant for second meningioma after primary cancers of the brain (p sub(Het) < 0.001) and ALL (p sub(Het) = 0.02). No statistically significant increased risks were detected for second acoustic neuromas (n = 114) following any first primary tumor. Conclusions: Risk of second benign brain tumors, particularly meningioma, is increased following first primary cancers of the brain/CNS, thyroid, prostate, and ALL. Radiation exposure likely contributes to these excess risks.
JF - Cancer Causes & Control
AU - Kutsenko, Alina
AU - Berrington de Gonzalez, Amy
AU - Curtis, Rochelle E
AU - Rajaraman, Preetha
AD - Radiation Epidemiology Branch, Division of Cancer Epidemiology and Genetics, NCI/NIH, 9609 Medical Center Drive, MSC 9778, Bethesda, MD, 20892, USA, alk2022@med.cornell.edu
Y1 - 2014/06//
PY - 2014
DA - Jun 2014
SP - 659
EP - 668
PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL - 25
IS - 6
SN - 0957-5243, 0957-5243
KW - Health & Safety Science Abstracts; Risk Abstracts
KW - Risk assessment
KW - Central nervous system
KW - Thyroid
KW - Brain
KW - Radiotherapy
KW - Tumors
KW - Cancer
KW - Brain tumors
KW - Leukemia
KW - Health risks
KW - Radiation
KW - Epidemiology
KW - Standards
KW - H 11000:Diseases/Injuries/Trauma
KW - R2 23060:Medical and environmental health
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534830371?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Causes+%26+Control&rft.atitle=Risk+of+second+benign+brain+tumors+among+cancer+survivors+in+the+surveillance%2C+epidemiology%2C+and+end+results+program&rft.au=Kutsenko%2C+Alina%3BBerrington+de+Gonzalez%2C+Amy%3BCurtis%2C+Rochelle+E%3BRajaraman%2C+Preetha&rft.aulast=Kutsenko&rft.aufirst=Alina&rft.date=2014-06-01&rft.volume=25&rft.issue=6&rft.spage=659&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/10.1007%2Fs10552-014-0367-5
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-01
N1 - Number of references - 36
N1 - Last updated - 2014-06-26
N1 - SubjectsTermNotLitGenreText - Risk assessment; Central nervous system; Brain; Thyroid; Radiotherapy; Tumors; Cancer; Brain tumors; Health risks; Leukemia; Epidemiology; Radiation; Standards
DO - http://dx.doi.org/10.1007/s10552-014-0367-5
ER -
TY - JOUR
T1 - Brucella arteritis: clinical manifestations, treatment, and prognosis
AN - 1534819831; 19918688
AB - Brucellosis is the most common bacterial zoonosis, and causes a considerable burden of disease in endemic countries. Cardiovascular involvement is the main cause of mortality due to infection with spp, and most commonly manifests as endocarditis, peripheral and cerebrovascular aneurysms, or arterial and venous thromboses. We report a case of brucellosis presenting as bacteraemia and aortic endarteritis 18 years after the last known exposure to risk factors for brucella infection. The patient was treated with doxycycline, rifampicin, and gentamicin, and underwent surgical repair of a penetrating aortic ulcer, with a good clinical recovery. We review the signs and symptoms, diagnostic approach, prognosis, and treatment of brucella arteritis. We draw attention to the absence of consensus about the optimum therapy for vascular brucellosis, and the urgent need for additional studies and renewed scientific interest in this major pathogen.
JF - Lancet Infectious Diseases
AU - Herrick, Jesica A
AU - Lederman, Robert J
AU - Sullivan, Brigit
AU - Powers, John H
AU - Palmore, Tara N
AD - Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD, USA
Y1 - 2014/06//
PY - 2014
DA - Jun 2014
SP - 520
EP - 526
PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands
VL - 14
IS - 6
SN - 1473-3099, 1473-3099
KW - Microbiology Abstracts B: Bacteriology
KW - Mortality
KW - Aneurysm
KW - Aorta
KW - Prognosis
KW - Bacteremia
KW - Brucella
KW - Pathogens
KW - Infection
KW - Endocarditis
KW - Gentamicin
KW - Rifampin
KW - Case reports
KW - Ulcers
KW - Risk factors
KW - Reviews
KW - Arteritis
KW - Brucellosis
KW - Doxycycline
KW - Endarteritis
KW - J 02400:Human Diseases
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534819831?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Lancet+Infectious+Diseases&rft.atitle=Brucella+arteritis%3A+clinical+manifestations%2C+treatment%2C+and+prognosis&rft.au=Herrick%2C+Jesica+A%3BLederman%2C+Robert+J%3BSullivan%2C+Brigit%3BPowers%2C+John+H%3BPalmore%2C+Tara+N&rft.aulast=Herrick&rft.aufirst=Jesica&rft.date=2014-06-01&rft.volume=14&rft.issue=6&rft.spage=520&rft.isbn=&rft.btitle=&rft.title=Lancet+Infectious+Diseases&rft.issn=14733099&rft_id=info:doi/10.1016%2FS1473-3099%2813%2970270-6
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-01
N1 - Last updated - 2014-06-26
N1 - SubjectsTermNotLitGenreText - Mortality; Aneurysm; Aorta; Prognosis; Bacteremia; Pathogens; Infection; Endocarditis; Gentamicin; Rifampin; Case reports; Ulcers; Reviews; Risk factors; Arteritis; Brucellosis; Endarteritis; Doxycycline; Brucella
DO - http://dx.doi.org/10.1016/S1473-3099(13)70270-6
ER -
TY - JOUR
T1 - HIV-1 Vaginal Transmission: Cell-Free or Cell-Associated Virus?
AN - 1534819384; 19972757
AB - The vast majority of new HIV infections in male-to-female transmission occurs through semen, where HIV-1 is present in two different forms: as free and as cell-associated virus. In the female lower genital tract, semen mixes with female genital secretions that contain various factors, some of which facilitate or inhibit HIV-1 transmission. Next, HIV-1 crosses the genital epithelia, reaches the regional lymph nodes, and disseminates through the female host. Cervico-vaginal mucosa contains multiple barriers, resulting in a low probability of vaginal transmission. However, in some cases, HIV-1 is able to break these barriers. Although the exact mechanisms of how these barriers function remain unclear, their levels of efficiency against cell-free and cell-associated HIV-1 are different, and both cell-free and cell-associated virions seem to use different strategies to overcome these barriers. Understanding the basic mechanisms of HIV-1 vaginal transmission is required for the development of new antiviral strategies to contain HIV-1 epidemics.
JF - American Journal of Reproductive Immunology
AU - Barreto-de-Souza, Victor
AU - Arakelyan, Anush
AU - Margolis, Leonid
AU - Vanpouille, Christophe
AD - Section of Intercellular Interactions Program in Physical Biology. Eunice Kennedy Shriver National Institute of Child Health and Human Development
Y1 - 2014/06//
PY - 2014
DA - Jun 2014
SP - 589
EP - 599
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 71
IS - 6
SN - 1046-7408, 1046-7408
KW - Health & Safety Science Abstracts; Virology & AIDS Abstracts; Immunology Abstracts
KW - Virions
KW - Epidemics
KW - Immunology
KW - Secretions
KW - Mucosa
KW - Infection
KW - Lymph nodes
KW - Disease transmission
KW - Human immunodeficiency virus
KW - Human immunodeficiency virus 1
KW - Vagina
KW - Semen
KW - Genital tract
KW - V 22360:AIDS and HIV
KW - H 11000:Diseases/Injuries/Trauma
KW - F 06935:Development, Aging & Organ Systems
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534819384?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Reproductive+Immunology&rft.atitle=HIV-1+Vaginal+Transmission%3A+Cell-Free+or+Cell-Associated+Virus%3F&rft.au=Barreto-de-Souza%2C+Victor%3BArakelyan%2C+Anush%3BMargolis%2C+Leonid%3BVanpouille%2C+Christophe&rft.aulast=Barreto-de-Souza&rft.aufirst=Victor&rft.date=2014-06-01&rft.volume=71&rft.issue=6&rft.spage=589&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Reproductive+Immunology&rft.issn=10467408&rft_id=info:doi/10.1111%2Faji.12240
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-01
N1 - Last updated - 2014-10-02
N1 - SubjectsTermNotLitGenreText - Virions; Epidemics; Mucosa; Secretions; Vagina; Semen; Genital tract; Infection; Lymph nodes; Disease transmission; Human immunodeficiency virus; Immunology; Human immunodeficiency virus 1
DO - http://dx.doi.org/10.1111/aji.12240
ER -
TY - JOUR
T1 - Maternal overweight and obesity and risk of congenital heart defects in offspring.
AN - 1534792383; 24362506
AB - Obesity is a risk factor for congenital heart defects (CHDs), but whether risk is independent of abnormal glucose metabolism remains unknown. Data on whether overweight status increases the risk are also conflicting.
We included 121 815 deliveries from a cohort study, the Consortium on Safe Labor (CSL), after excluding women with pregestational diabetes as recorded in the electronic medical record. CHD was identified via medical record discharge summaries. Adjusted odds ratios (ORs) for any CHD were calculated for prepregnancy body mass index (BMI) categories of overweight (25-<30 kg m(-2)), obese (30-<40 kg m(-2)) and morbidly obese (≥40 kg m(-2)) compared with normal weight (18.5-<25 kg m(-2)) women, and for specific CHD with obese groups combined (≥30 kg m(-2)). A subanalysis adjusting for oral glucose tolerance test (OGTT) results where available was performed as a proxy for potential abnormal glucose metabolism present at the time of organogenesis.
There were 1388 (1%) infants with CHD. Overweight (OR=1.15, 95% confidence interval (95% CI): 1.01-1.32), obese (OR=1.26, 95% CI: 1.09-1.44) and morbidly obese (OR=1.34, 95% CI: 1.02-1.76) women had greater OR of having a neonate with CHD than normal weight women (P<0.001 for trend). Obese women (BMI≥30 kg m(-2)) had higher OR of having an infant with conotruncal defects (OR = 1.33, 95% CI: (1.03–1.72) [corrected], atrial septal defects (OR=1.22, 95% CI: 1.04-1.43) and ventricular septal defects (OR=1.38, 95% CI: 1.06-1.79). Being obese remained a significant predictor of CHD risk after adjusting for OGTT. Increasing maternal weight class was associated with an increased risk for CHD. In obese women, abnormal glucose metabolism did not completely explain the increased risk for CHD; the possibility that other obesity-related factors are teratogenic requires further investigation.
JF - International journal of obesity (2005)
AU - Brite, J
AU - Laughon, S K
AU - Troendle, J
AU - Mills, J
AD - 1] Epidemiology Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD, USA [2] Epidemiology and Biostatistics, CUNY School of Public Health at Hunter College, New York, NY, USA [3] CUNY Institute for Demographic Research (CIDR), New York, NY, USA. ; Epidemiology Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD, USA. ; Office of Biostatistics Research, Division of Cardiovascular Sciences, National Heart, Lung, and Blood Institute, Bethesda, MD, USA.
Y1 - 2014/06//
PY - 2014
DA - June 2014
SP - 878
EP - 882
VL - 38
IS - 6
KW - Index Medicus
KW - Odds Ratio
KW - Prospective Studies
KW - Logistic Models
KW - Risk Factors
KW - Humans
KW - Cohort Studies
KW - Adult
KW - Infant, Newborn
KW - Body Mass Index
KW - Female
KW - Risk Assessment
KW - Pregnancy
KW - Heart Defects, Congenital -- epidemiology
KW - Pregnancy Complications -- etiology
KW - Heart Defects, Congenital -- etiology
KW - Mothers
KW - Glucose Metabolism Disorders -- epidemiology
KW - Obesity -- epidemiology
KW - Glucose Metabolism Disorders -- etiology
KW - Pregnancy Complications -- epidemiology
KW - Obesity -- complications
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534792383?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+obesity+%282005%29&rft.atitle=Maternal+overweight+and+obesity+and+risk+of+congenital+heart+defects+in+offspring.&rft.au=Brite%2C+J%3BLaughon%2C+S+K%3BTroendle%2C+J%3BMills%2C+J&rft.aulast=Brite&rft.aufirst=J&rft.date=2014-06-01&rft.volume=38&rft.issue=6&rft.spage=878&rft.isbn=&rft.btitle=&rft.title=International+journal+of+obesity+%282005%29&rft.issn=1476-5497&rft_id=info:doi/10.1038%2Fijo.2013.244
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-03-30
N1 - Date created - 2014-06-10
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
JAMA. 2012 Feb 1;307(5):491-7 [22253363]
Am J Obstet Gynecol. 2010 Oct;203(4):326.e1-326.e10 [20708166]
Congenit Heart Dis. 2013 Mar-Apr;8(2):131-41 [22967199]
Obes Res. 2003 Sep;11(9):1065-71 [12972676]
Am J Obstet Gynecol. 2012 May;206(5):419.e1-9 [22542117]
Paediatr Perinat Epidemiol. 2000 Jul;14(3):234-9 [10949215]
Epidemiology. 2000 Nov;11(6):689-94 [11055631]
Obstet Gynecol. 2001 Sep;98(3):525-38 [11547793]
Scand J Work Environ Health. 2002 Feb;28(1):12-7 [11873776]
Pediatrics. 2003 May;111(5 Pt 2):1152-8 [12728129]
Am J Epidemiol. 1991 Aug 15;134(4):393-402 [1877600]
Arch Pediatr Adolesc Med. 2007 Aug;161(8):745-50 [17679655]
Birth Defects Res A Clin Mol Teratol. 2007 Oct;79(10):714-27 [17729292]
N Engl J Med. 2008 May 8;358(19):1991-2002 [18463375]
Epidemiology. 2008 Jul;19(4):616-20 [18552593]
Am J Obstet Gynecol. 2008 Sep;199(3):237.e1-9 [18674752]
Int J Obes (Lond). 2008 Sep;32(9):1431-7 [18607383]
Cardiol Young. 2008 Dec;18 Suppl 2:92-100 [19063779]
JAMA. 2009 Feb 11;301(6):636-50 [19211471]
Diabetes Care. 2009 Sep;32(9):1639-43 [19549728]
Birth Defects Res A Clin Mol Teratol. 2010 Jan;88(1):35-40 [19711433]
Am J Obstet Gynecol. 2010 Jan;202(1):51.e1-51.e10 [19796755]
Am J Clin Nutr. 2010 Jun;91(6):1543-9 [20375192]
Erratum In:
Int J Obes (Lond). 2014 Jun;38(6):886
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1038/ijo.2013.244
ER -
TY - JOUR
T1 - Exploitation of Langerhans cells for in vivo DNA vaccine delivery into the lymph nodes.
AN - 1534102037; 24694539
AB - There is no clinically available cancer immunotherapy that exploits Langerhans cells (LCs), the epidermal precursors of dendritic cells (DCs) that are the natural agent of antigen delivery. We developed a DNA formulation with a polymer and obtained synthetic 'pathogen-like' nanoparticles that preferentially targeted LCs in epidermal cultures. These nanoparticles applied topically under a patch-elicited robust immune responses in human subjects. To demonstrate the mechanism of action of this novel vaccination strategy in live animals, we assembled a high-resolution two-photon laser scanning-microscope. Nanoparticles applied on the native skin poorly penetrated and poorly induced LC motility. The combination of nanoparticle administration and skin treatment was essential both for efficient loading the vaccine into the epidermis and for potent activation of the LCs to migrate into the lymph nodes. LCs in the epidermis picked up nanoparticles and accumulated them in the nuclear region demonstrating an effective nuclear DNA delivery in vivo. Tissue distribution studies revealed that the majority of the DNA was targeted to the lymph nodes. Preclinical toxicity of the LC-targeting DNA vaccine was limited to mild and transient local erythema caused by the skin treatment. This novel, clinically proven LC-targeting DNA vaccine platform technology broadens the options on DC-targeting vaccines to generate therapeutic immunity against cancer.
JF - Gene therapy
AU - Tőke, E R
AU - Lőrincz, O
AU - Csiszovszki, Z
AU - Somogyi, E
AU - Felföldi, G
AU - Molnár, L
AU - Szipőcs, R
AU - Kolonics, A
AU - Malissen, B
AU - Lori, F
AU - Trocio, J
AU - Bakare, N
AU - Horkay, F
AU - Romani, N
AU - Tripp, C H
AU - Stoitzner, P
AU - Lisziewicz, J
AD - Genetic Immunity Kft, H-1045 Budapest, Hungary. ; 1] Wigner RCP of HAS, H-1121 Budapest, Hungary [2] R&D Ultrafast Lasers Ltd, H-1539 Budapest, Hungary. ; Centre d'Immunologie de Marseille-Luminy, INSERM U1104, CNRS UMR7280, Aix Marseille Université, Marseille, France. ; Research Institute for Genetic and Human Therapy (RIGHT), Bethesda, MD, USA. ; Section on Tissue Biophysics and Biomimetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development, NIH, Bethesda, MD, USA. ; Department of Dermatology and Venereology, Innsbruck Medical University, Innsbruck, Austria.
Y1 - 2014/06//
PY - 2014
DA - June 2014
SP - 566
EP - 574
VL - 21
IS - 6
KW - Vaccines, DNA
KW - 0
KW - Index Medicus
KW - Cell Movement
KW - Drug Delivery Systems
KW - Animals
KW - Epidermis -- drug effects
KW - Microscopy, Confocal -- instrumentation
KW - Epidermis -- cytology
KW - Rabbits
KW - Tissue Distribution
KW - Microscopy, Confocal -- methods
KW - Mice, Transgenic
KW - Nanoparticles -- administration & dosage
KW - Administration, Topical
KW - Immunotherapy -- methods
KW - Langerhans Cells
KW - Vaccines, DNA -- administration & dosage
KW - Vaccines, DNA -- pharmacokinetics
KW - Lymph Nodes -- drug effects
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534102037?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gene+therapy&rft.atitle=Exploitation+of+Langerhans+cells+for+in+vivo+DNA+vaccine+delivery+into+the+lymph+nodes.&rft.au=T%C5%91ke%2C+E+R%3BL%C5%91rincz%2C+O%3BCsiszovszki%2C+Z%3BSomogyi%2C+E%3BFelf%C3%B6ldi%2C+G%3BMoln%C3%A1r%2C+L%3BSzip%C5%91cs%2C+R%3BKolonics%2C+A%3BMalissen%2C+B%3BLori%2C+F%3BTrocio%2C+J%3BBakare%2C+N%3BHorkay%2C+F%3BRomani%2C+N%3BTripp%2C+C+H%3BStoitzner%2C+P%3BLisziewicz%2C+J&rft.aulast=T%C5%91ke&rft.aufirst=E&rft.date=2014-06-01&rft.volume=21&rft.issue=6&rft.spage=566&rft.isbn=&rft.btitle=&rft.title=Gene+therapy&rft.issn=1476-5462&rft_id=info:doi/10.1038%2Fgt.2014.29
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-05-12
N1 - Date created - 2014-06-06
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1038/gt.2014.29
ER -
TY - JOUR
T1 - Dietary flavonoid intake and thyroid cancer risk in the NIH-AARP diet and health study.
AN - 1532951261; 24686895
AB - Experimental studies suggested that flavonoids may influence thyroid carcinogenesis, but epidemiologic evidence is sparse. No study has examined different classes of flavonoids in relation to thyroid cancer risk. Using data from the NIH-AARP Diet and Health Study, which enrolled 491,840 U.S. men and women, ages 50 to 71 years at baseline, we prospectively examined the risk of thyroid cancer in relation to dietary intakes of catechins, flavanones, flavonols, anthocyanidins, flavones, isoflavones, and total flavonoids. Dietary intakes were assessed using a food frequency questionnaire. Cancer cases were ascertained by linkage to state cancer registries. Multivariable-adjusted Cox proportional hazard models were used to estimate HRs and 95% confidence intervals (CI). During follow up (mean = 9 years), we identified 586 thyroid cancer cases. Thyroid cancer risk was inversely associated with dietary flavan-3-ols [HRQ5 vs. Q1 (95% CI): 0.70 (0.55, 0.91), PTrend = 0.03], but positively associated with flavanones [HRQ5 vs. Q1 (95% CI): 1.50 (1.14, 1.96), PTrend = 0.004]. Other classes of flavonoids and total flavonoids were not associated with thyroid cancer risk. Similar associations were found for papillary thyroid cancer. Our findings suggest that dietary intake of different classes of dietary flavonoids may have divergent effects on thyroid cancer risk. More studies are needed to clarify a role of flavonoids in thyroid cancer development. Results from our study suggest a potential nutritional etiology of thyroid cancer. Cancer Epidemiol Biomarkers Prev; 23(6); 1102-8. ©2014 AACR.
©2014 American Association for Cancer Research.
JF - Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
AU - Xiao, Qian
AU - Park, Yikyung
AU - Hollenbeck, Albert R
AU - Kitahara, Cari M
AD - Authors' Affiliations: Nutritional Epidemiology Branch and Radiation Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland; and AARP, Washington, District of Columbia qian.xiao@nih.gov. ; Authors' Affiliations: Nutritional Epidemiology Branch and Radiation Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland; and AARP, Washington, District of Columbia.
Y1 - 2014/06//
PY - 2014
DA - June 2014
SP - 1102
EP - 1108
VL - 23
IS - 6
KW - Flavonoids
KW - 0
KW - Index Medicus
KW - United States
KW - Prospective Studies
KW - Risk Factors
KW - Humans
KW - National Institutes of Health (U.S.)
KW - Aged
KW - Middle Aged
KW - Diet
KW - Male
KW - Female
KW - Thyroid Neoplasms -- diet therapy
KW - Flavonoids -- therapeutic use
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1532951261?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+epidemiology%2C+biomarkers+%26+prevention+%3A+a+publication+of+the+American+Association+for+Cancer+Research%2C+cosponsored+by+the+American+Society+of+Preventive+Oncology&rft.atitle=Dietary+flavonoid+intake+and+thyroid+cancer+risk+in+the+NIH-AARP+diet+and+health+study.&rft.au=Xiao%2C+Qian%3BPark%2C+Yikyung%3BHollenbeck%2C+Albert+R%3BKitahara%2C+Cari+M&rft.aulast=Xiao&rft.aufirst=Qian&rft.date=2014-06-01&rft.volume=23&rft.issue=6&rft.spage=1102&rft.isbn=&rft.btitle=&rft.title=Cancer+epidemiology%2C+biomarkers+%26+prevention+%3A+a+publication+of+the+American+Association+for+Cancer+Research%2C+cosponsored+by+the+American+Society+of+Preventive+Oncology&rft.issn=1538-7755&rft_id=info:doi/10.1158%2F1055-9965.EPI-13-1150
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2016-05-15
N1 - Date created - 2014-06-04
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Am J Epidemiol. 2001 Dec 15;154(12):1119-25 [11744517]
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Chem Res Toxicol. 1996 Jan-Feb;9(1):16-23 [8924586]
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Future Oncol. 2010 Nov;6(11):1771-9 [21142662]
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Cancer Causes Control. 2011 Jul;22(7):985-93 [21562752]
Food Chem Toxicol. 2011 Oct;49(10):2495-502 [21745527]
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Cancer Causes Control. 2012 Oct;23(10):1615-24 [22843022]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1158/1055-9965.EPI-13-1150
ER -
TY - JOUR
T1 - Novel DNA motif binding activity observed in vivo with an estrogen receptor α mutant mouse.
AN - 1532947160; 24713037
AB - Estrogen receptor α (ERα) interacts with DNA directly or indirectly via other transcription factors, referred to as "tethering." Evidence for tethering is based on in vitro studies and a widely used "KIKO" mouse model containing mutations that prevent direct estrogen response element DNA- binding. KIKO mice are infertile, due in part to the inability of estradiol (E2) to induce uterine epithelial proliferation. To elucidate the molecular events that prevent KIKO uterine growth, regulation of the pro-proliferative E2 target gene Klf4 and of Klf15, a progesterone (P4) target gene that opposes the pro-proliferative activity of KLF4, was evaluated. Klf4 induction was impaired in KIKO uteri; however, Klf15 was induced by E2 rather than by P4. Whole uterine chromatin immunoprecipitation-sequencing revealed enrichment of KIKO ERα binding to hormone response elements (HREs) motifs. KIKO binding to HRE motifs was verified using reporter gene and DNA-binding assays. Because the KIKO ERα has HRE DNA-binding activity, we evaluated the "EAAE" ERα, which has more severe DNA-binding domain mutations, and demonstrated a lack of estrogen response element or HRE reporter gene induction or DNA-binding. The EAAE mouse has an ERα null-like phenotype, with impaired uterine growth and transcriptional activity. Our findings demonstrate that the KIKO mouse model, which has been used by numerous investigators, cannot be used to establish biological functions for ERα tethering, because KIKO ERα effectively stimulates transcription using HRE motifs. The EAAE-ERα DNA-binding domain mutant mouse demonstrates that ERα DNA-binding is crucial for biological and transcriptional processes in reproductive tissues and that ERα tethering may not contribute to estrogen responsiveness in vivo.
JF - Molecular endocrinology (Baltimore, Md.)
AU - Hewitt, Sylvia C
AU - Li, Leping
AU - Grimm, Sara A
AU - Winuthayanon, Wipawee
AU - Hamilton, Katherine J
AU - Pockette, Brianna
AU - Rubel, Cory A
AU - Pedersen, Lars C
AU - Fargo, David
AU - Lanz, Rainer B
AU - DeMayo, Francesco J
AU - Schütz, Günther
AU - Korach, Kenneth S
AD - Receptor Biology (S.C.H., W.W., K.J.H., B.P., K.S.K.), Laboratory of Reproductive and Developmental Toxicology, Biostatistics Branch (L.L.), Integrative Bioinformatics (S.A.G., D.F.), Laboratory of Structural Biology (L.C.P.), National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709; Department of Molecular and Cellular Biology (C.A.R., R.B.L., F.J.D.), Baylor College of Medicine, Houston, Texas 77030; and Department of Molecular Biology of the Cell (G.S.), German Cancer Research Center, 69121 Heidelberg, Germany.
Y1 - 2014/06//
PY - 2014
DA - June 2014
SP - 899
EP - 911
VL - 28
IS - 6
KW - Estrogen Receptor alpha
KW - 0
KW - GKLF protein
KW - KLF15 protein, human
KW - Kruppel-Like Transcription Factors
KW - Nuclear Proteins
KW - Estradiol
KW - 4TI98Z838E
KW - Index Medicus
KW - Animals
KW - Nuclear Proteins -- genetics
KW - Estradiol -- physiology
KW - Protein Binding
KW - Mutation, Missense
KW - Mice, Knockout
KW - Uterus -- metabolism
KW - Phenotype
KW - Mice, 129 Strain
KW - Base Sequence
KW - Mice, Inbred C57BL
KW - Kruppel-Like Transcription Factors -- metabolism
KW - Consensus Sequence
KW - Response Elements
KW - Nuclear Proteins -- metabolism
KW - Female
KW - Kruppel-Like Transcription Factors -- genetics
KW - Estrogen Receptor alpha -- genetics
KW - Estrogen Receptor alpha -- metabolism
KW - Transcriptional Activation
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+endocrinology+%28Baltimore%2C+Md.%29&rft.atitle=Novel+DNA+motif+binding+activity+observed+in+vivo+with+an+estrogen+receptor+%CE%B1+mutant+mouse.&rft.au=Hewitt%2C+Sylvia+C%3BLi%2C+Leping%3BGrimm%2C+Sara+A%3BWinuthayanon%2C+Wipawee%3BHamilton%2C+Katherine+J%3BPockette%2C+Brianna%3BRubel%2C+Cory+A%3BPedersen%2C+Lars+C%3BFargo%2C+David%3BLanz%2C+Rainer+B%3BDeMayo%2C+Francesco+J%3BSch%C3%BCtz%2C+G%C3%BCnther%3BKorach%2C+Kenneth+S&rft.aulast=Hewitt&rft.aufirst=Sylvia&rft.date=2014-06-01&rft.volume=28&rft.issue=6&rft.spage=899&rft.isbn=&rft.btitle=&rft.title=Molecular+endocrinology+%28Baltimore%2C+Md.%29&rft.issn=1944-9917&rft_id=info:doi/10.1210%2Fme.2014-1051
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-01-20
N1 - Date created - 2014-06-04
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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Proc Natl Acad Sci U S A. 2010 Jul 20;107(29):13057-62 [20616010]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1210/me.2014-1051
ER -
TY - JOUR
T1 - Breast cancer risk after occupational solvent exposure: the influence of timing and setting.
AN - 1531956773; 24879566
AB - Organic solvents are ubiquitous in occupational settings where they may contribute to risks for carcinogenesis. However, there is limited information on organic solvents as human breast carcinogens. We examined the relationship between occupational exposure to solvents and breast cancer in a prospective study of 47,661 women with an occupational history in the Sister Study cohort. Occupational solvent exposure was categorized using self-reported job-specific solvent use collected at baseline. Multivariable Cox regression analyses were used to assess breast cancer risk, adjusting for established breast cancer risk factors. A total of 1,798 women were diagnosed with breast cancer during follow-up, including 1,255 invasive cases. Overall the risk of invasive breast cancer was not associated with lifetime exposure to solvents [HR, 1.04; 95% confidence interval (CI), 0.88-1.24]. Parous women who worked with solvents before their first full-term birth had an increased risk of estrogen receptor-positive invasive breast cancer compared with women who never worked with solvents (HR, 1.39; 95% CI, 1.03-1.86). A significantly elevated risk for estrogen receptor-positive invasive breast cancer was associated with solvent exposure among clinical laboratory technologists and technicians (HR, 2.00; 95% CI, 1.07-3.73). Occupational exposure to solvents before first birth, a critical period of breast tissue differentiation, may result in increased vulnerability for breast cancer. Our findings suggest a need for future studies in this area to focus on exposure time windows and solvent types in different occupational settings. ©2014 American Association for Cancer Research.
JF - Cancer research
AU - Ekenga, Christine C
AU - Parks, Christine G
AU - D'Aloisio, Aimee A
AU - DeRoo, Lisa A
AU - Sandler, Dale P
AD - Authors' Affiliations: Epidemiology Branch, National Institute of Environmental Health Sciences, NIH, Department of Health and Human Services, Research Triangle Park, North Carolina; and Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway christine.ekenga@nih.gov. ; Authors' Affiliations: Epidemiology Branch, National Institute of Environmental Health Sciences, NIH, Department of Health and Human Services, Research Triangle Park, North Carolina; and Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway. ; Authors' Affiliations: Epidemiology Branch, National Institute of Environmental Health Sciences, NIH, Department of Health and Human Services, Research Triangle Park, North Carolina; and Department of Global Public Health and Primary Care, University of Bergen, Bergen, NorwayAuthors' Affiliations: Epidemiology Branch, National Institute of Environmental Health Sciences, NIH, Department of Health and Human Services, Research Triangle Park, North Carolina; and Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway.
Y1 - 2014/06/01/
PY - 2014
DA - 2014 Jun 01
SP - 3076
EP - 3083
VL - 74
IS - 11
KW - Receptors, Estrogen
KW - 0
KW - Solvents
KW - Index Medicus
KW - Self Report
KW - Prospective Studies
KW - Risk Factors
KW - Humans
KW - Cohort Studies
KW - Middle Aged
KW - Receptors, Estrogen -- metabolism
KW - United States -- epidemiology
KW - Puerto Rico -- epidemiology
KW - Female
KW - Occupational Exposure -- statistics & numerical data
KW - Occupational Diseases -- metabolism
KW - Solvents -- poisoning
KW - Occupational Exposure -- adverse effects
KW - Breast Neoplasms -- metabolism
KW - Occupational Diseases -- epidemiology
KW - Breast Neoplasms -- epidemiology
KW - Breast Neoplasms -- chemically induced
KW - Occupational Diseases -- chemically induced
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1531956773?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Breast+cancer+risk+after+occupational+solvent+exposure%3A+the+influence+of+timing+and+setting.&rft.au=Ekenga%2C+Christine+C%3BParks%2C+Christine+G%3BD%27Aloisio%2C+Aimee+A%3BDeRoo%2C+Lisa+A%3BSandler%2C+Dale+P&rft.aulast=Ekenga&rft.aufirst=Christine&rft.date=2014-06-01&rft.volume=74&rft.issue=11&rft.spage=3076&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=1538-7445&rft_id=info:doi/10.1158%2F0008-5472.CAN-13-2430
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-08-28
N1 - Date created - 2014-06-02
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Am J Ind Med. 2000 Apr;37(4):349-52 [10706746]
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Occup Environ Med. 1998 Mar;55(3):161-71 [9624267]
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Epidemiology. 1999 Jan;10(1):37-48 [9888278]
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Scand J Work Environ Health. 1999 Jun;25(3):215-21 [10450771]
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Endocr Rev. 2009 Jun;30(4):293-342 [19502515]
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Occup Environ Med. 2010 Apr;67(4):263-9 [20360196]
Environ Health. 2010;9:40 [20646273]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1158/0008-5472.CAN-13-2430
ER -
TY - JOUR
T1 - Predictive value of a proteomic signature in patients with non-small-cell lung cancer treated with second-line erlotinib or chemotherapy (PROSE): a biomarker-stratified, randomised phase 3 trial.
AN - 1530958099; 24831979
AB - An established multivariate serum protein test can be used to classify patients according to whether they are likely to have a good or poor outcome after treatment with EGFR tyrosine-kinase inhibitors. We assessed the predictive power of this test in the comparison of erlotinib and chemotherapy in patients with non-small-cell lung cancer.
From Feb 26, 2008, to April 11, 2012, patients (aged ≥18 years) with histologically or cytologically confirmed, second-line, stage IIIB or IV non-small-cell lung cancer were enrolled in 14 centres in Italy. Patients were stratified according to a minimisation algorithm by Eastern Cooperative Oncology Group performance status, smoking history, centre, and masked pretreatment serum protein test classification, and randomly assigned centrally in a 1:1 ratio to receive erlotinib (150 mg/day, orally) or chemotherapy (pemetrexed 500 mg/m(2), intravenously, every 21 days, or docetaxel 75 mg/m(2), intravenously, every 21 days). The proteomic test classification was masked for patients and investigators who gave treatments, and treatment allocation was masked for investigators who generated the proteomic classification. The primary endpoint was overall survival and the primary hypothesis was the existence of a significant interaction between the serum protein test classification and treatment. Analyses were done on the per-protocol population. This trial is registered with ClinicalTrials.gov, number NCT00989690. 142 patients were randomly assigned to chemotherapy and 143 to erlotinib, and 129 (91%) and 134 (94%), respectively, were included in the per-protocol analysis. 88 (68%) patients in the chemotherapy group and 96 (72%) in the erlotinib group had a proteomic test classification of good. Median overall survival was 9·0 months (95% CI 6·8-10·9) in the chemotherapy group and 7·7 months (5·9-10·4) in the erlotinib group. We noted a significant interaction between treatment and proteomic classification (pinteraction=0·017 when adjusted for stratification factors; pinteraction=0·031 when unadjusted for stratification factors). Patients with a proteomic test classification of poor had worse survival on erlotinib than on chemotherapy (hazard ratio 1·72 [95% CI 1·08-2·74], p=0·022). There was no significant difference in overall survival between treatments for patients with a proteomic test classification of good (adjusted HR 1·06 [0·77-1·46], p=0·714). In the group of patients who received chemotherapy, the most common grade 3 or 4 toxic effect was neutropenia (19 [15%] vs one [<1%] in the erlotinib group), whereas skin toxicity (one [<1%] vs 22 [16%]) was the most frequent in the erlotinib group.
Our findings indicate that serum protein test status is predictive of differential benefit in overall survival for erlotinib versus chemotherapy in the second-line setting. Patients classified as likely to have a poor outcome have better outcomes on chemotherapy than on erlotinib. Italian Ministry of Health, Italian Association of Cancer Research, and Biodesix.
Copyright © 2014 Elsevier Ltd. All rights reserved.
JF - The Lancet. Oncology
AU - Gregorc, Vanesa
AU - Novello, Silvia
AU - Lazzari, Chiara
AU - Barni, Sandro
AU - Aieta, Michele
AU - Mencoboni, Manlio
AU - Grossi, Francesco
AU - De Pas, Tommaso
AU - de Marinis, Filippo
AU - Bearz, Alessandra
AU - Floriani, Irene
AU - Torri, Valter
AU - Bulotta, Alessandra
AU - Cattaneo, Angela
AU - Grigorieva, Julia
AU - Tsypin, Maxim
AU - Roder, Joanna
AU - Doglioni, Claudio
AU - Levra, Matteo Giaj
AU - Petrelli, Fausto
AU - Foti, Silvia
AU - Viganò, Mariagrazia
AU - Bachi, Angela
AU - Roder, Heinrich
AD - Department of Medical Oncology, Istituto di Ricovero e Cura a Carattere Scientifico, Ospedale San Raffaele, Milan, Italy. Electronic address: vanesa.gregorc@hsr.it. ; Department of Oncology, University of Turin, Azienda Ospedaliera Universitaria San Luigi Orbassano, Turin, Italy. ; Department of Medical Oncology, Istituto di Ricovero e Cura a Carattere Scientifico, Ospedale San Raffaele, Milan, Italy. ; Division of Medical Oncology, Department of Medical Oncology, Azienda Ospedaliera Treviglio, Treviglio, Italy. ; Division of Medical Oncology, Centro di Riferimento Oncologico di Basilicata, Istituto di Ricovero e Cura a Carattere Scientifico, Rionero in Vulture, Italy. ; Oncology Unit, Villa Scassi Hospital, Azienda Sanitaria Locale 3, Genoa, Italy. ; Lung Cancer Unit, Istituto di Ricovero e Cura a Carattere Scientifico, Azienda Ospedaliera Universitaria San Martino, Istituto Nazionale per la Ricerca sul Cancro, Genoa, Italy. ; Division of Thoracic Oncology, European Institute of Oncology, Milan, Italy. ; Division of Thoracic Oncology, European Institute of Oncology, Milan, Italy; 1st Oncological Pulmonary Unit, San Camillo, High Specialization Hospital, Rome, Italy. ; Department of Medical Oncology, National Cancer Institute of Aviano, Aviano, Italy. ; Department of Oncology, Istituto di Ricovero e Cura a Carattere Scientifico-Istituto di Richerche Farmacologiche Mario Negri, Milan, Italy. ; Biodesix, Boulder, CO, USA. ; Università Vita-Salute San Raffaele, School of Medicine, Department of Pathology, Istituto di Ricovero e Cura a Carattere Scientifico, Ospedale San Raffaele, Milan, Italy.
Y1 - 2014/06//
PY - 2014
DA - June 2014
SP - 713
EP - 721
VL - 15
IS - 7
KW - Biomarkers, Tumor
KW - 0
KW - Blood Proteins
KW - Protein Kinase Inhibitors
KW - Quinazolines
KW - Erlotinib Hydrochloride
KW - DA87705X9K
KW - Receptor, Epidermal Growth Factor
KW - EC 2.7.10.1
KW - Index Medicus
KW - Disease-Free Survival
KW - Receptor, Epidermal Growth Factor -- genetics
KW - Humans
KW - Male
KW - Female
KW - Carcinoma, Non-Small-Cell Lung -- blood
KW - Protein Kinase Inhibitors -- therapeutic use
KW - Carcinoma, Non-Small-Cell Lung -- mortality
KW - Lung Neoplasms -- blood
KW - Proteomics
KW - Lung Neoplasms -- drug therapy
KW - Quinazolines -- therapeutic use
KW - Lung Neoplasms -- mortality
KW - Carcinoma, Non-Small-Cell Lung -- drug therapy
KW - Blood Proteins -- analysis
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1530958099?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Lancet.+Oncology&rft.atitle=Predictive+value+of+a+proteomic+signature+in+patients+with+non-small-cell+lung+cancer+treated+with+second-line+erlotinib+or+chemotherapy+%28PROSE%29%3A+a+biomarker-stratified%2C+randomised+phase+3+trial.&rft.au=Gregorc%2C+Vanesa%3BNovello%2C+Silvia%3BLazzari%2C+Chiara%3BBarni%2C+Sandro%3BAieta%2C+Michele%3BMencoboni%2C+Manlio%3BGrossi%2C+Francesco%3BDe+Pas%2C+Tommaso%3Bde+Marinis%2C+Filippo%3BBearz%2C+Alessandra%3BFloriani%2C+Irene%3BTorri%2C+Valter%3BBulotta%2C+Alessandra%3BCattaneo%2C+Angela%3BGrigorieva%2C+Julia%3BTsypin%2C+Maxim%3BRoder%2C+Joanna%3BDoglioni%2C+Claudio%3BLevra%2C+Matteo+Giaj%3BPetrelli%2C+Fausto%3BFoti%2C+Silvia%3BVigan%C3%B2%2C+Mariagrazia%3BBachi%2C+Angela%3BRoder%2C+Heinrich&rft.aulast=Gregorc&rft.aufirst=Vanesa&rft.date=2014-06-01&rft.volume=15&rft.issue=7&rft.spage=713&rft.isbn=&rft.btitle=&rft.title=The+Lancet.+Oncology&rft.issn=1474-5488&rft_id=info:doi/10.1016%2FS1470-2045%2814%2970162-7
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-07-30
N1 - Date created - 2014-05-29
N1 - Date revised - 2017-01-14
N1 - Genetic sequence - NCT00989690; ClinicalTrials.gov
N1 - SuppNotes - Comment In:
Lancet Oncol. 2014 Jun;15(7):671-2 [24831978]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/S1470-2045(14)70162-7
ER -
TY - JOUR
T1 - Lenalidomide plus R-CHOP21 in elderly patients with untreated diffuse large B-cell lymphoma: results of the REAL07 open-label, multicentre, phase 2 trial.
AN - 1530957903; 24831981
AB - Up to 40% of elderly patients with untreated diffuse large B-cell lymphoma (DLBCL) given a regimen of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone every 21 days (R-CHOP21) relapse or develop refractory disease. Lenalidomide has high activity in relapsed or refractory aggressive B-cell lymphomas. In phase 2 of the REAL07 trial, we aimed to establish the safety and efficacy of the combination of lenalidomide and R-CHOP21 in elderly patients with untreated DLBCL.
REAL07 was an open-label, multicentre trial that was done in 13 centres in Italy and one in Germany. Eligible patients were aged 60-80 years; had newly diagnosed, untreated, CD20-positive, Ann Arbor stage II-IV DLBCL or grade 3b follicular lymphoma; had an Eastern Cooperative Oncology Group performance status of 0-2; had an International Prognostic Index (IPI) risk of low-intermediate, intermediate-high, or high; and were fit according to comprehensive geriatric assessment. Participants were to receive 15 mg oral lenalidomide on days 1-14 of six 21-day cycles, and standard doses of R-CHOP21 chemotherapy (375 mg/m(2) intravenous rituximab, 750 mg/m(2) intravenous cyclophosphamide, 50 mg/m(2) intravenous doxorubicin, and 1·4 mg/m(2) intravenous vincristine on day 1, and 40 mg/m(2) oral prednisone on days 1-5). The primary endpoint was frequency of overall response (complete response [CR] and partial response [PR]), which was assessed by (18)F-fluorodeoxyglucose ((18)F-FDG) PET at the end of the treatment. Analyses were by intention to treat. This trial is registered with ClinicalTrials.gov, number NCT00907348. 49 patients were included in phase 2: nine had been enrolled into phase 1 between Oct 23, 2008, and June 4, 2009, and had received the maximum tolerated dose of 15 mg lenalidomide; and 40 were enrolled into phase 2 between April 28, 2010, and June 3, 2011. 45 patients (92%, 95% CI 81-97) achieved a response (42 [86%] CR; three [6%] PR). Three patients (6%) did not respond and one (2%) died for reasons unrelated to treatment or disease. 277 (94%) of 294 planned cycles of lenalidomide and R-CHOP21 were completed. Grade 3-4 neutropenia was reported in 87 cycles (31%), grade 3-4 leukopenia in 77 (28%), and grade 3-4 thrombocytopenia in 35 (13%). No grade 4 non-haematological adverse events were reported. No patients died during the study as a result of toxic effects.
Lenalidomide with R-CHOP21 is effective and safe in elderly patients with untreated DLBCL. Fondazione Italiana Linfomi and Celgene.
Copyright © 2014 Elsevier Ltd. All rights reserved.
JF - The Lancet. Oncology
AU - Vitolo, Umberto
AU - Chiappella, Annalisa
AU - Franceschetti, Silvia
AU - Carella, Angelo Michele
AU - Baldi, Ileana
AU - Inghirami, Giorgio
AU - Spina, Michele
AU - Pavone, Vincenzo
AU - Ladetto, Marco
AU - Liberati, Anna Marina
AU - Molinari, Anna Lia
AU - Zinzani, Pierluigi
AU - Salvi, Flavia
AU - Fattori, Pier Paolo
AU - Zaccaria, Alfonso
AU - Dreyling, Martin
AU - Botto, Barbara
AU - Castellino, Alessia
AU - Congiu, Angela
AU - Gaudiano, Marcello
AU - Zanni, Manuela
AU - Ciccone, Giovannino
AU - Gaidano, Gianluca
AU - Rossi, Giuseppe
AU - Fondazione Italiana Linfomi
AD - Hematology, Azienda Ospedaliero Universitaria Città della Salute e della Scienza di Torino, Turin, Italy. Electronic address: uvitolo@cittadellasalute.to.it. ; Hematology, Azienda Ospedaliero Universitaria Città della Salute e della Scienza di Torino, Turin, Italy. ; Division of Hematology, Department of Translational Medicine, Amedeo Avogadro University of Eastern Piedmont, Azienda Ospedaliero-Universitaria Maggiore della Carità, Novara, Italy. ; Unit of Hematology 1, Istituto di Ricovero e Cura a Carattere Scientifico Hospital and University, Istituto dei Tumori San Martino, Genoa, Italy. ; Unit of Biostatistics, Epidemiology and Public Health, Department of Cardiac, Thoracic and Vascular Sciences, University of Padua, Padua, Italy. ; Department of Molecular Biotechnology and Health Science and Center for Experimental Research and Medical Studies, University of Turin, Turin, Italy; Department of Pathology and Laboratory Medicine, Weill Cornell Medical College, New York, NY, USA. ; Division of Medical Oncology A, Centro di Riferimento Oncologico Aviano National Cancer Institute, Aviano, Italy. ; Unit of Hematology and Hemopoietic Stem Cell Transplantation, Ospedale Cardinale G Panico, Tricase, Italy. ; Department of Molecular Biotechnologies and Health Sciences, University of Turin, Turin, Italy. ; Università degli studi di Perugia, Azienda Ospedaliera Santa Maria, Terni, Italy. ; Department of Oncology and Hematology, Infermi Hospital, Rimini, Italy. ; Institute of Hematology Lorenzo ed Ariosto Seràgnoli, University of Bologna, Bologna, Italy. ; Hematology Unit, S S Antonio e Biagio e Cesare Arrigo Hospital, Alessandria, Italy. ; Istituto Scientifico Romagnolo per lo studio e la Cura dei Tumori, Istituti di Ricovero e Cura a Carattere Scientifico, Meldola, Italy. ; Hematology Unit, Department of Oncology and Hematology, Santa Maria delle Croci Hospital, Ravenna, Italy. ; Medizinische Klinik und Poliklinik III, Klinikum der Universität München, Munich, Germany. ; Unit of Clinical Epidemiology, Azienda Ospedaliero Universitaria Città della Salute e della Scienza di Torino and Centro di Riferimento per l'Epidemiologia e la Prevenzione Oncologica in Piemonte, Turin, Italy. ; Struttura Complessa Ematologia e Dipartimento Oncologia Medica, Spedali Civili, Brescia, Italy. ; Fondazione Italiana Linfomi
Y1 - 2014/06//
PY - 2014
DA - June 2014
SP - 730
EP - 737
VL - 15
IS - 7
KW - Antibodies, Monoclonal, Murine-Derived
KW - 0
KW - R-CHOP protocol
KW - Thalidomide
KW - 4Z8R6ORS6L
KW - Vincristine
KW - 5J49Q6B70F
KW - Doxorubicin
KW - 80168379AG
KW - Cyclophosphamide
KW - 8N3DW7272P
KW - lenalidomide
KW - F0P408N6V4
KW - Prednisone
KW - VB0R961HZT
KW - Index Medicus
KW - Cyclophosphamide -- administration & dosage
KW - Doxorubicin -- adverse effects
KW - Vincristine -- adverse effects
KW - Thalidomide -- adverse effects
KW - Humans
KW - Vincristine -- administration & dosage
KW - Aged
KW - Antibodies, Monoclonal, Murine-Derived -- adverse effects
KW - Doxorubicin -- administration & dosage
KW - Cyclophosphamide -- adverse effects
KW - Prednisone -- adverse effects
KW - Aged, 80 and over
KW - Antibodies, Monoclonal, Murine-Derived -- administration & dosage
KW - Thalidomide -- administration & dosage
KW - Middle Aged
KW - Prednisone -- administration & dosage
KW - Female
KW - Male
KW - Thalidomide -- analogs & derivatives
KW - Lymphoma, Large B-Cell, Diffuse -- mortality
KW - Lymphoma, Large B-Cell, Diffuse -- drug therapy
KW - Antineoplastic Combined Chemotherapy Protocols -- administration & dosage
KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects
KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1530957903?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Lancet.+Oncology&rft.atitle=Lenalidomide+plus+R-CHOP21+in+elderly+patients+with+untreated+diffuse+large+B-cell+lymphoma%3A+results+of+the+REAL07+open-label%2C+multicentre%2C+phase+2+trial.&rft.au=Vitolo%2C+Umberto%3BChiappella%2C+Annalisa%3BFranceschetti%2C+Silvia%3BCarella%2C+Angelo+Michele%3BBaldi%2C+Ileana%3BInghirami%2C+Giorgio%3BSpina%2C+Michele%3BPavone%2C+Vincenzo%3BLadetto%2C+Marco%3BLiberati%2C+Anna+Marina%3BMolinari%2C+Anna+Lia%3BZinzani%2C+Pierluigi%3BSalvi%2C+Flavia%3BFattori%2C+Pier+Paolo%3BZaccaria%2C+Alfonso%3BDreyling%2C+Martin%3BBotto%2C+Barbara%3BCastellino%2C+Alessia%3BCongiu%2C+Angela%3BGaudiano%2C+Marcello%3BZanni%2C+Manuela%3BCiccone%2C+Giovannino%3BGaidano%2C+Gianluca%3BRossi%2C+Giuseppe%3BFondazione+Italiana+Linfomi&rft.aulast=Vitolo&rft.aufirst=Umberto&rft.date=2014-06-01&rft.volume=15&rft.issue=7&rft.spage=730&rft.isbn=&rft.btitle=&rft.title=The+Lancet.+Oncology&rft.issn=1474-5488&rft_id=info:doi/10.1016%2FS1470-2045%2814%2970191-3
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-07-30
N1 - Date created - 2014-05-29
N1 - Date revised - 2017-01-14
N1 - Genetic sequence - NCT00907348; ClinicalTrials.gov
N1 - SuppNotes - Comment In:
Lancet Oncol. 2014 Jun;15(7):674-5 [24872095]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/S1470-2045(14)70191-3
ER -
TY - JOUR
T1 - A recurrent neomorphic mutation in MYOD1 defines a clinically aggressive subset of embryonal rhabdomyosarcoma associated with PI3K-AKT pathway mutations.
AN - 1530319319; 24793135
AB - Rhabdomyosarcoma, a cancer of skeletal muscle lineage, is the most common soft-tissue sarcoma in children. Major subtypes of rhabdomyosarcoma include alveolar (ARMS) and embryonal (ERMS) tumors. Whereas ARMS tumors typically contain translocations generating PAX3-FOXO1 or PAX7-FOXO1 fusions that block terminal myogenic differentiation, no functionally comparable genetic event has been found in ERMS tumors. Here we report the discovery, through whole-exome sequencing, of a recurrent somatic mutation encoding p.Leu122Arg in the myogenic transcription factor MYOD1 in a distinct subset of ERMS tumors with poor outcomes that also often contain mutations altering PI3K-AKT pathway components. Previous mutagenesis studies had shown that MYOD1 with a p.Leu122Arg substitution can block wild-type MYOD1 function and bind to MYC consensus sequences, suggesting a possible switch from differentiation to proliferation. Our functional data now confirm this prediction. Thus, MYOD1 p.Leu122Arg defines a subset of rhabdomyosarcomas eligible for high-risk protocols and the development of targeted therapeutics.
JF - Nature genetics
AU - Kohsaka, Shinji
AU - Shukla, Neerav
AU - Ameur, Nabahet
AU - Ito, Tatsuo
AU - Ng, Charlotte K Y
AU - Wang, Lu
AU - Lim, Diana
AU - Marchetti, Angela
AU - Viale, Agnes
AU - Pirun, Mono
AU - Socci, Nicholas D
AU - Qin, Li-Xuan
AU - Sciot, Raf
AU - Bridge, Julia
AU - Singer, Samuel
AU - Meyers, Paul
AU - Wexler, Leonard H
AU - Barr, Frederic G
AU - Dogan, Snjezana
AU - Fletcher, Jonathan A
AU - Reis-Filho, Jorge S
AU - Ladanyi, Marc
AD - 1] Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York, USA. [2] Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York, USA. [3]. ; 1] Department of Pediatrics, Memorial Sloan Kettering Cancer Center, New York, New York, USA. [2]. ; Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York, USA. ; Genomics Core Laboratory, Memorial Sloan Kettering Cancer Center, New York, New York, USA. ; Bioinformatics Core Facility, Memorial Sloan Kettering Cancer Center, New York, New York, USA. ; Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, New York, USA. ; Department of Pathology, University Hospital Gasthuisberg and University of Leuven, Leuven, Belgium. ; Department of Pathology, University of Nebraska Medical Center, Omaha, Nebraska, USA. ; Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, New York, USA. ; Department of Pediatrics, Memorial Sloan Kettering Cancer Center, New York, New York, USA. ; Laboratory of Pathology, National Cancer Institute, Bethesda, Maryland, USA. ; Department of Pathology, Brigham and Women's Hospital, Boston, Massachusetts, USA. ; 1] Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York, USA. [2] Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York, USA.
Y1 - 2014/06//
PY - 2014
DA - June 2014
SP - 595
EP - 600
VL - 46
IS - 6
KW - MyoD Protein
KW - 0
KW - MyoD1 myogenic differentiation protein
KW - Phosphatidylinositol 3-Kinases
KW - EC 2.7.1.-
KW - AKT1 protein, human
KW - EC 2.7.11.1
KW - Proto-Oncogene Proteins c-akt
KW - Index Medicus
KW - Young Adult
KW - Animals
KW - DNA Mutational Analysis
KW - Humans
KW - Mice
KW - Amino Acid Sequence
KW - Child
KW - Cell Proliferation
KW - Mutagenesis
KW - Genotype
KW - Exome
KW - Adult
KW - Molecular Sequence Data
KW - Sequence Homology, Amino Acid
KW - Adolescent
KW - Transcriptome
KW - Male
KW - Female
KW - High-Throughput Nucleotide Sequencing
KW - Proto-Oncogene Proteins c-akt -- genetics
KW - Phosphatidylinositol 3-Kinases -- genetics
KW - Rhabdomyosarcoma, Embryonal -- genetics
KW - MyoD Protein -- genetics
KW - Mutation
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1530319319?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+genetics&rft.atitle=A+recurrent+neomorphic+mutation+in+MYOD1+defines+a+clinically+aggressive+subset+of+embryonal+rhabdomyosarcoma+associated+with+PI3K-AKT+pathway+mutations.&rft.au=Kohsaka%2C+Shinji%3BShukla%2C+Neerav%3BAmeur%2C+Nabahet%3BIto%2C+Tatsuo%3BNg%2C+Charlotte+K+Y%3BWang%2C+Lu%3BLim%2C+Diana%3BMarchetti%2C+Angela%3BViale%2C+Agnes%3BPirun%2C+Mono%3BSocci%2C+Nicholas+D%3BQin%2C+Li-Xuan%3BSciot%2C+Raf%3BBridge%2C+Julia%3BSinger%2C+Samuel%3BMeyers%2C+Paul%3BWexler%2C+Leonard+H%3BBarr%2C+Frederic+G%3BDogan%2C+Snjezana%3BFletcher%2C+Jonathan+A%3BReis-Filho%2C+Jorge+S%3BLadanyi%2C+Marc&rft.aulast=Kohsaka&rft.aufirst=Shinji&rft.date=2014-06-01&rft.volume=46&rft.issue=6&rft.spage=595&rft.isbn=&rft.btitle=&rft.title=Nature+genetics&rft.issn=1546-1718&rft_id=info:doi/10.1038%2Fng.2969
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-08-08
N1 - Date created - 2014-05-28
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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Comment In:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1038/ng.2969
ER -
TY - JOUR
T1 - Essential Role for the Response Regulator PmrA in Coxiella burnetii Type 4B Secretion and Colonization of Mammalian Host Cells
AN - 1529932114; 19846360
AB - Successful host cell colonization by the Q fever pathogen, Coxiella burnetii, requires translocation of effector proteins into the host cytosol by a Dot/Icm type 4B secretion system (T4BSS). In Legionella pneumophila, the two-component system (TCS) PmrAB regulates the Dot/Icm T4BSS and several additional physiological processes associated with pathogenesis. Because PmrA consensus regulatory elements are associated with some dot/icm and substrate genes, a similar role for PmrA in regulation of the C. burnetii T4BSS has been proposed. Here, we constructed a C. burnetii pmrA deletion mutant to directly probe PmrA-mediated gene regulation. Compared to wild-type bacteria, C. burnetii Delta pmrA exhibited severe intracellular growth defects that coincided with failed secretion of effector proteins. Luciferase gene reporter assays demonstrated PmrA-dependent expression of 5 of 7 dot/icm operons and 9 of 11 effector-encoding genes with a predicted upstream PmrA regulatory element. Mutational analysis verified consensus sequence nucleotides required for PmrA-directed transcription. RNA sequencing and whole bacterial cell mass spectrometry of wild-type C. burnetii and the Delta pmrA mutant uncovered new components of the PmrA regulon, including several genes lacking PmrA motifs that encoded Dot/Icm substrates. Collectively, our results indicate that the PmrAB TCS is a critical virulence factor that regulates C. burnetii Dot/Icm secretion. The presence of PmrA-responsive genes lacking PmrA regulatory elements also suggests that the PmrAB TCS controls expression of regulatory systems associated with the production of additional C. burnetii proteins involved in host cell parasitism.
JF - Journal of Bacteriology
AU - Beare, Paul A
AU - Sandoz, Kelsi M
AU - Larson, Charles L
AU - Howe, Dale
AU - Kronmiller, Brent
AU - Heinzen, Robert A
AD - Coxiella Pathogenesis Section, Laboratory of Intracellular Parasites, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, USA, rheinzen@niaid.nih.gov.
Y1 - 2014/06//
PY - 2014
DA - June 2014
SP - 1925
EP - 1940
PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL - 196
IS - 11
SN - 0021-9193, 0021-9193
KW - Microbiology Abstracts B: Bacteriology
KW - Legionella pneumophila
KW - Deletion mutant
KW - virulence factors
KW - Nucleotide sequence
KW - Regulatory sequences
KW - Secretion
KW - DNA probes
KW - Transcription
KW - Pathogens
KW - Parasitism
KW - Mass spectroscopy
KW - Coxiella burnetii
KW - Colonization
KW - RNA
KW - Gene regulation
KW - Cytosol
KW - Conserved sequence
KW - Operons
KW - Q fever
KW - Translocation
KW - J 02310:Genetics & Taxonomy
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-05-01
N1 - Number of references - 76
N1 - Last updated - 2016-08-03
N1 - SubjectsTermNotLitGenreText - Deletion mutant; virulence factors; DNA probes; Secretion; Regulatory sequences; Nucleotide sequence; Transcription; Pathogens; Parasitism; Mass spectroscopy; Colonization; RNA; Gene regulation; Cytosol; Conserved sequence; Operons; Translocation; Q fever; Legionella pneumophila; Coxiella burnetii
DO - http://dx.doi.org/10.1128/JB.01532-14
ER -
TY - JOUR
T1 - Evaluation of intracellular and extracellular trehalose as a cryoprotectant of stem cells obtained from umbilical cord blood.
AN - 1529843315; 24769312
AB - Cord blood is a source of hematopoietic stem cells used in transplantation in which hematopoietic reconstitution is necessary. This transplant modality requires the cryopreservation of hematopoietic stem cells (HSCs). Dimethyl sulfoxide has been used as a cryoprotectant (CPA) in the cryopreservation of HSCs; however, it has been demonstrated that Me2SO exhibits toxic side effects to the human body. Due to its stability upon freezing, disaccharides such as trehalose have been investigated as a cryoprotectant. This study investigated the hypothesis that a cryopreservation solution containing intracellular and extracellular trehalose improves the recovery of stem cells after cryopreservation. After thawing, the cells were tested for their viability using the 7AAD stain, CD45+/CD34+ cells were assessed using flow cytometry and the MTT viability assay, and the proportion of hematopoietic progenitor cells was measured using the CFU assay. Our results showed the effectiveness of the solution containing intracellular and extracellular trehalose in the cryopreservation of cord blood cells, demonstrating that trehalose may be an optimal cryoprotectant when present both inside and outside of cells.
Copyright © 2014 Elsevier Inc. All rights reserved.
JF - Cryobiology
AU - Motta, Juliana Pessanha Rodrigues
AU - Paraguassú-Braga, Flávio Henrique
AU - Bouzas, Luis Fernando
AU - Porto, Luís Cristóvão
AD - Histocompatibility and Cryopreservation Laboratory, Department of Histology and Embryology, Institute of Biology Roberto Alcantara Gomes, Rio de Janeiro State University, Pav. Jose Roberto Feresin Moraes, Av Marechal Rondon 381, São Francisco Xavier, 20950-003 Rio de Janeiro, Brazil. ; Umbilical Cord Blood Bank, Bone Marrow Transplantation Unit, National Cancer Institute, Rio de Janeiro, Brazil. ; Histocompatibility and Cryopreservation Laboratory, Department of Histology and Embryology, Institute of Biology Roberto Alcantara Gomes, Rio de Janeiro State University, Pav. Jose Roberto Feresin Moraes, Av Marechal Rondon 381, São Francisco Xavier, 20950-003 Rio de Janeiro, Brazil. Electronic address: lcporto@uerj.br.
Y1 - 2014/06//
PY - 2014
DA - June 2014
SP - 343
EP - 348
VL - 68
IS - 3
KW - Cryoprotective Agents
KW - 0
KW - Liposomes
KW - Trehalose
KW - B8WCK70T7I
KW - Index Medicus
KW - Cord blood
KW - Liposome
KW - Me(2)SO
KW - Cryopreservation
KW - Cells, Cultured
KW - Humans
KW - Female
KW - Cell Survival
KW - Fetal Blood -- cytology
KW - Cryoprotective Agents -- analysis
KW - Cryoprotective Agents -- metabolism
KW - Trehalose -- analysis
KW - Hematopoietic Stem Cells -- cytology
KW - Trehalose -- administration & dosage
KW - Cryopreservation -- methods
KW - Hematopoietic Stem Cells -- metabolism
KW - Trehalose -- metabolism
KW - Cryoprotective Agents -- administration & dosage
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-01-05
N1 - Date created - 2014-05-27
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.cryobiol.2014.04.007
ER -
TY - JOUR
T1 - Sputum neutrophil counts are associated with more severe asthma phenotypes using cluster analysis
AN - 1529150333; 24332216
AB - Background
Clinical cluster analysis from the Severe Asthma Research Program (SARP) identified 5 asthma subphenotypes that represent the severity spectrum of early-onset allergic asthma, late-onset severe asthma, and severe asthma with chronic obstructive pulmonary disease characteristics. Analysis of induced sputum from a subset of SARP subjects showed 4 sputum inflammatory cellular patterns. Subjects with concurrent increases in eosinophil (>=2%) and neutrophil (>=40%) percentages had characteristics of very severe asthma.
Objective
To better understand interactions between inflammation and clinical subphenotypes, we integrated inflammatory cellular measures and clinical variables in a new cluster analysis.
Methods
Participants in SARP who underwent sputum induction at 3 clinical sites were included in this analysis (n = 423). Fifteen variables, including clinical characteristics and blood and sputum inflammatory cell assessments, were selected using factor analysis for unsupervised cluster analysis.
Results
Four phenotypic clusters were identified. Cluster A (n = 132) and B (n = 127) subjects had mild-to-moderate early-onset allergic asthma with paucigranulocytic or eosinophilic sputum inflammatory cell patterns. In contrast, these inflammatory patterns were present in only 7% of cluster C (n = 117) and D (n = 47) subjects who had moderate-to-severe asthma with frequent health care use despite treatment with high doses of inhaled or oral corticosteroids and, in cluster D, reduced lung function. The majority of these subjects (>83%) had sputum neutrophilia either alone or with concurrent sputum eosinophilia. Baseline lung function and sputum neutrophil percentages were the most important variables determining cluster assignment.
Conclusion
This multivariate approach identified 4 asthma subphenotypes representing the severity spectrum from mild-to-moderate allergic asthma with minimal or eosinophil-predominant sputum inflammation to moderate-to-severe asthma with neutrophil-predominant or mixed granulocytic inflammation.
JF - Journal of Allergy and Clinical Immunology
AU - Moore, Wendy C
AU - Hastie, Annette T
AU - Li, Xingnan
AU - Li, Huashi
AU - Busse, William W
AU - Jarjour, Nizar N
AU - Wenzel, Sally E
AU - Peters, Stephen P
AU - Meyers, Deborah A
AU - Bleecker, Eugene R
Y1 - 2014/06//
PY - 2014
DA - Jun 2014
SP - 1557
EP - 63.e5
CY - St. Louis
PB - Elsevier Science Ltd.
VL - 133
IS - 6
SN - 00916749
KW - Abstracting And Indexing Services
KW - Cluster analysis
KW - Asthma
KW - Colleges & universities
KW - Statistical methods
KW - Age
KW - Body mass index
KW - Multivariate analysis
KW - Family medical history
KW - Discriminant analysis
KW - Respiratory Function Tests
KW - Granulocytes
KW - Young Adult
KW - Age Factors
KW - Asthma -- blood
KW - Risk Factors
KW - Humans
KW - Adult
KW - Middle Aged
KW - Adolescent
KW - Male
KW - Female
KW - Asthma -- physiopathology
KW - Severity of Illness Index
KW - Phenotype
KW - Sputum -- cytology
KW - Neutrophils
KW - Asthma -- diagnosis
KW - Cluster Analysis
KW - Leukocyte Count
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LA - English
DB - ProQuest Central
N1 - Copyright - Copyright Elsevier Limited Jun 2014
N1 - Last updated - 2014-07-19
DO - http://dx.doi.org/10.1016/j.jaci.2013.10.011
ER -
TY - JOUR
T1 - Effects of prenatal methamphetamine exposure on behavioral and cognitive findings at 7.5 years of age.
AN - 1528884286; 24630350
AB - To examine child behavioral and cognitive outcomes after prenatal exposure to methamphetamine.
We enrolled 412 mother-infant pairs (204 methamphetamine-exposed and 208 unexposed matched comparisons) in the Infant Development, Environment, and Lifestyle study. The 151 children exposed to methamphetamine and 147 comparisons who attended the 7.5-year visit were included. Exposure was determined by maternal self-report and/or positive meconium toxicology. Maternal interviews assessed behavioral and cognitive outcomes using the Conners' Parent Rating Scale-Revised: Short Form. After adjusting for covariates, children exposed to methamphetamine had significantly higher cognitive problems subscale scores than comparisons and were 2.8 times more likely to have cognitive problems scores that were above average on the Conners' Parent Rating Scale-Revised: Short Form. No association between prenatal methamphetamine exposure and behavioral problems, measured by the oppositional, hyperactivity, and attention-deficit/hyperactivity disorder index subscales, were found.
Prenatal methamphetamine exposure was associated with increased cognitive problems, which may affect academic achievement and lead to increased negative behavioral outcomes. Copyright © 2014 Elsevier Inc. All rights reserved.
JF - The Journal of pediatrics
AU - Diaz, Sabrina D
AU - Smith, Lynne M
AU - LaGasse, Linda L
AU - Derauf, Chris
AU - Newman, Elana
AU - Shah, Rizwan
AU - Arria, Amelia
AU - Huestis, Marilyn A
AU - Della Grotta, Sheri
AU - Dansereau, Lynne M
AU - Neal, Charles
AU - Lester, Barry M
AD - LA Biomed Institute at Harbor-UCLA Medical Center and David Geffen School of Medicine at UCLA, Los Angeles, CA. ; LA Biomed Institute at Harbor-UCLA Medical Center and David Geffen School of Medicine at UCLA, Los Angeles, CA. Electronic address: smith@labiomed.org. ; Brown Center for the Study of Children at Risk, Warren Alpert Medical School of Brown University, Women and Infants Hospital, Providence, RI. ; Mayo Clinic, Rochester, MN. ; Department of Psychology, The University of Tulsa, Tulsa, OK. ; Blank Hospital Regional Child Protection Center-Iowa Health, Des Moines, IA. ; Center on Young Adult Health and Development, University of Maryland, School of Public Health, College Park, MD. ; Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD. ; John A. Burns School of Medicine, University of Hawaii, Honolulu, HI.
Y1 - 2014/06//
PY - 2014
DA - June 2014
SP - 1333
EP - 1338
VL - 164
IS - 6
KW - Methamphetamine
KW - 44RAL3456C
KW - Abridged Index Medicus
KW - Index Medicus
KW - Severity of Illness Index
KW - Amphetamine-Related Disorders -- epidemiology
KW - Age Factors
KW - Methamphetamine -- adverse effects
KW - Humans
KW - Retrospective Studies
KW - Prognosis
KW - Infant, Newborn
KW - Child
KW - Risk Assessment
KW - Pregnancy
KW - Child, Preschool
KW - Infant
KW - Case-Control Studies
KW - Incidence
KW - Amphetamine-Related Disorders -- diagnosis
KW - Time Factors
KW - Female
KW - Male
KW - Maternal Exposure -- adverse effects
KW - Attention Deficit Disorder with Hyperactivity -- diagnosis
KW - Attention Deficit Disorder with Hyperactivity -- epidemiology
KW - Child Behavior
KW - Prenatal Exposure Delayed Effects -- psychology
KW - Cognition Disorders -- epidemiology
KW - Prenatal Exposure Delayed Effects -- epidemiology
KW - Prenatal Exposure Delayed Effects -- diagnosis
KW - Cognition Disorders -- chemically induced
KW - Cognition Disorders -- physiopathology
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-08-18
N1 - Date created - 2014-05-26
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Am J Obstet Gynecol. 2002 Mar;186(3):487-95 [11904612]
Pediatrics. 2002 Dec;110(6):1182-92 [12456917]
J Pers Assess. 2003 Jun;80(3):252-9 [12763699]
JAMA. 2004 May 26;291(20):2448-56 [15161895]
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Psychol Bull. 1992 Jan;111(1):127-55 [1539086]
Child Abuse Negl. 1994 Jan;18(1):3-9 [7510211]
Acta Paediatr. 1996 Feb;85(2):204-8 [8640051]
Neurotoxicol Teratol. 1996 Nov-Dec;18(6):627-34 [8947939]
J Am Acad Child Adolesc Psychiatry. 1997 Jan;36(1):123-31 [9000790]
Integr Physiol Behav Sci. 1997 Jan-Mar;32(1):62-74 [9105915]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.jpeds.2014.01.053
ER -
TY - JOUR
T1 - A novel trafficking-defective HCN4 mutation is associated with early-onset atrial fibrillation.
AN - 1528873564; 24607718
AB - Atrial fibrillation (AF) is the most common arrhythmia, and a recent genome-wide association study identified the hyperpolarization-activated cyclic nucleotide-gated channel 4 (HCN4) as a novel AF susceptibility locus. HCN4 encodes for the cardiac pacemaker channel, and HCN4 mutations are associated with familial sinus bradycardia and AF.
The purpose of this study was to determine whether novel variants in the coding region of HCN4 contribute to the susceptibility for AF. We sequenced the coding region of HCN4 for novel variants from 527 cases with early-onset AF from the Massachusetts General Hospital AF Study and 443 referents from the Framingham Heart Study. We used site-directed mutagenesis, cellular electrophysiology, immunocytochemistry, and confocal microscopy to functionally characterize novel variants.
We found the frequency of novel coding HCN4 variants was 2-fold greater for individuals with AF (7 variants) compared to the referents (3 variants). We determined that of the 7 novel HCN4 variants in our AF cases, 1 (p.Pro257Ser, located in the amino-terminus adjacent to the first transmembrane spanning domain) did not traffic to cell membrane, whereas the remaining 6 were not functionally different from wild type. In addition, the 3 novel variants in our referents did not alter function compared to wild-type. Coexpression studies showed that the p.Pro257Ser mutant channel failed to colocalize with the wild-type HCN4 channel on the cell membrane. Our findings are consistent with HCN4 haploinsufficiency as the likely mechanism for early-onset AF in the p.Pro257Ser carrier.
Copyright © 2014 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.
JF - Heart rhythm
AU - Macri, Vincenzo
AU - Mahida, Saagar N
AU - Zhang, Michael L
AU - Sinner, Moritz F
AU - Dolmatova, Elena V
AU - Tucker, Nathan R
AU - McLellan, Micheal
AU - Shea, Marisa A
AU - Milan, David J
AU - Lunetta, Kathryn L
AU - Benjamin, Emelia J
AU - Ellinor, Patrick T
AD - Cardiovascular Research Center, Massachusetts General Hospital, Charlestown, Massachusetts; Harvard Medical School, Boston, Massachusetts. ; Cardiovascular Research Center, Massachusetts General Hospital, Charlestown, Massachusetts. ; Cardiovascular Research Center, Massachusetts General Hospital, Charlestown, Massachusetts; Department of Medicine I, University Hospital Grosshadern, Ludwig-Maximilians University, Munich, Germany; National Heart, Lung, and Blood Institute's and Boston University's Framingham Heart Study, Framingham, Massachusetts. ; Cardiac Arrhythmia Service, Massachusetts General Hospital, Boston, Massachusetts. ; National Heart, Lung, and Blood Institute's and Boston University's Framingham Heart Study, Framingham, Massachusetts; Department of Epidemiology, Boston University School of Public Health, Boston, Massachusetts; Department of Biostatistics, Boston University School of Public Health, Boston, Massachusetts. ; National Heart, Lung, and Blood Institute's and Boston University's Framingham Heart Study, Framingham, Massachusetts; Department of Epidemiology, Boston University School of Public Health, Boston, Massachusetts; Preventive Medicine Section, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts; Cardiology Section, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts. ; Cardiovascular Research Center, Massachusetts General Hospital, Charlestown, Massachusetts; Harvard Medical School, Boston, Massachusetts; Cardiac Arrhythmia Service, Massachusetts General Hospital, Boston, Massachusetts. Electronic address: ellinor@mgh.harvard.edu.
Y1 - 2014/06//
PY - 2014
DA - June 2014
SP - 1055
EP - 1062
VL - 11
IS - 6
KW - HCN4 protein, human
KW - 0
KW - Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels
KW - Muscle Proteins
KW - Potassium Channels
KW - Index Medicus
KW - Electrophysiology
KW - Atrial fibrillation
KW - HCN4
KW - Mutation
KW - Mutagenesis, Site-Directed
KW - Microscopy, Confocal
KW - Animals
KW - Cricetulus
KW - Age of Onset
KW - Electrophysiologic Techniques, Cardiac
KW - Humans
KW - CHO Cells
KW - Middle Aged
KW - Haploinsufficiency
KW - Male
KW - Female
KW - Protein Transport
KW - Muscle Proteins -- metabolism
KW - Muscle Proteins -- genetics
KW - Potassium Channels -- metabolism
KW - Atrial Fibrillation -- genetics
KW - Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels -- metabolism
KW - Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels -- genetics
KW - Potassium Channels -- genetics
KW - Atrial Fibrillation -- epidemiology
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-02-12
N1 - Date created - 2014-05-26
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.hrthm.2014.03.002
ER -
TY - JOUR
T1 - Deleted in liver cancer-1 (DLC1): an emerging metastasis suppressor gene.
AN - 1528341063; 24519699
AB - While significant progress continues to be made in the early detection and therapeutic management of primary tumors, the incidence of metastatic disease remains the major cause of mortality. Accordingly, the development of novel effective therapies that can ameliorate dissemination and secondary tumor growth are a clinical priority. The identification of genetic and functional alterations in cancer cells that affect factors implicated in the metastatic process is critical for designing preventive and therapeutic strategies. Evidence implicating the protein deleted in liver cancer-1 (DLC1), a Rho GTPase activator, in metastasis has accumulated to a point where DLC1 may be considered as a metastasis suppressor gene. This review presents evidence supporting an anti-metastatic role for DLC1 in several human cancers and discusses the mechanisms contributing to its inhibitory effects. In addition, promising opportunities for therapeutic interventions based on DLC1 function and downstream pathways involved in the metastatic process are considered.
JF - Molecular diagnosis & therapy
AU - Popescu, Nicholas C
AU - Goodison, Steve
AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Building 37, Room 4140, 37 Convent Dr., MSC 4262, Bethesda, MD, 20892-4262, USA, popescun@dc37a.nci.nih.gov.
Y1 - 2014/06//
PY - 2014
DA - June 2014
SP - 293
EP - 302
VL - 18
IS - 3
KW - Antineoplastic Agents
KW - 0
KW - DLC1 protein, human
KW - GTPase-Activating Proteins
KW - Tumor Suppressor Proteins
KW - Index Medicus
KW - Gene Expression Regulation, Neoplastic
KW - Genes, Tumor Suppressor
KW - Humans
KW - Antineoplastic Agents -- therapeutic use
KW - Antineoplastic Agents -- pharmacology
KW - GTPase-Activating Proteins -- genetics
KW - Neoplasms -- pathology
KW - Neoplasm Metastasis -- genetics
KW - GTPase-Activating Proteins -- metabolism
KW - Tumor Suppressor Proteins -- metabolism
KW - Tumor Suppressor Proteins -- genetics
KW - Neoplasm Metastasis -- pathology
KW - Neoplasms -- genetics
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1528341063?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+diagnosis+%26+therapy&rft.atitle=Deleted+in+liver+cancer-1+%28DLC1%29%3A+an+emerging+metastasis+suppressor+gene.&rft.au=Popescu%2C+Nicholas+C%3BGoodison%2C+Steve&rft.aulast=Popescu&rft.aufirst=Nicholas&rft.date=2014-06-01&rft.volume=18&rft.issue=3&rft.spage=293&rft.isbn=&rft.btitle=&rft.title=Molecular+diagnosis+%26+therapy&rft.issn=1179-2000&rft_id=info:doi/10.1007%2Fs40291-014-0086-3
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-01-12
N1 - Date created - 2014-05-23
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1007/s40291-014-0086-3
ER -
TY - JOUR
T1 - Learning phenotype densities conditional on many interacting predictors.
AN - 1528337791; 24501099
AB - Estimating a phenotype distribution conditional on a set of discrete-valued predictors is a commonly encountered task. For example, interest may be in how the density of a quantitative trait varies with single nucleotide polymorphisms and patient characteristics. The subset of important predictors is not usually known in advance. This becomes more challenging with a high-dimensional predictor set when there is the possibility of interaction.
We demonstrate a novel non-parametric Bayes method based on a tensor factorization of predictor-dependent weights for Gaussian kernels. The method uses multistage predictor selection for dimension reduction, providing succinct models for the phenotype distribution. The resulting conditional density morphs flexibly with the selected predictors. In a simulation study and an application to molecular epidemiology data, we demonstrate advantages over commonly used methods. © The Author 2014. Published by Oxford University Press. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.
JF - Bioinformatics (Oxford, England)
AU - Kessler, David C
AU - Taylor, Jack A
AU - Dunson, David B
AD - Advanced Analytics Division, SAS Institute Inc., Cary, NC 27513, Molecular and Genetic Epidemiology Section, Epidemiology Branch and Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709 and Department of Statistical Science, Duke University, Durham, NC 27708.
Y1 - 2014/06/01/
PY - 2014
DA - 2014 Jun 01
SP - 1562
EP - 1568
VL - 30
IS - 11
KW - Index Medicus
KW - Polymorphism, Single Nucleotide
KW - Humans
KW - Bayes Theorem
KW - Algorithms
KW - Phenotype
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1528337791?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Bioinformatics+%28Oxford%2C+England%29&rft.atitle=Learning+phenotype+densities+conditional+on+many+interacting+predictors.&rft.au=Kessler%2C+David+C%3BTaylor%2C+Jack+A%3BDunson%2C+David+B&rft.aulast=Kessler&rft.aufirst=David&rft.date=2014-06-01&rft.volume=30&rft.issue=11&rft.spage=1562&rft.isbn=&rft.btitle=&rft.title=Bioinformatics+%28Oxford%2C+England%29&rft.issn=1367-4811&rft_id=info:doi/10.1093%2Fbioinformatics%2Fbtu040
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-07-28
N1 - Date created - 2014-05-22
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Psychometrika. 1966 Sep;31(3):279-311 [5221127]
Biometrics. 2011 Sep;67(3):886-95 [21039398]
Biostatistics. 2009 Jan;10(1):155-71 [18708650]
Cancer Res. 1991 Sep 1;51(17):4671-6 [1873812]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/bioinformatics/btu040
ER -
TY - JOUR
T1 - Phase I/Ib study of olaparib and carboplatin in BRCA1 or BRCA2 mutation-associated breast or ovarian cancer with biomarker analyses.
AN - 1526731510; 24842883
AB - Olaparib has single-agent activity against breast/ovarian cancer (BrCa/OvCa) in germline BRCA1 or BRCA2 mutation carriers (gBRCAm). We hypothesized addition of olaparib to carboplatin can be administered safely and yield preliminary clinical activity.
Eligible patients had measurable or evaluable disease, gBRCAm, and good end-organ function. A 3 + 3 dose escalation tested daily oral capsule olaparib (100 or 200mg every 12 hours; dose level1 or 2) with carboplatin area under the curve (AUC) on day 8 (AUC3 day 8), then every 21 days. For dose levels 3 to 6, patients were given olaparib days 1 to 7 at 200 and 400 mg every 12 hours, with carboplatin AUC3 to 5 on day 1 or 2 every 21 days; a maximum of eight combination cycles were permitted, after which daily maintenance of olaparib 400mg every12 hours continued until progression. Dose-limiting toxicity was defined in the first two cycles. Peripheral blood mononuclear cells were collected for polymorphism analysis and polyADP-ribose incorporation. Paired tumor biopsies (before/after cycle 1) were obtained for biomarker proteomics and apoptosis endpoints. Forty-five women (37 OvCa/8 BrCa) were treated. Dose-limiting toxicity was not reached on the intermittent schedule. Expansion proceeded with olaparib 400mg every 12 hours on days 1 to 7/carboplatin AUC5. Grade 3/4 adverse events included neutropenia (42.2%), thrombocytopenia (20.0%), and anemia (15.6%). Responses included 1 complete response (1 BrCa; 23 months) and 21 partial responses (50.0%; 15 OvCa; 6 BrCa; median = 16 [4 to >45] in OvCa and 10 [6 to >40] months in BrCa). Proteomic analysis suggests high pretreatment pS209-eIF4E and FOXO3a correlated with duration of response (two-sided P < .001; Pearson's R (2) = 0.94).
Olaparib capsules 400mg every 12 hours on days 1 to 7/carboplatin AUC5 is safe and has activity in gBRCAm BrCa/OvCa patients. Exploratory translational studies indicate pretreatment tissue FOXO3a expression may be predictive for response to therapy, requiring prospective validation. Published by Oxford University Press 2014.
JF - Journal of the National Cancer Institute
AU - Lee, Jung-Min
AU - Hays, John L
AU - Annunziata, Christina M
AU - Noonan, Anne M
AU - Minasian, Lori
AU - Zujewski, Jo Anne
AU - Yu, Minshu
AU - Gordon, Nicolas
AU - Ji, Jiuping
AU - Sissung, Tristan M
AU - Figg, William D
AU - Azad, Nilofer
AU - Wood, Bradford J
AU - Doroshow, James
AU - Kohn, Elise C
AD - Affiliations of authors: Medical Oncology Branch, Center for Cancer Research (J-ML, JLH, CMA, AMN, LM, JAZ, MY, NG, TMS, WDF, NA, ECK), National Clinical Target Validation Laboratory, Leidos Biomedical Research, Frederick National Laboratory for Cancer Research (JJ), Center for Interventional Oncology, Radiology, and Imaging Sciences, Clinical Center and National Cancer Institute (BJW), and Division of Cancer Treatment and Diagnosis, National Cancer Institute (JD), National Institutes of Health, Bethesda, MD. leej6@mail.nih.gov. ; Affiliations of authors: Medical Oncology Branch, Center for Cancer Research (J-ML, JLH, CMA, AMN, LM, JAZ, MY, NG, TMS, WDF, NA, ECK), National Clinical Target Validation Laboratory, Leidos Biomedical Research, Frederick National Laboratory for Cancer Research (JJ), Center for Interventional Oncology, Radiology, and Imaging Sciences, Clinical Center and National Cancer Institute (BJW), and Division of Cancer Treatment and Diagnosis, National Cancer Institute (JD), National Institutes of Health, Bethesda, MD.
Y1 - 2014/06//
PY - 2014
DA - June 2014
SP - 1
VL - 106
IS - 6
KW - BRCA1 Protein
KW - 0
KW - BRCA1 protein, human
KW - BRCA2 Protein
KW - BRCA2 protein, human
KW - FOXO3 protein, human
KW - Forkhead Box Protein O3
KW - Forkhead Transcription Factors
KW - Phthalazines
KW - Piperazines
KW - Poly Adenosine Diphosphate Ribose
KW - 26656-46-2
KW - Carboplatin
KW - BG3F62OND5
KW - olaparib
KW - WOH1JD9AR8
KW - Index Medicus
KW - Administration, Oral
KW - Phthalazines -- adverse effects
KW - Drug Administration Schedule
KW - Humans
KW - Aged
KW - Predictive Value of Tests
KW - Piperazines -- adverse effects
KW - Piperazines -- administration & dosage
KW - Carboplatin -- administration & dosage
KW - Carboplatin -- adverse effects
KW - Gene Expression Regulation, Neoplastic -- drug effects
KW - Phthalazines -- administration & dosage
KW - Monocytes -- metabolism
KW - Adult
KW - Monocytes -- drug effects
KW - Middle Aged
KW - Genetic Predisposition to Disease
KW - Poly Adenosine Diphosphate Ribose -- metabolism
KW - Female
KW - Breast Neoplasms -- genetics
KW - Breast Neoplasms -- drug therapy
KW - Ovarian Neoplasms -- genetics
KW - BRCA1 Protein -- genetics
KW - Antineoplastic Combined Chemotherapy Protocols -- administration & dosage
KW - Forkhead Transcription Factors -- drug effects
KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects
KW - Forkhead Transcription Factors -- metabolism
KW - Mutation
KW - Ovarian Neoplasms -- drug therapy
KW - BRCA2 Protein -- genetics
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1526731510?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=Phase+I%2FIb+study+of+olaparib+and+carboplatin+in+BRCA1+or+BRCA2+mutation-associated+breast+or+ovarian+cancer+with+biomarker+analyses.&rft.au=Lee%2C+Jung-Min%3BHays%2C+John+L%3BAnnunziata%2C+Christina+M%3BNoonan%2C+Anne+M%3BMinasian%2C+Lori%3BZujewski%2C+Jo+Anne%3BYu%2C+Minshu%3BGordon%2C+Nicolas%3BJi%2C+Jiuping%3BSissung%2C+Tristan+M%3BFigg%2C+William+D%3BAzad%2C+Nilofer%3BWood%2C+Bradford+J%3BDoroshow%2C+James%3BKohn%2C+Elise+C&rft.aulast=Lee&rft.aufirst=Jung-Min&rft.date=2014-06-01&rft.volume=106&rft.issue=6&rft.spage=dju089&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=1460-2105&rft_id=info:doi/10.1093%2Fjnci%2Fdju089
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-07-07
N1 - Date created - 2014-05-20
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/jnci/dju089
ER -
TY - JOUR
T1 - Treatment outcomes of female germ cell tumors: the Egyptian National Cancer Institute experience.
AN - 1526731459; 24841162
AB - Female germ cell tumors (GCTS) are rare tumors that carry a good prognosis.
To report the experience of the Egyptian National Cancer Institute (ENCI) in managing female GCTs. This retrospective study included 19 females with ovarian GCTs presenting to the ENCI between 2006 and 2010.
The median age was 23years. Ovaries were the primary site in all patients. Dysgerminoma and teratoma were the predominant pathologies followed by mixed GCT in females. Unilateral ovariectomy or ovarian tumorectomy were the classic surgical procedures with R0 resection being feasible in most cases. Surveillance was adopted in six patients with stage I disease. Chemotherapy was administered in 63% of ovarian GCTs with BEP being the commonest regimen with reasonable tolerability and good response rates. The median OS and EFS were not reached. The projected 5-year OS rate was 93.8%. Both OS and EFS were better in patients responding to chemotherapy than non-responders (p<0.002). Stage of disease did not significantly affect OS or EFS.
Female GCTs rarely affect Egyptian females. They have good prognosis. Copyright © 2014. Production and hosting by Elsevier B.V.
JF - Journal of the Egyptian National Cancer Institute
AU - Saber, Magdy M
AU - Zeeneldin, Ahmed A
AU - El Gammal, Mosaad M
AU - Salem, Salem E
AU - Darweesh, Amira D
AU - Abdelaziz, Alshaymaa A
AU - Monir, Manar
AD - Medical Oncology Department, NCI, Cairo University, Egypt. ; Medical Oncology Department, NCI, Cairo University, Egypt. Electronic address: elgammalmosaad@yahoo.com. ; Department of Medical Statics, NCI, Cairo University, Egypt.
Y1 - 2014/06//
PY - 2014
DA - June 2014
SP - 103
EP - 108
VL - 26
IS - 2
SN - 1110-0362, 1110-0362
KW - Etoposide
KW - 6PLQ3CP4P3
KW - Cisplatin
KW - Q20Q21Q62J
KW - Index Medicus
KW - Chemotherapy
KW - Survival
KW - Female germ-cell tumors
KW - Treatment
KW - Side effects
KW - Disease-Free Survival
KW - Neoplasm Staging
KW - Etoposide -- administration & dosage
KW - Humans
KW - Adult
KW - Retrospective Studies
KW - Prognosis
KW - Aged
KW - Middle Aged
KW - Adolescent
KW - Female
KW - Cisplatin -- administration & dosage
KW - Genital Neoplasms, Female -- surgery
KW - Genital Neoplasms, Female -- pathology
KW - Treatment Outcome
KW - Neoplasms, Germ Cell and Embryonal -- pathology
KW - Neoplasms, Germ Cell and Embryonal -- drug therapy
KW - Neoplasms, Germ Cell and Embryonal -- surgery
KW - Genital Neoplasms, Female -- drug therapy
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-12-30
N1 - Date created - 2014-05-20
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.jnci.2014.03.001
ER -
TY - JOUR
T1 - The origin of cancer stem cells.
AN - 1526133491; 24631602
JF - Journal of hepatology
AU - Dang, Hien T
AU - Budhu, Anuradha
AU - Wang, Xin W
AD - Liver Carcinogenesis Section, Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. ; Liver Carcinogenesis Section, Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: xw3u@nih.gov.
Y1 - 2014/06//
PY - 2014
DA - June 2014
SP - 1304
EP - 1305
VL - 60
IS - 6
KW - Interleukin-6
KW - 0
KW - Index Medicus
KW - IL-6
KW - HCC progenitor cells
KW - Foci altered hepatocytes
KW - Cancer stem cells
KW - Hepatocellular carcinoma
KW - Hepatocarcinogenesis
KW - Animals
KW - Gene Expression Regulation, Neoplastic
KW - Liver Neoplasms -- pathology
KW - Interleukin-6 -- metabolism
KW - Autocrine Communication
KW - Neoplastic Stem Cells -- metabolism
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-01-06
N1 - Date created - 2014-05-19
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Comment On:
Cell. 2013 Oct 10;155(2):384-96 [24120137]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.jhep.2014.03.001
ER -
TY - JOUR
T1 - Immunomodulatory activity of orphan drug Elmiron® in female B6C3F1/N mice.
AN - 1526129724; 24657363
AB - Interstitial cystitis (IC) is a chronic disorder characterized by bladder discomfort and urinary urgency in the absence of identifiable infection. Despite the expanding use in IC treatment and other chronic conditions, the effects of Elmiron® treatment on immune system remain unknown. Therefore, female B6C3F1/N mice were orally administered Elmiron® daily for 28-days at doses of 63, 125, 250, 500 or 1000mg/kg to evaluate its immunomodulatory effects. Mice treated with Elmiron® had a significant increase in absolute numbers of splenic macrophages (63, 500 and 1000mg/kg) and natural killer (NK) cells (250 and 1000mg/kg). Elmiron® treatment did not affect the humoral immune response or T cell proliferative response. However, innate immune responses such as phagocytosis by liver macrophages (1000mg/kg) and NK cell activity were enhanced (500 and 1000mg/kg). Further analysis using a disease resistance model showed that Elmiron®-treated mice demonstrated significantly increased anti-tumor activity against B16F10 melanoma cells at the 500 and 1000mg/kg doses. Collectively, we conclude that Elmiron® administration stimulates the immune system, increasing numbers of specific cell populations and enhancing macrophage phagocytosis and NK cell activity in female B6C3F1/N mice. This augmentation may have largely contributed to the reduced number of B16F10 melanoma tumors.
Published by Elsevier Ltd.
JF - Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
AU - Thakur, Sheetal A
AU - Nyska, Abraham
AU - White, Kimber L
AU - Smith, Matthew J
AU - Auttachoat, Wimolnut
AU - Germolec, Dori R
AD - Toxicology Branch, Division of National Toxicology Program, National Institute of Environmental Health Sciences, NIH, RTP, NC, United States. Electronic address: thakursa@niehs.nih.gov. ; Integrated Laboratory Systems, RTP, NC, United States. ; Virginia Commonwealth University, Richmond, VA, United States. ; Toxicology Branch, Division of National Toxicology Program, National Institute of Environmental Health Sciences, NIH, RTP, NC, United States. Electronic address: germolec@niehs.nih.gov.
Y1 - 2014/06//
PY - 2014
DA - June 2014
SP - 196
EP - 203
VL - 68
KW - Antineoplastic Agents
KW - 0
KW - Immunoglobulin M
KW - Pentosan Sulfuric Polyester
KW - 37300-21-3
KW - Index Medicus
KW - Interstitial cystitis
KW - Immunotoxicity
KW - Sodium pentosan polysulfate
KW - Orphan drug
KW - Cell Proliferation -- drug effects
KW - Animals
KW - Immunity, Innate -- drug effects
KW - Spleen -- metabolism
KW - Spleen -- cytology
KW - Dose-Response Relationship, Drug
KW - Immunoglobulin M -- metabolism
KW - Liver -- metabolism
KW - Mice
KW - Cell Line, Tumor
KW - Macrophages -- drug effects
KW - Killer Cells, Natural -- drug effects
KW - Mice, Inbred Strains
KW - T-Lymphocytes -- metabolism
KW - Liver -- drug effects
KW - Body Weight -- drug effects
KW - T-Lymphocytes -- drug effects
KW - Phagocytosis -- drug effects
KW - Spleen -- drug effects
KW - Antineoplastic Agents -- pharmacology
KW - Female
KW - Organ Size -- drug effects
KW - Macrophages -- metabolism
KW - Pentosan Sulfuric Polyester -- pharmacology
KW - Immunomodulation -- drug effects
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-01-05
N1 - Date created - 2014-05-19
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.fct.2014.03.015
ER -
TY - JOUR
T1 - Probing the molecular mechanism of action of the HIV-1 reverse transcriptase inhibitor 4'-ethynyl-2-fluoro-2'-deoxyadenosine (EFdA) using pre-steady-state kinetics.
AN - 1524822356; 24632447
AB - The novel antiretroviral 4'-ethynyl-2-fluoro-2'-deoxyadenosine (EFdA) is a potent nucleoside HIV-1 reverse transcriptase (RT) inhibitor (NRTI). Unlike other FDA-approved NRTIs, EFdA contains a 3'-hydroxyl. Pre-steady-state kinetics showed RT preferred incorporating EFdA-TP over native dATP. Moreover, RT slowly inserted nucleotides past an EFdA-terminated primer, resulting in delayed chain termination with unaffected fidelity. This is distinct from KP1212, another 3'-hydroxyl-containing RT inhibitor considered to promote viral lethal mutagenesis. New mechanistic features of RT inhibition by EFdA are revealed.
Copyright © 2014 Elsevier B.V. All rights reserved.
JF - Antiviral research
AU - Muftuoglu, Yagmur
AU - Sohl, Christal D
AU - Mislak, Andrea C
AU - Mitsuya, Hiroaki
AU - Sarafianos, Stefan G
AU - Anderson, Karen S
AD - Department of Pharmacology, Yale University School of Medicine, New Haven, CT 06520, United States. ; Department of Infectious Diseases, Kumamoto University Graduate School of Medical Sciences, Kumamoto 860-8556, Japan; Department of Hematology, Kumamoto University Graduate School of Medical Sciences, Kumamoto 860-8556, Japan; Experimental Retrovirology Section, HIV and AIDS Malignancy Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, United States. ; CS Bond Life Sciences Center and Department of Molecular Microbiology and Immunology, University of Missouri, School of Medicine, Columbia, MO 65211, United States; Department of Biochemistry, University of Missouri, School of Medicine, Columbia, MO 65211, United States. ; Department of Pharmacology, Yale University School of Medicine, New Haven, CT 06520, United States. Electronic address: karen.anderson@yale.edu.
Y1 - 2014/06//
PY - 2014
DA - June 2014
SP - 1
EP - 4
VL - 106
KW - 4'-ethynyl-2-fluoro-2'-deoxyadenosine
KW - 0
KW - Anti-HIV Agents
KW - Deoxyadenosines
KW - Reverse Transcriptase Inhibitors
KW - reverse transcriptase, Human immunodeficiency virus 1
KW - EC 2.7.7.-
KW - HIV Reverse Transcriptase
KW - EC 2.7.7.49
KW - Index Medicus
KW - Polymerase
KW - Reverse transcriptase
KW - EFdA
KW - Enzyme kinetics
KW - HIV
KW - Kinetics
KW - Reverse Transcriptase Inhibitors -- pharmacology
KW - Anti-HIV Agents -- pharmacology
KW - HIV Reverse Transcriptase -- antagonists & inhibitors
KW - Deoxyadenosines -- pharmacology
KW - HIV-1 -- enzymology
KW - HIV-1 -- drug effects
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Antiviral+research&rft.atitle=Probing+the+molecular+mechanism+of+action+of+the+HIV-1+reverse+transcriptase+inhibitor+4%27-ethynyl-2-fluoro-2%27-deoxyadenosine+%28EFdA%29+using+pre-steady-state+kinetics.&rft.au=Muftuoglu%2C+Yagmur%3BSohl%2C+Christal+D%3BMislak%2C+Andrea+C%3BMitsuya%2C+Hiroaki%3BSarafianos%2C+Stefan+G%3BAnderson%2C+Karen+S&rft.aulast=Muftuoglu&rft.aufirst=Yagmur&rft.date=2014-06-01&rft.volume=106&rft.issue=&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Antiviral+research&rft.issn=1872-9096&rft_id=info:doi/10.1016%2Fj.antiviral.2014.03.001
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-12-19
N1 - Date created - 2014-05-14
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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J Biol Chem. 2001 Nov 2;276(44):40847-57 [11526116]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.antiviral.2014.03.001
ER -
TY - JOUR
T1 - Vitamin D-binding protein, circulating vitamin D and risk of renal cell carcinoma
AN - 1524426150; 19553242
AB - Cell culture experiments suggest that vitamin D may inhibit renal carcinogenesis, but human studies of circulating 25-hydroxyvitamin D [25(OH)D], the accepted measure of vitamin D status, and kidney cancer have been null. Limited research has examined the role of circulating vitamin D-binding protein (DBP) in the association between 25(OH)D and disease risk, and it is unclear whether free 25(OH)D in circulation is a better measure of effective exposure, or if DBP may independently impact outcomes. We conducted a nested case-control analysis within the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study to examine whether circulating DBP concentration was prospectively associated with risk of renal cell carcinoma, and whether it modified the association with 25(OH)D. Renal cell carcinoma cases (n = 262) were matched 1:1 to controls on age ( plus or minus 1 year) and date of blood collection ( plus or minus 30 days). We estimated odds ratios (ORs) and 95% confidence intervals (CIs) of renal cell carcinoma risk by quartiles of 25(OH)D, DBP and the molar ratio of 25(OH)D:DBP, a proxy for free circulating 25(OH)D. Men with higher DBP concentrations were at significantly decreased risk of kidney cancer (Q4 vs. Q1: OR = 0.17, 95% CI = 0.08-0.33; p-trend < 0.0001), a finding unchanged by adjustment for 25(OH)D. Although we observed no association with total 25(OH)D, we found slightly increased risk with higher levels of estimated free 25(OH)D [Q4 vs. Q1 of the 25(OH)D:DBP ratio, OR = 1.61, 95% CI = 0.95-2.73; p-trend = 0.09]. The strong protective association observed between higher circulating DBP concentration and kidney cancer risk requires replication but suggests a vitamin D-independent influence of DBP. What's new? Circulating vitamin D binding protein (DBP) has been implicated in the etiology of certain cancers, where it may act directly or by modifying circulating vitamin D concentrations and disease risk. In this examination of the association between DBP and renal cell carcinoma (RCC) specifically, a strong protective association was found between elevated circulating DBP concentrations and kidney cancer. The association was unchanged after adjustment for circulating vitamin D. The results suggest that DBP may influence risk of RCC through a biologic mechanism unrelated to vitamin D status.
JF - International Journal of Cancer
AU - Mondul, Alison M
AU - Weinstein, Stephanie J
AU - Moy, Kristin A
AU - Maennisto, Satu
AU - Albanes, Demetrius
AD - Nutritional Epidemiology Branch Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Rockville, MD.
Y1 - 2014/06//
PY - 2014
DA - Jun 2014
SP - 2699
EP - 2706
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 134
IS - 11
SN - 0020-7136, 0020-7136
KW - Health & Safety Science Abstracts; Risk Abstracts
KW - renal cell carcinoma
KW - vitamin D-binding protein
KW - 25-hydroxyvitamin D
KW - prospective studies
KW - Renal
KW - Health risks
KW - Prevention
KW - Age
KW - Etiology
KW - Vitamin D
KW - Vitamins
KW - Carcinogenesis
KW - Kidney
KW - Proteins
KW - Cancer
KW - H 6000:Natural Disasters/Civil Defense/Emergency Management
KW - R2 23060:Medical and environmental health
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1524426150?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Cancer&rft.atitle=Vitamin+D-binding+protein%2C+circulating+vitamin+D+and+risk+of+renal+cell+carcinoma&rft.au=Mondul%2C+Alison+M%3BWeinstein%2C+Stephanie+J%3BMoy%2C+Kristin+A%3BMaennisto%2C+Satu%3BAlbanes%2C+Demetrius&rft.aulast=Mondul&rft.aufirst=Alison&rft.date=2014-06-01&rft.volume=134&rft.issue=11&rft.spage=2699&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.28596
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-05-01
N1 - Last updated - 2014-10-30
N1 - SubjectsTermNotLitGenreText - Renal; Health risks; Etiology; Age; Prevention; Vitamin D; Vitamins; Carcinogenesis; Kidney; Proteins; Cancer
DO - http://dx.doi.org/10.1002/ijc.28596
ER -
TY - JOUR
T1 - Dietary nitrate and nitrite intake and risk of colorectal cancer in the Shanghai Women's Health Study
AN - 1524397976; 19625526
AB - Nitrate and nitrite are precursors of endogenously formed N-nitroso compounds (NOC), known animal carcinogens. Nitrosation reactions forming NOCs can be inhibited by vitamin C and other antioxidants. We prospectively investigated the association between dietary nitrate and nitrite intake and risk of colorectal cancer in the Shanghai Women's Health Study, a cohort of 73,118 women ages 40-70 residing in Shanghai. We evaluated effect modification by factors that affect endogenous formation of NOCs: vitamin C (at or above/below median) and red meat intake (at or above/below median). Nitrate, nitrite and other dietary intakes were estimated from a 77-item food frequency questionnaire administered at baseline. Over a mean of 11 years of follow-up, we identified 619 colorectal cancer cases (n=383, colon; n=236, rectum). Hazard ratios (HR) and 95% confidence intervals (CI) were estimated using Cox proportional hazard regression. Overall, nitrate intake was not associated with colorectal cancer risk (HR=1.08; 95% CI: 0.73-1.59). However, among women with vitamin C intake below the median (83.9 mg day super(-1)) and hence higher potential exposure to NOCs, risk of colorectal cancer increased with increasing quintiles of nitrate intake (highest vs. lowest quintile HR=2.45; 95% CI: 1.15-5.18; p trend=0.02). There was no association among women with higher vitamin C intake. We found no association between nitrite intake and risk of colorectal cancer overall or by intake level of vitamin C. Our findings suggest that high dietary nitrate intake among subgroups expected to have higher exposure to endogenously formed NOCs increases risk of colorectal cancer. What's new? Nitrate and nitrite are precursors in the endogenous formation of potentially carcinogenic N-nitroso compounds (NOC). These nitrosation reactions are linked to the consumption of red meat and can be inhibited by vitamin C and other antioxidants. Here, a potential association of dietary nitrate, nitrite and vitamin C intake with the risk of colorectal cancer was investigated in Chinese women. The authors find an increased risk of colorectal cancer in women with high nitrate intake and low vitamin C consumption linking high endogenous NOC exposure to colorectal carcinogenesis.
JF - International Journal of Cancer
AU - DellaValle, Curt T
AU - Xiao, Qian
AU - Yang, Gong
AU - Shu, Xiao-Ou
AU - Aschebrook-Kilfoy, Briseis
AU - Zheng, Wei
AU - Lan Li, Hong
AU - Ji, Bu-Tian
AU - Rothman, Nathaniel
AU - Chow, Wong-Ho
AU - Gao, Yu-Tang
AU - Ward, Mary H
AD - Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD.
Y1 - 2014/06//
PY - 2014
DA - Jun 2014
SP - 2917
EP - 2926
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 134
IS - 12
SN - 0020-7136, 0020-7136
KW - Health & Safety Science Abstracts; Risk Abstracts
KW - Diets
KW - Antioxidants
KW - Nitrates
KW - Ingestion
KW - Cancer
KW - Meat
KW - Health risks
KW - Nitrites
KW - Carcinogenicity
KW - Risk factors
KW - Vitamins
KW - Carcinogenesis
KW - Colorectal carcinoma
KW - China, People's Rep., Shanghai
KW - Females
KW - H 11000:Diseases/Injuries/Trauma
KW - R2 23060:Medical and environmental health
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Cancer&rft.atitle=Dietary+nitrate+and+nitrite+intake+and+risk+of+colorectal+cancer+in+the+Shanghai+Women%27s+Health+Study&rft.au=DellaValle%2C+Curt+T%3BXiao%2C+Qian%3BYang%2C+Gong%3BShu%2C+Xiao-Ou%3BAschebrook-Kilfoy%2C+Briseis%3BZheng%2C+Wei%3BLan+Li%2C+Hong%3BJi%2C+Bu-Tian%3BRothman%2C+Nathaniel%3BChow%2C+Wong-Ho%3BGao%2C+Yu-Tang%3BWard%2C+Mary+H&rft.aulast=DellaValle&rft.aufirst=Curt&rft.date=2014-06-01&rft.volume=134&rft.issue=12&rft.spage=2917&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.28612
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-05-01
N1 - Last updated - 2014-06-26
N1 - SubjectsTermNotLitGenreText - Diets; Antioxidants; Nitrates; Ingestion; Cancer; Meat; Health risks; Nitrites; Carcinogenicity; Vitamins; Risk factors; Carcinogenesis; Colorectal carcinoma; Females; China, People's Rep., Shanghai
DO - http://dx.doi.org/10.1002/ijc.28612
ER -
TY - JOUR
T1 - Ribonucleotide incorporation by yeast DNA polymerase ζ.
AN - 1524176962; 24674899
AB - During replication in yeast, the three B family DNA replicases frequently incorporate ribonucleotides (rNMPs) into DNA, and their presence in the nuclear genome can affect genome stability. This prompted us to examine ribonucleotide incorporation by the fourth B family member, Pol ζ, the enzyme responsible for the majority of damage-induced mutagenesis in eukaryotes. We first show that Pol ζ inserts rNMPs into DNA and can extend primer termini containing 3'-ribonucleotides. We then measure rNMP incorporation by Pol ζ in the presence of its cofactors, RPA, RFC and PCNA and at normal cellular dNTP and rNTP concentrations that exist under unstressed conditions. Under these conditions, Pol ζ stably incorporates one rNMP for every 200-300 dNMPs incorporated, a frequency that is slightly higher than for the high fidelity replicative DNA polymerases. Under damage-induced conditions wherein cellular dNTP concentrations are elevated 5-fold, Pol ζ only incorporates one rNMP per 1300 dNMPs. Functional interaction of Pol ζ with the mutasome assembly factor Rev1 gives comparable rNMP incorporation frequencies. These results suggest that ribonucleotide incorporation into DNA during Pol ζ-mediated mutagenesis in vivo may be rare.
Copyright © 2014 Elsevier B.V. All rights reserved.
JF - DNA repair
AU - Makarova, Alena V
AU - Nick McElhinny, Stephanie A
AU - Watts, Brian E
AU - Kunkel, Thomas A
AU - Burgers, Peter M
AD - Department of Biochemistry and Molecular Biophysics, Washington University School of Medicine, St. Louis, MO 63110, USA. ; Laboratory of Molecular Genetics and Laboratory of Structural Biology, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, NC 27709, USA. ; Department of Biochemistry and Molecular Biophysics, Washington University School of Medicine, St. Louis, MO 63110, USA. Electronic address: burgers@biochem.wustl.edu.
Y1 - 2014/06//
PY - 2014
DA - June 2014
SP - 63
EP - 67
VL - 18
KW - DNA, Fungal
KW - 0
KW - Deoxyribonucleotides
KW - REV7 protein, S cerevisiae
KW - RFA1 protein, S cerevisiae
KW - Replication Protein A
KW - Ribonucleotides
KW - Saccharomyces cerevisiae Proteins
KW - DNA polymerase zeta
KW - EC 2.7.7.-
KW - Nucleotidyltransferases
KW - REV1 protein, S cerevisiae
KW - DNA-Directed DNA Polymerase
KW - EC 2.7.7.7
KW - REV3 protein, S cerevisiae
KW - Index Medicus
KW - DNA polymerase
KW - Translesion synthesis
KW - Mutagenesis
KW - Nucleotidyltransferases -- metabolism
KW - Nucleotidyltransferases -- genetics
KW - DNA Damage
KW - Deoxyribonucleotides -- metabolism
KW - Replication Protein A -- metabolism
KW - Mutation
KW - DNA Replication
KW - Saccharomyces cerevisiae Proteins -- metabolism
KW - Saccharomyces cerevisiae Proteins -- genetics
KW - Ribonucleotides -- metabolism
KW - Saccharomyces cerevisiae -- enzymology
KW - DNA, Fungal -- metabolism
KW - DNA-Directed DNA Polymerase -- metabolism
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-01-06
N1 - Date created - 2014-05-12
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
J Biol Chem. 2000 May 12;275(19):14541-9 [10799539]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.dnarep.2014.02.017
ER -
TY - JOUR
T1 - Randomized, double-blind, placebo-controlled trial of soluble tumor necrosis factor receptor: enbrel (etanercept) for the treatment of idiopathic pneumonia syndrome after allogeneic stem cell transplantation: blood and marrow transplant clinical trials network protocol.
AN - 1524174464; 24607553
AB - Idiopathic pneumonia syndrome (IPS) is a diffuse, noninfectious lung injury that occurs acutely after allogeneic hematopoietic cell transplantation (HCT). IPS-related mortality has been historically high (>50%) despite treatment with systemic corticosteroids and supportive care measures. We have now examined the role of tumor necrosis factor inhibition in a randomized, double-blind, placebo-controlled trial of corticosteroids with etanercept or placebo. Thirty-four subjects (≥18 years) with IPS after HCT were randomized to receive methylprednisolone (2 mg/kg/day) plus etanercept (0.4 mg/kg twice weekly × 4 weeks; n = 16) or placebo (n = 18). No active infections and a pathogen-negative bronchoscopy were required at study entry. Response (alive, with complete discontinuation of supplemental oxygen support) and overall survival were examined. This study, originally planned to accrue 120 patients, was terminated prematurely due to slow accrual. In the limited number of patients examined, there were no differences in response rates at day 28 of study. Ten of 16 patients (62.5% [95% confidence interval {CI}, 35.4% to 84.8%]) receiving etanercept and 12 of 18 patients (66.7% [95% CI, 41.0% to 86.7%]) receiving placebo met the day 28 response definition (P = 1.00). The median survival was 170 days (95% CI, 11 to 362) with etanercept versus 64 days (95% CI, 26 to 209) with placebo (P = .51). Among responders, the median time to discontinuation of supplemental oxygen was 9 days (etanercept) versus 7 days (placebo). Therapy was well tolerated, with 1 toxicity-related death from infectious pneumonia in the placebo arm. The treatment of IPS with corticosteroids in adult HCT recipients was associated with high early response rates (>60%) compared with historical reports, with poor overall survival. The addition of etanercept did not lead to further increases in response, although the sample size of this truncated trial preclude a definitive conclusion.
Copyright © 2014. Published by Elsevier Inc.
JF - Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
AU - Yanik, Gregory A
AU - Horowitz, Mary M
AU - Weisdorf, Daniel J
AU - Logan, Brent R
AU - Ho, Vincent T
AU - Soiffer, Robert J
AU - Carter, Shelly L
AU - Wu, Juan
AU - Wingard, John R
AU - Difronzo, Nancy L
AU - Ferrara, James L
AU - Giralt, Sergio
AU - Madtes, David K
AU - Drexler, Rebecca
AU - White, Eric S
AU - Cooke, Kenneth R
AD - Department of Pediatrics and Internal Medicine, Blood and Marrow Transplant Program, University of Michigan Medical Center, Ann Arbor, Michigan. Electronic address: gyanik@umich.edu. ; Center for International Blood and Marrow Transplant Research, Medical College of Wisconsin, Milwaukee, Wisconsin. ; Department of Internal Medicine, University of Minnesota Blood and Marrow Transplantation Program, Minneapolis, Minnesota. ; Department of Hematologic Malignancies, Dana Farber Cancer Institute, Boston, Massachusetts. ; The EMMES Corporation, Rockville, Maryland. ; Department of Medicine, University of Florida, Gainesville, Florida. ; Division of Blood Diseases and Resources, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland. ; Department of Pediatrics and Internal Medicine, Blood and Marrow Transplant Program, University of Michigan Medical Center, Ann Arbor, Michigan. ; Department of Stem Cell Transplantation, Memorial Sloan Kettering Cancer Center, New York, New York. ; Clinical Research Division, Fred Hutchinson Cancer Research Center and Division of Pulmonary and Critical Care Medicine, University of Washington, Seattle, Washington. ; National Marrow Donor Program, Minneapolis, Minnesota; Center for International Blood and Marrow Transplant Research, Minneapolis, Minnesota. ; Department of Internal Medicine, Pulmonary and Critical Care Medicine, University of Michigan Medical Center, Ann Arbor, Michigan. ; Department of Oncology, Sidney Kimmel Cancer Center, Johns Hopkins University, School of Medicine, Baltimore, Maryland.
Y1 - 2014/06//
PY - 2014
DA - June 2014
SP - 858
EP - 864
VL - 20
IS - 6
KW - Adrenal Cortex Hormones
KW - 0
KW - Immunoglobulin G
KW - Receptors, Tumor Necrosis Factor
KW - Etanercept
KW - OP401G7OJC
KW - Index Medicus
KW - TNF
KW - Pulmonary
KW - IPS
KW - Pneumonia
KW - Bone marrow transplantation
KW - Young Adult
KW - Double-Blind Method
KW - Humans
KW - Adult
KW - Treatment Outcome
KW - Aged
KW - Middle Aged
KW - Transplantation, Homologous
KW - Male
KW - Female
KW - Adrenal Cortex Hormones -- therapeutic use
KW - Idiopathic Interstitial Pneumonias -- etiology
KW - Receptors, Tumor Necrosis Factor -- therapeutic use
KW - Idiopathic Interstitial Pneumonias -- drug therapy
KW - Immunoglobulin G -- therapeutic use
KW - Hematopoietic Stem Cell Transplantation -- adverse effects
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biology+of+blood+and+marrow+transplantation+%3A+journal+of+the+American+Society+for+Blood+and+Marrow+Transplantation&rft.atitle=Randomized%2C+double-blind%2C+placebo-controlled+trial+of+soluble+tumor+necrosis+factor+receptor%3A+enbrel+%28etanercept%29+for+the+treatment+of+idiopathic+pneumonia+syndrome+after+allogeneic+stem+cell+transplantation%3A+blood+and+marrow+transplant+clinical+trials+network+protocol.&rft.au=Yanik%2C+Gregory+A%3BHorowitz%2C+Mary+M%3BWeisdorf%2C+Daniel+J%3BLogan%2C+Brent+R%3BHo%2C+Vincent+T%3BSoiffer%2C+Robert+J%3BCarter%2C+Shelly+L%3BWu%2C+Juan%3BWingard%2C+John+R%3BDifronzo%2C+Nancy+L%3BFerrara%2C+James+L%3BGiralt%2C+Sergio%3BMadtes%2C+David+K%3BDrexler%2C+Rebecca%3BWhite%2C+Eric+S%3BCooke%2C+Kenneth+R&rft.aulast=Yanik&rft.aufirst=Gregory&rft.date=2014-06-01&rft.volume=20&rft.issue=6&rft.spage=858&rft.isbn=&rft.btitle=&rft.title=Biology+of+blood+and+marrow+transplantation+%3A+journal+of+the+American+Society+for+Blood+and+Marrow+Transplantation&rft.issn=1523-6536&rft_id=info:doi/10.1016%2Fj.bbmt.2014.02.026
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-04-09
N1 - Date created - 2014-05-12
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Transplantation. 2000 Jul 27;70(2):272-9 [10933148]
J Immunol. 2000 Dec 1;165(11):6612-9 [11086106]
Biol Blood Marrow Transplant. 2002;8(7):395-400 [12171486]
Blood. 2003 Oct 15;102(8):2777-85 [12855568]
Am Rev Respir Dis. 1993 Jun;147(6 Pt 1):1393-400 [8503550]
Am Rev Respir Dis. 1993 Jun;147(6 Pt 1):1601-6 [8503576]
Blood. 1996 Oct 15;88(8):3230-9 [8963063]
Transplantation. 1997 Apr 27;63(8):1079-86 [9133468]
Crit Care Med. 1999 Sep;27(9):1800-6 [10507601]
Blood. 2008 Oct 15;112(8):3073-81 [18664626]
Biol Blood Marrow Transplant. 2010 Jan;16(1 Suppl):S106-14 [19896545]
Bone Marrow Transplant. 2010 Apr;45(4):647-55 [19684637]
Am J Respir Crit Care Med. 2011 May 1;183(9):1262-79 [21531955]
Pediatr Blood Cancer. 2012 May;58(5):780-4 [21922645]
Mol Cell Proteomics. 2012 Jun;11(6):M111.015479 [22337588]
Bone Marrow Transplant. 2012 Oct;47(10):1332-7 [22307018]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.bbmt.2014.02.026
ER -
TY - JOUR
T1 - Relative potency for altered humoral immunity induced by polybrominated and polychlorinated dioxins/furans in female B6C3F1/N mice.
AN - 1524168409; 24713691
AB - The use of brominated flame retardants and incineration of bromine-containing materials has lead to an increase in polybrominated dibenzo-p-dioxins and dibenzofurans (PBDD/Fs) in the environment. Measurable amounts of PBDD/Fs have been detected in soil, seafood, and human breast milk and serum. Studies indicate that the relative potencies of some PBDD/Fs based on enzyme induction are equivalent to those of some polychlorinated dibenzo-p-dioxins and dibenzofurans. To assess the humoral immunity relative potencies of PBDD/Fs and compare them to their chlorinated analogs, female B6C3F1/N mice received a single oral exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 2,3,7,8-tetrabromodibenzofuran (TBDF), 2,3,7,8-tetrachlorodibenzofuran (TCDF), 1,2,3,7,8-pentabromodibenzofuran (1PeBDF), 1,2,3,7,8-pentachlorodibenzofuran (1PeCDF), 2,3,4,7,8-pentabromodibenzofuran (4PeBDF), 2,3,4,7,8-pentachlorodibenzofuran (4PeCDF), 2,3-dibromo-7,8-dichlorodibenzo-p-dioxin (DBDCDD), or 2,3,7-tribromodibenzo-p-dioxin (TriBDD). Inhibition of the immunoglobulin M (IgM) antibody forming cell response was measured 4 days following immunization with sheep red blood cells. The data were fit to a Hill model to estimate the ED50 for inhibition. Expression of xenobiotic metabolizing enzyme (XME) and thyroxine transport protein (Ttr) genes in liver was measured by PCR to assess aryl hydrocarbon-mediated responses. TCDD, TBDF, TCDF, 1PeBDF, 4PeBDF, 4PeCDF, and DBDCDD suppressed the IgM antibody response and Ttr gene expression, and upregulated phase I XME genes. 1PeCDF suppressed the IgM antibody response but only upregulated phase I XME genes; TriBDD had no effect on antibody response. The rank order of potency (ED50) for these chemicals was TCDD>TBDF>4PeBDF>TCDF/4PeCDF/1PeBDF>1PeCDF. Whereas TCDD was the most potent compound tested, the brominated analogs were more potent than their chlorinated analogs, suggesting that these compounds should be considered in toxic equivalency factor evaluation and risk assessment.
JF - Toxicological sciences : an official journal of the Society of Toxicology
AU - Frawley, Rachel
AU - DeVito, Michael
AU - Walker, Nigel J
AU - Birnbaum, Linda
AU - White, Kimber
AU - Smith, Matthew
AU - Maynor, Timothy
AU - Recio, Leslie
AU - Germolec, Dori
AD - Division of the National Toxicology Program, National Institute of Environmental Health Sciences.
Y1 - 2014/06//
PY - 2014
DA - June 2014
SP - 488
EP - 500
VL - 139
IS - 2
KW - Benzofurans
KW - 0
KW - Dioxins
KW - Hydrocarbons, Brominated
KW - Hydrocarbons, Chlorinated
KW - Immunoglobulin M
KW - Index Medicus
KW - 3
KW - 2
KW - brominated furans
KW - IgM antibody forming cell
KW - 7
KW - toxic equivalency factor
KW - 8-tetrachlorodibenzo-p-dioxin
KW - relative potency
KW - chlorinated furans
KW - TEF
KW - brominated dioxins
KW - Molecular Structure
KW - Animals
KW - Liver -- enzymology
KW - Dose-Response Relationship, Drug
KW - Immunoglobulin M -- immunology
KW - Liver -- metabolism
KW - Gene Expression Profiling
KW - Mice, Inbred Strains
KW - Liver -- drug effects
KW - Spleen -- immunology
KW - Spleen -- drug effects
KW - Transcriptome
KW - Erythrocytes -- immunology
KW - Female
KW - Immunity, Humoral -- drug effects
KW - Hydrocarbons, Chlorinated -- toxicity
KW - Dioxins -- chemistry
KW - Hydrocarbons, Chlorinated -- chemistry
KW - Dioxins -- toxicity
KW - Hydrocarbons, Brominated -- chemistry
KW - Hydrocarbons, Brominated -- toxicity
KW - Benzofurans -- toxicity
KW - Benzofurans -- chemistry
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicological+sciences+%3A+an+official+journal+of+the+Society+of+Toxicology&rft.atitle=Relative+potency+for+altered+humoral+immunity+induced+by+polybrominated+and+polychlorinated+dioxins%2Ffurans+in+female+B6C3F1%2FN+mice.&rft.au=Frawley%2C+Rachel%3BDeVito%2C+Michael%3BWalker%2C+Nigel+J%3BBirnbaum%2C+Linda%3BWhite%2C+Kimber%3BSmith%2C+Matthew%3BMaynor%2C+Timothy%3BRecio%2C+Leslie%3BGermolec%2C+Dori&rft.aulast=Frawley&rft.aufirst=Rachel&rft.date=2014-06-01&rft.volume=139&rft.issue=2&rft.spage=488&rft.isbn=&rft.btitle=&rft.title=Toxicological+sciences+%3A+an+official+journal+of+the+Society+of+Toxicology&rft.issn=1096-0929&rft_id=info:doi/10.1093%2Ftoxsci%2Fkfu041
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-12-29
N1 - Date created - 2014-05-12
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Toxicology. 2000 Dec 7;156(1):1-11 [11162871]
Toxicol Lett. 2013 Jul 18;220(3):294-302 [23680695]
Environ Int. 2001 Nov;27(5):413-39 [11757855]
Toxicol Sci. 2002 Aug;68(2):372-80 [12151633]
Environ Sci Technol. 2003 Mar 1;37(5):817-21 [12666907]
Environ Int. 2003 Sep;29(6):855-60 [12850101]
Environ Int. 2003 Sep;29(6):861-77 [12850102]
Food Cosmet Toxicol. 1980 Aug;18(4):387-92 [7461518]
Toxicol Lett. 1983 Feb;15(2-3):259-64 [6829049]
Annu Rev Pharmacol Toxicol. 1986;26:371-99 [3013079]
Toxicology. 1987 Jun;44(3):245-55 [3033849]
Toxicol Appl Pharmacol. 1988 Jun 15;94(1):141-9 [2836965]
Fundam Appl Toxicol. 1992 Feb;18(2):200-10 [1534777]
Fundam Appl Toxicol. 1993 Nov;21(4):412-9 [8253294]
Fundam Appl Toxicol. 1995 Jan;24(1):145-8 [7713338]
Environ Health Perspect. 1998 Dec;106(12):775-92 [9831538]
Science. 1963 Apr 26;140(3565):405 [13957684]
Toxicol Sci. 2006 Oct;93(2):223-41 [16829543]
Toxicol Sci. 2008 Sep;105(1):33-43 [18566023]
Toxicol Sci. 2009 Jan;107(1):27-39 [18978342]
Environ Int. 2009 Apr;35(3):588-93 [19121869]
J Nutr Biochem. 2009 Jun;20(6):469-76 [18789671]
Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2009 Jun;26(6):918-27 [19680967]
Environ Sci Technol. 2009 Oct 1;43(19):7350-6 [19848145]
Chemosphere. 2010 Jan;78(2):113-20 [19897226]
Methods Mol Biol. 2010;598:173-84 [19967513]
Biol Chem. 2009 Dec;390(12):1225-35 [19747074]
Biol Chem. 2010 Oct;391(10):1205-19 [20707612]
Environ Health Perspect. 2011 Mar;119(3):371-6 [21041162]
J Steroid Biochem Mol Biol. 2011 Oct;127(1-2):96-101 [21168493]
J Chromatogr A. 2011 Dec 23;1218(51):9279-87 [22098927]
Drug Metab Dispos. 2012 Mar;40(3):588-95 [22187485]
Chemosphere. 2012 May;87(9):1063-9 [22405723]
J Biopharm Stat. 2013 May;23(3):648-61 [23611201]
Toxicol Sci. 2013 Jun;133(2):197-208 [23492812]
Curr Drug Metab. 2001 Jun;2(2):149-64 [11469723]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/toxsci/kfu041
ER -
TY - JOUR
T1 - The effects of add-on low-dose memantine on cytokine levels in bipolar II depression: a 12-week double-blind, randomized controlled trial.
AN - 1521329320; 24717258
AB - Memantine, a noncompetitive N-methyl-d-aspartate receptor antagonist with a mood-stabilizing effect, and an association between bipolar disorder and proinflammatory cytokine levels have been reported. Whether adding-on memantine would reduce cytokine levels and is more effective than valproic acid (VPA) alone in bipolar II disorder was investigated. A randomized, double-blind, controlled, 12-week study was conducted. Patients undergoing regular VPA treatments were randomly assigned to a group: VPA + memantine (5 mg/d) (n = 106) or VPA + placebo (n = 108). The Hamilton Depression Rating Scale (HDRS) and Young Mania Rating Scale (YMRS) were used to evaluate clinical response. Symptom severity, plasma tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), IL-8, and IL-1 levels were examined during weeks 0, 1, 2, 4, 8, and 12. To adjust within-subject dependence over repeated assessments, multiple linear regressions with generalized estimating equation methods were used to examine the therapeutic effect. Tumor necrosis factor α levels were significantly lower in the VPA + memantine group than in the VPA + placebo group (P = 0.013). Posttreatment HDRS and YMRS scores decreased significantly in both groups, but not significant, nor was the other between-group cytokine level difference pretreatment and posttreatment. The HDRS score changes were significantly associated with IL-6 (P = 0.012) and IL-1 (P = 0.005) level changes and changes in YMRS score changes with TNF-α (P = 0.005) level changes. Treating bipolar II depression with VPA + memantine may improve the plasma TNF-α level. However, adding-on memantine may not improve clinical symptoms or cytokine levels other than TNF-α. Clinical symptoms may be correlated with certain cytokines.
JF - Journal of clinical psychopharmacology
AU - Lee, Sheng-Yu
AU - Chen, Shiou-Lan
AU - Chang, Yun-Hsuan
AU - Chen, Po See
AU - Huang, San-Yuan
AU - Tzeng, Nian-Sheng
AU - Wang, Yu-Shan
AU - Wang, Liang-Jen
AU - Lee, I Hui
AU - Wang, Tzu-Yun
AU - Yeh, Tzung Lieh
AU - Yang, Yen Kuang
AU - Hong, Jau-Shyong
AU - Lu, Ru-Band
AD - From the *Department of Psychiatry, †Institute of Behavioral Medicine, and ‡Institute of Allied Health Sciences, College of Medicine and Hospital, National Cheng Kung University, Tainan; §Department of Psychiatry, Tri-Service General Hospital, National Defense Medical Center, Taipei; ∥Department of Child and Adolescent Psychiatry, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung; ¶Department of Psychiatry, Tainan Hospital, Department of Health, Executive Yuan, Tainan; #Addiction Research Center, National Cheng Kung University, Tainan, Taiwan; and **Laboratory of Toxicology and Pharmacology, NIH/NIEHS, Research Triangle Park, NC.
Y1 - 2014/06//
PY - 2014
DA - June 2014
SP - 337
EP - 343
VL - 34
IS - 3
KW - Antimanic Agents
KW - 0
KW - Cytokines
KW - Excitatory Amino Acid Antagonists
KW - Receptors, N-Methyl-D-Aspartate
KW - Valproic Acid
KW - 614OI1Z5WI
KW - Memantine
KW - W8O17SJF3T
KW - Index Medicus
KW - Severity of Illness Index
KW - Young Adult
KW - Double-Blind Method
KW - Humans
KW - Linear Models
KW - Excitatory Amino Acid Antagonists -- administration & dosage
KW - Drug Therapy, Combination
KW - Psychiatric Status Rating Scales
KW - Adult
KW - Antimanic Agents -- administration & dosage
KW - Excitatory Amino Acid Antagonists -- therapeutic use
KW - Treatment Outcome
KW - Receptors, N-Methyl-D-Aspartate -- antagonists & inhibitors
KW - Antimanic Agents -- therapeutic use
KW - Female
KW - Male
KW - Cytokines -- drug effects
KW - Memantine -- therapeutic use
KW - Memantine -- administration & dosage
KW - Bipolar Disorder -- drug therapy
KW - Cytokines -- metabolism
KW - Valproic Acid -- therapeutic use
KW - Valproic Acid -- administration & dosage
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+psychopharmacology&rft.atitle=The+effects+of+add-on+low-dose+memantine+on+cytokine+levels+in+bipolar+II+depression%3A+a+12-week+double-blind%2C+randomized+controlled+trial.&rft.au=Lee%2C+Sheng-Yu%3BChen%2C+Shiou-Lan%3BChang%2C+Yun-Hsuan%3BChen%2C+Po+See%3BHuang%2C+San-Yuan%3BTzeng%2C+Nian-Sheng%3BWang%2C+Yu-Shan%3BWang%2C+Liang-Jen%3BLee%2C+I+Hui%3BWang%2C+Tzu-Yun%3BYeh%2C+Tzung+Lieh%3BYang%2C+Yen+Kuang%3BHong%2C+Jau-Shyong%3BLu%2C+Ru-Band&rft.aulast=Lee&rft.aufirst=Sheng-Yu&rft.date=2014-06-01&rft.volume=34&rft.issue=3&rft.spage=337&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+psychopharmacology&rft.issn=1533-712X&rft_id=info:doi/10.1097%2FJCP.0000000000000109
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-02-09
N1 - Date created - 2014-05-05
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1097/JCP.0000000000000109
ER -
TY - JOUR
T1 - S6 kinase 2 is bound to chromatin-nuclear matrix cellular fractions and is able to phosphorylate histone H3 at threonine 45 in vitro and in vivo.
AN - 1517398440; 23564320
AB - The activity of S6 kinases (S6K) is highly induced in cancer cells highlighting an essential role in carcinogenesis. The S6K family has two members: S6K1 and S6K2 which bear common as well as distinct features. In an attempt to identify S6K2 unique sequence features compared to S6K1, we applied extensive bioinformatic analysis and motif search approaches. Interestingly, we identified 14 unique protein signatures which are present in proteins directly connected to chromatin and/or involved in transcription regulation. Using chromatin binding assay, we biochemically showed that S6K2 is bound to chromatin as well as nuclear matrix cellular fractions in HEK293 cells. The presence of S6K2 in chromatin fractions raised the possibility that it may be in close proximity to a number of chromatin substrates. For that, we then searched for S6K phosphorylation consensus sites RXRXXT/S in mammalian proteins using the SWISS-PROT database. Interestingly, we identified some potential phosphorylation sites in histone H3 (Thr45). Using in vitro kinase assays and siRNA-based knockdown strategy; we confirmed that S6K2 but not S6K1 or AKT is essential for histone H3-Thr45 phosphorylation in HEK293 cells. Furthermore, we show that the nuclear localisation sequence in the S6K2 C-terminus is essential for this modification. We have found that, H3-Thr45 phosphorylation correlates to S6K activation in response to mitogens and TPA-induced cell differentiation of leukaemic cell lines U937, HL60 and THP1. Overall, we demonstrate that S6K2 is a novel kinase that can phosphorylate histone H3 at position Thr45, which may play a role during cell proliferation and/or differentiation.
© 2014 Wiley Periodicals, Inc.
JF - Journal of cellular biochemistry
AU - Ismail, Heba M S
AU - Hurd, Paul J
AU - Khalil, Mahmoud I M
AU - Kouzarides, Tony
AU - Bannister, Andrew
AU - Gout, Ivan
AD - Institute of Structural and Molecular Biology, University College London, London, WC1E 6BT, United Kingdom; Cancer Biology Department, National Cancer Institute, Cairo University, Cairo, Egypt.
Y1 - 2014/06//
PY - 2014
DA - June 2014
SP - 1048
EP - 1062
VL - 115
IS - 6
KW - Chromatin
KW - 0
KW - Histones
KW - Threonine
KW - 2ZD004190S
KW - Proto-Oncogene Proteins c-akt
KW - EC 2.7.11.1
KW - Ribosomal Protein S6 Kinases, 70-kDa
KW - Ribosomal Protein S6 Kinases, 90-kDa
KW - ribosomal protein S6 kinase, 70kD, polypeptide 1
KW - ribosomal protein S6 kinase, 90kDa, polypeptide 3
KW - Tetradecanoylphorbol Acetate
KW - NI40JAQ945
KW - Index Medicus
KW - S6K2
KW - CHROMATIN
KW - H3 PHOSPHORYLATION
KW - Proto-Oncogene Proteins c-akt -- genetics
KW - Proto-Oncogene Proteins c-akt -- metabolism
KW - Animals
KW - HL-60 Cells
KW - HEK293 Cells
KW - Humans
KW - Amino Acid Sequence
KW - Cell Line, Tumor
KW - Mice
KW - Ribosomal Protein S6 Kinases, 70-kDa -- metabolism
KW - Protein Binding
KW - Ribosomal Protein S6 Kinases, 70-kDa -- genetics
KW - NIH 3T3 Cells
KW - Cell Fractionation
KW - Blotting, Western
KW - Phosphorylation
KW - Molecular Sequence Data
KW - Tetradecanoylphorbol Acetate -- pharmacology
KW - Middle Aged
KW - RNA Interference
KW - Cell Differentiation -- drug effects
KW - U937 Cells
KW - Ribosomal Protein S6 Kinases, 90-kDa -- metabolism
KW - Chromatin -- metabolism
KW - Threonine -- metabolism
KW - Nuclear Matrix -- metabolism
KW - Histones -- metabolism
KW - Ribosomal Protein S6 Kinases, 90-kDa -- genetics
KW - Chromatin -- genetics
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-12-15
N1 - Date created - 2014-04-16
N1 - Date revised - 2017-01-13
N1 - Last updated - 2017-01-18
DO - http://dx.doi.org/10.1002/jcb.24566
ER -
TY - JOUR
T1 - Characterization of an anti-Bla g 1 scFv: epitope mapping and cross-reactivity.
AN - 1514436205; 24667070
AB - Bla g 1 is a major allergen from Blatella germanica and one of the primary allergens used to assess cockroach allergen exposure. The epitope of an anti-Bla g 1 scFv was mapped in order to better understand cross reactivity with other group 1 cockroach allergens and patient IgE epitopes. X-ray crystallography was used to determine the structure of the scFv. The scFv epitope on Bla g 1 was located by alanine scanning site-directed mutagenesis and ELISA. Twenty-six rBla g 1-GST alanine mutants were evaluated for variations in binding to the scFv compared to the wild type allergen. Six mutants showed a significant difference in scFv binding affinity. These mutations clustered to form a discontinuous epitope mainly comprising two helices of Bla g 1. The allergen-scFv complex was modeled based on the results, and the epitope region was found to have low sequence similarity with Per a 1, especially among the residues identified as functionally important for the scFv binding to Bla g 1. Indeed, the scFv failed to bind Per a 1 in American cockroach extract. The scFv was unable to inhibit the binding of IgE antibodies from a highly cockroach allergic patient to Bla g 1. Based on the surface area of Bla g 1 occluded by the scFv, putative regions of patient IgE-Bla g 1 interactions can be inferred. This scFv could be best utilized as a capture antibody in an IgE detection ELISA, or to differentiate Bla g 1 from Per a 1 in environmental exposure assays.
Published by Elsevier Ltd.
JF - Molecular immunology
AU - Mueller, Geoffrey A
AU - Ankney, John A
AU - Glesner, Jill
AU - Khurana, Taruna
AU - Edwards, Lori L
AU - Pedersen, Lars C
AU - Perera, Lalith
AU - Slater, Jay E
AU - Pomés, Anna
AU - London, Robert E
AD - National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. Electronic address: mueller3@niehs.nih.gov. ; National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. ; Indoor Biotechnologies, Inc., Charlottesville, VA 22903, USA. ; U.S. Food and Drug Administration, Bethesda, MD 20892, USA.
Y1 - 2014/06//
PY - 2014
DA - June 2014
SP - 200
EP - 207
VL - 59
IS - 2
KW - Allergens
KW - 0
KW - Epitopes
KW - Single-Chain Antibodies
KW - allergen Bla g 1
KW - allergen Per a I
KW - Immunoglobulin E
KW - 37341-29-0
KW - Index Medicus
KW - Allergen
KW - Epitope
KW - Structure
KW - Bla g 1
KW - Cockroach
KW - scFv
KW - Animals
KW - Immunoglobulin E -- immunology
KW - Models, Molecular
KW - Humans
KW - Epitopes -- ultrastructure
KW - Crystallography, X-Ray
KW - Epitopes -- immunology
KW - Binding Sites, Antibody -- immunology
KW - Mutation
KW - Epitope Mapping
KW - Cross Reactions -- immunology
KW - Allergens -- immunology
KW - Single-Chain Antibodies -- immunology
KW - Single-Chain Antibodies -- ultrastructure
KW - Cockroaches -- immunology
KW - Allergens -- genetics
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-06-05
N1 - Date created - 2014-04-07
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
J Biol Chem. 2001 Mar 23;276(12):9359-65 [11134039]
Clin Exp Allergy. 2002 May;32(5):721-7 [11994096]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.molimm.2014.02.003
ER -
TY - JOUR
T1 - Targeting STAT3 phosphorylation by neem leaf glycoprotein prevents immune evasion exerted by supraglottic laryngeal tumor induced M2 macrophages.
AN - 1514435985; 24607970
AB - Tumor-associated macrophages (TAMs) are preferentially M2 skewed and promote tumor growth, angiogenesis, invasion, and/or metastasis. In this study, we have analyzed the in vitro immunomodulatory potential of a non-toxic neem leaf glycoprotein (NLGP) in reprogramming Stage III supraglottic laryngeal tumor cell lysate (SLTCL) induced M2 TAMs to their classical anti-tumor shape (M1). Data generated from this study support that NLGP is effective in preventing the SLTCL induced generation (CD68(+)CD206(+)IL-10(high) to CD68(+)CD206(-)IL-10(low) TAMs) and functions (NO(low) to NO(high), MHC-I(low) to MHC-I(high), CD80(low) to CD80(high)) of pro-tumorous M2 macrophages, which in turn associated with sustained anti-tumor effector functions by promoting cytotoxic T cell activities and suppressing regulatory T cells. Furthermore, our data also suggest that NLGP prevents M2 skewness of TAMs by downregulating phosphorylation of targeted STAT3.
Copyright © 2014 Elsevier Ltd. All rights reserved.
JF - Molecular immunology
AU - Goswami, K K
AU - Barik, S
AU - Sarkar, M
AU - Bhowmick, A
AU - Biswas, J
AU - Bose, A
AU - Baral, R
AD - Department of Immunoregulation and Immunodiagnostics, Chittaranjan National Cancer Institute (CNCI), 37, S. P. Mukherjee Road, Kolkata, 700026, India. ; Department of ENT and Head-Neck Oncology, Chittaranjan National Cancer Institute (CNCI), 37, S. P. Mukherjee Road, Kolkata, 700026, India. ; Department of Surgical Oncology and Medical Oncology, Chittaranjan National Cancer Institute (CNCI), 37, S. P. Mukherjee Road, Kolkata 700026, India. ; Department of Molecular Medicine, Bose Institute, C.I.T. Scheme, Kolkata, India. ; Department of Immunoregulation and Immunodiagnostics, Chittaranjan National Cancer Institute (CNCI), 37, S. P. Mukherjee Road, Kolkata, 700026, India. Electronic address: rathindranath.baral@cnci.org.in.
Y1 - 2014/06//
PY - 2014
DA - June 2014
SP - 119
EP - 127
VL - 59
IS - 2
KW - Glycoproteins
KW - 0
KW - IL10 protein, human
KW - Immunologic Factors
KW - Plant Extracts
KW - RNA, Small Interfering
KW - STAT3 Transcription Factor
KW - STAT3 protein, human
KW - Interleukin-10
KW - 130068-27-8
KW - Interleukin-12
KW - 187348-17-0
KW - Nitric Oxide
KW - 31C4KY9ESH
KW - NOS2 protein, human
KW - EC 1.14.13.39
KW - Nitric Oxide Synthase Type II
KW - Index Medicus
KW - Tumor-associated macrophages
KW - Supraglottic laryngeal tumor cell lysate
KW - T cells
KW - Neem leaf glycoprotein
KW - Humans
KW - Cell Line, Tumor
KW - T-Lymphocytes, Cytotoxic -- immunology
KW - Nitric Oxide -- biosynthesis
KW - Nitric Oxide Synthase Type II -- biosynthesis
KW - Plant Extracts -- pharmacology
KW - Phosphorylation
KW - Interleukin-12 -- biosynthesis
KW - Interleukin-10 -- biosynthesis
KW - Down-Regulation -- drug effects
KW - RNA Interference
KW - T-Lymphocytes, Regulatory -- immunology
KW - Macrophages -- immunology
KW - Immune Evasion -- drug effects
KW - Glycoproteins -- pharmacology
KW - Laryngeal Neoplasms -- immunology
KW - Immunologic Factors -- pharmacology
KW - Azadirachta -- chemistry
KW - STAT3 Transcription Factor -- genetics
KW - STAT3 Transcription Factor -- metabolism
KW - Plant Leaves -- chemistry
KW - Macrophages -- drug effects
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1514435985?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+immunology&rft.atitle=Targeting+STAT3+phosphorylation+by+neem+leaf+glycoprotein+prevents+immune+evasion+exerted+by+supraglottic+laryngeal+tumor+induced+M2+macrophages.&rft.au=Goswami%2C+K+K%3BBarik%2C+S%3BSarkar%2C+M%3BBhowmick%2C+A%3BBiswas%2C+J%3BBose%2C+A%3BBaral%2C+R&rft.aulast=Goswami&rft.aufirst=K&rft.date=2014-06-01&rft.volume=59&rft.issue=2&rft.spage=119&rft.isbn=&rft.btitle=&rft.title=Molecular+immunology&rft.issn=1872-9142&rft_id=info:doi/10.1016%2Fj.molimm.2014.01.015
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-06-05
N1 - Date created - 2014-04-07
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.molimm.2014.01.015
ER -
TY - JOUR
T1 - Repair of DNA double-strand breaks by templated nucleotide sequence insertions derived from distant regions of the genome.
AN - 1534796520; 24821809
AB - We used the I-SceI endonuclease to produce DNA double-strand breaks (DSBs) and observed that a fraction of these DSBs were repaired by insertion of sequences, which we termed "templated sequence insertions" (TSIs), derived from distant regions of the genome. These TSIs were derived from genic, retrotransposon, or telomere sequences and were not deleted from the donor site in the genome, leading to the hypothesis that they were derived from reverse-transcribed RNA. Cotransfection of RNA and an I-SceI expression vector demonstrated insertion of RNA-derived sequences at the DNA-DSB site, and TSIs were suppressed by reverse-transcriptase inhibitors. Both observations support the hypothesis that TSIs were derived from RNA templates. In addition, similar insertions were detected at sites of DNA DSBs induced by transcription activator-like effector nuclease proteins. Whole-genome sequencing of myeloma cell lines revealed additional TSIs, demonstrating that repair of DNA DSBs via insertion was not restricted to experimentally produced DNA DSBs. Analysis of publicly available databases revealed that many of these TSIs are polymorphic in the human genome. Taken together, these results indicate that insertional events should be considered as alternatives to gross chromosomal rearrangements in the interpretation of whole-genome sequence data and that this mutagenic form of DNA repair may play a role in genetic disease, exon shuffling, and mammalian evolution.
JF - Proceedings of the National Academy of Sciences of the United States of America
AU - Onozawa, Masahiro
AU - Zhang, Zhenhua
AU - Kim, Yoo Jung
AU - Goldberg, Liat
AU - Varga, Tamas
AU - Bergsagel, P Leif
AU - Kuehl, W Michael
AU - Aplan, Peter D
AD - Genetics Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892; and. ; Comprehensive Cancer Center, Mayo Clinic, Scottsdale, AZ 85259. ; Genetics Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892; and aplanp@mail.nih.gov.
Y1 - 2014/05/27/
PY - 2014
DA - 2014 May 27
SP - 7729
EP - 7734
VL - 111
IS - 21
KW - Cinnamates
KW - 0
KW - DNA Primers
KW - Retroelements
KW - Hygromycin B
KW - 3XQ2233B0B
KW - hygromycin A
KW - 3YJY415DDI
KW - Index Medicus
KW - TSIP
KW - LINE-1
KW - polymorphism
KW - DNA patch
KW - Polymerase Chain Reaction
KW - DNA Copy Number Variations
KW - DNA Primers -- genetics
KW - Humans
KW - Cell Line, Tumor
KW - Genetic Vectors -- genetics
KW - Computational Biology
KW - Hygromycin B -- analogs & derivatives
KW - DNA Repair -- genetics
KW - Retroelements -- genetics
KW - Telomere -- genetics
KW - DNA Breaks, Double-Stranded
KW - Mutagenesis, Insertional -- genetics
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534796520?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Repair+of+DNA+double-strand+breaks+by+templated+nucleotide+sequence+insertions+derived+from+distant+regions+of+the+genome.&rft.au=Onozawa%2C+Masahiro%3BZhang%2C+Zhenhua%3BKim%2C+Yoo+Jung%3BGoldberg%2C+Liat%3BVarga%2C+Tamas%3BBergsagel%2C+P+Leif%3BKuehl%2C+W+Michael%3BAplan%2C+Peter+D&rft.aulast=Onozawa&rft.aufirst=Masahiro&rft.date=2014-05-27&rft.volume=111&rft.issue=21&rft.spage=7729&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=1091-6490&rft_id=info:doi/10.1073%2Fpnas.1321889111
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-09-02
N1 - Date created - 2014-06-10
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Annu Rev Biochem. 2006;75:493-517 [16756500]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1073/pnas.1321889111
ER -
TY - JOUR
T1 - 3,4-Methylenedioxypyrovalerone (MDPV) and metabolites quantification in human and rat plasma by liquid chromatography-high resolution mass spectrometry.
AN - 1525764939; 24832995
AB - Synthetic cathinones are recreational drugs that mimic the effects of illicit stimulants like cocaine, amphetamine or Ecstasy. Among the available synthetic cathinones in the United States, 3,4-methylenedioxypyrovalerone (MDPV) is commonly abused and associated with dangerous side effects. MDPV is a dopamine transporter blocker 10-fold more potent than cocaine as a locomotor stimulant in rats. Previous in vitro and in vivo studies examining MDPV metabolism reported 3,4-dihydroxypyrovalerone (3,4-catechol-PV) and 4-hydroxy-3-methoxypyrovalerone (4-OH-3-MeO-PV) as the two primary metabolites. We developed and validated a liquid chromatography-high resolution mass spectrometry method to quantify MDPV and its primary metabolites in 100 μL human and rat plasma. Plasma hydrolysis was followed by protein precipitation before analysis. Limits of detection were 0.1 μg L(-1), with linear ranges from 0.25 to 1000 μg L(-1). Process efficiency, matrix effect, total imprecision (%CV) and accuracy (%target) were 36-93%, from -8 to 12%, 2.1 to 7.3% and 86 to 109%, respectively. MDPV and metabolites were stable at room temperature for 24 h, 4 °C for 72 h and after 3 freeze-thaw cycles with less than 10% variability. Human-rat plasma cross validation demonstrated that rat plasma could be accurately quantified against a human plasma calibration curve. As proof of this method, rat plasma specimens were analyzed after intraperitoneal and subcutaneous dosing with MDPV (0.5 mg kg(-1)). MDPV, 3,4-catechol-PV and 4-OH-3-MeO-PV concentrations ranged from not detected to 107.5 μg L(-1) prior to and up to 8h after dosing. This method provides a simultaneous quantification of MDPV and two metabolites in plasma with good selectivity and sensitivity.
Published by Elsevier B.V.
JF - Analytica chimica acta
AU - Anizan, Sebastien
AU - Ellefsen, Kayla
AU - Concheiro, Marta
AU - Suzuki, Masaki
AU - Rice, Kenner C
AU - Baumann, Michael H
AU - Huestis, Marilyn A
AD - Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD, USA. ; Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD, USA; Program in Toxicology, University of Maryland Baltimore, Baltimore, MD, USA. ; Drug Design and Synthesis Section, Intramural Research Program, National Institute on Drug Abuse and National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Baltimore, MD, USA; On leave from the Medicinal Chemistry Group, Qs' Research Institute, Otsuka Pharmaceutical Co., Ltd., Tokushima, Japan. ; Drug Design and Synthesis Section, Intramural Research Program, National Institute on Drug Abuse and National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Baltimore, MD, USA. ; Designer Drug Research Unit, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD, USA. ; Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD, USA. Electronic address: mhuestis@intra.nida.nih.gov.
Y1 - 2014/05/27/
PY - 2014
DA - 2014 May 27
SP - 54
EP - 63
VL - 827
KW - 3,4-methylenedioxypyrovalerone
KW - 0
KW - Benzodioxoles
KW - Pyrrolidines
KW - Index Medicus
KW - Synthetic cathinones
KW - MDPV
KW - Metabolites
KW - HRMS
KW - LC–MS/MS
KW - Rats
KW - Animals
KW - Reproducibility of Results
KW - Humans
KW - Linear Models
KW - Chromatography, Liquid
KW - Limit of Detection
KW - Hydrolysis
KW - Male
KW - Mass Spectrometry
KW - Benzodioxoles -- blood
KW - Pyrrolidines -- chemistry
KW - Blood Chemical Analysis -- methods
KW - Pyrrolidines -- metabolism
KW - Pyrrolidines -- blood
KW - Benzodioxoles -- metabolism
KW - Benzodioxoles -- chemistry
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1525764939?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Analytica+chimica+acta&rft.atitle=3%2C4-Methylenedioxypyrovalerone+%28MDPV%29+and+metabolites+quantification+in+human+and+rat+plasma+by+liquid+chromatography-high+resolution+mass+spectrometry.&rft.au=Anizan%2C+Sebastien%3BEllefsen%2C+Kayla%3BConcheiro%2C+Marta%3BSuzuki%2C+Masaki%3BRice%2C+Kenner+C%3BBaumann%2C+Michael+H%3BHuestis%2C+Marilyn+A&rft.aulast=Anizan&rft.aufirst=Sebastien&rft.date=2014-05-27&rft.volume=827&rft.issue=&rft.spage=54&rft.isbn=&rft.btitle=&rft.title=Analytica+chimica+acta&rft.issn=1873-4324&rft_id=info:doi/10.1016%2Fj.aca.2014.04.015
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-08-19
N1 - Date created - 2014-05-16
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Chem Res Toxicol. 2001 Sep;14(9):1203-8 [11559034]
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Clin Chem. 1984 Feb;30(2):290-2 [6692538]
Ann Emerg Med. 1993 Dec;22(12):1897-903 [8239113]
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Anal Bioanal Chem. 2009 Mar;393(6-7):1607-17 [19183967]
Rapid Commun Mass Spectrom. 2010 Sep;24(18):2706-14 [20814976]
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Forensic Sci Int. 2011 Jul 15;210(1-3):195-200 [21477955]
Drug Test Anal. 2011 Jul-Aug;3(7-8):439-53 [21755607]
Clin Toxicol (Phila). 2011 Jul;49(6):499-505 [21824061]
J Anal Toxicol. 2011 Sep;35(7):470-80 [21871156]
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Anal Bioanal Chem. 2013 Nov;405(29):9437-48 [24196122]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.aca.2014.04.015
ER -
TY - JOUR
T1 - Divalent metal ions enhance DOPAL-induced oligomerization of alpha-synuclein.
AN - 1521344182; 24670480
AB - Parkinson disease (PD) features profound striatal dopamine depletion and Lewy bodies containing abundant precipitated alpha-synuclein. Mechanisms linking alpha-synucleinopathy with the death of dopamine neurons remain incompletely understood. One such link may be 3,4-dihydroxyphenylacetaldehyde (DOPAL). All of the intra-neuronal metabolism of dopamine passes through DOPAL, which is toxic. DOPAL also potently oligomerizes alpha-synuclein and alpha-synuclein oligomers are thought to be pathogenic in PD. Another implicated factor in PD pathogenesis is metal ions, and alpha-synuclein contains binding sites for these ions. In this study we tested whether divalent metal ions augment DOPAL-induced oligomerization of alpha-synuclein in cell-free system and in PC12 cells conditionally over-expressing alpha-synuclein. Incubation with divalent metal ions augmented DOPAL-induced oligomerization of alpha-synuclein (Cu(2+)>Fe(2+)>Mn(2+)), whereas monovalent Cu(1+) and trivalent Fe(3+) were without effect. Other dopamine metabolites, dopamine itself, and metal ions alone or in combination with dopamine, also had no effect. Antioxidant treatment with ascorbic acid and divalent cation chelation with EDTA attenuated the augmentation by Cu(2+) of DOPAL-induced alpha-synuclein oligomerization. Incubation of PC12 cells with L-DOPA markedly increased intracellular DOPAL content and promoted alpha-synuclein dimerization. Co-incubation with Cu(2+) amplified (p=0.01), while monoamine oxidase inhibition prevented, L-DOPA-related dimerization of alpha-synuclein (p=0.01). We conclude that divalent metal ions augment DOPAL-induced oligomerization of alpha-synuclein. Drugs that interfere with this interaction might constitute a novel approach for future treatment or prevention approaches.
Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.
JF - Neuroscience letters
AU - Jinsmaa, Yunden
AU - Sullivan, Patricia
AU - Gross, Daniel
AU - Cooney, Adele
AU - Sharabi, Yehonatan
AU - Goldstein, David S
AD - Clinical Neurocardiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 10 Center Drive MSC-1620, Bethesda, MD 20892-1620, USA. ; Clinical Neurocardiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 10 Center Drive MSC-1620, Bethesda, MD 20892-1620, USA. Electronic address: goldsteind@ninds.nih.gov.
Y1 - 2014/05/21/
PY - 2014
DA - 2014 May 21
SP - 27
EP - 32
VL - 569
KW - Antioxidants
KW - 0
KW - Cations, Divalent
KW - Chelating Agents
KW - Protein Aggregates
KW - alpha-Synuclein
KW - 3,4-Dihydroxyphenylacetic Acid
KW - 102-32-9
KW - 3,4-dihydroxyphenylethanol
KW - 10597-60-1
KW - Manganese
KW - 42Z2K6ZL8P
KW - 3,4-dihydroxyphenylacetaldehyde
KW - 5707-55-1
KW - Copper
KW - 789U1901C5
KW - Edetic Acid
KW - 9G34HU7RV0
KW - Iron
KW - E1UOL152H7
KW - Phenylethyl Alcohol
KW - ML9LGA7468
KW - Ascorbic Acid
KW - PQ6CK8PD0R
KW - Dopamine
KW - VTD58H1Z2X
KW - Index Medicus
KW - Alpha-synuclein
KW - Parkinson disease
KW - Oligomerization
KW - DOPAL
KW - Rats
KW - Animals
KW - Chelating Agents -- chemistry
KW - Dopamine -- chemistry
KW - Phenylethyl Alcohol -- analogs & derivatives
KW - Humans
KW - Phenylethyl Alcohol -- chemistry
KW - Ascorbic Acid -- chemistry
KW - Antioxidants -- chemistry
KW - Protein Multimerization
KW - Edetic Acid -- chemistry
KW - PC12 Cells
KW - 3,4-Dihydroxyphenylacetic Acid -- chemistry
KW - alpha-Synuclein -- metabolism
KW - alpha-Synuclein -- chemistry
KW - Manganese -- chemistry
KW - 3,4-Dihydroxyphenylacetic Acid -- pharmacology
KW - Iron -- chemistry
KW - Copper -- pharmacology
KW - Copper -- chemistry
KW - 3,4-Dihydroxyphenylacetic Acid -- analogs & derivatives
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1521344182?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuroscience+letters&rft.atitle=Divalent+metal+ions+enhance+DOPAL-induced+oligomerization+of+alpha-synuclein.&rft.au=Jinsmaa%2C+Yunden%3BSullivan%2C+Patricia%3BGross%2C+Daniel%3BCooney%2C+Adele%3BSharabi%2C+Yehonatan%3BGoldstein%2C+David+S&rft.aulast=Jinsmaa&rft.aufirst=Yunden&rft.date=2014-05-21&rft.volume=569&rft.issue=&rft.spage=27&rft.isbn=&rft.btitle=&rft.title=Neuroscience+letters&rft.issn=1872-7972&rft_id=info:doi/10.1016%2Fj.neulet.2014.03.016
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-12-09
N1 - Date created - 2014-05-05
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Arch Biochem Biophys. 2000 Jun 15;378(2):269-77 [10860544]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.neulet.2014.03.016
ER -
TY - JOUR
T1 - Oral anticancer drugs: how limited dosing options and dose reductions may affect outcomes in comparative trials and efficacy in patients.
AN - 1526127380; 24711558
AB - Historically, cancer medicine has avoided the problem of unequal dosing by comparing maximum-tolerated doses of intravenous regimens with proportionate dose reductions for toxicity. However, in recent years, with the development of numerous oral anticancer agents, dosing options are arbitrarily and increasingly limited by the size of pills. We contend that an underappreciated consequence of pill size is unequal dosing in comparative clinical trials and that this can have an impact on outcomes. We discuss how comparative effectiveness trials can be unbalanced and how the use of doses that are not sustainable might affect outcomes, especially marginal ones. We further argue that because of their poor tolerability and their limited dosing options, which often result in large dose adjustments in response to toxicity, the real-world clinical effectiveness of oral anticancer agents may be diminished and may not emulate results achieved in registration trials.
© 2014 by American Society of Clinical Oncology.
JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology
AU - Prasad, Vinay
AU - Massey, Paul R
AU - Fojo, Tito
AD - Vinay Prasad and Tito Fojo, National Cancer Institute, National Institutes of Health, Bethesda, MD; and Paul R. Massey, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA. vinayak.prasad@nih.gov. ; Vinay Prasad and Tito Fojo, National Cancer Institute, National Institutes of Health, Bethesda, MD; and Paul R. Massey, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA.
Y1 - 2014/05/20/
PY - 2014
DA - 2014 May 20
SP - 1620
EP - 1629
VL - 32
IS - 15
KW - Antineoplastic Agents
KW - 0
KW - Index Medicus
KW - Administration, Oral
KW - Dose-Response Relationship, Drug
KW - Humans
KW - Treatment Outcome
KW - Neoplasms -- drug therapy
KW - Antineoplastic Agents -- administration & dosage
KW - Drug Dosage Calculations
KW - Comparative Effectiveness Research
KW - Research Design
KW - Clinical Trials as Topic -- methods
KW - Antineoplastic Agents -- adverse effects
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-07-03
N1 - Date created - 2014-05-19
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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Comment In:
J Clin Oncol. 2014 May 20;32(15):1537-9 [24711547]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1200/JCO.2013.53.0204
ER -
TY - CPAPER
T1 - HIV-Related Malignancies: Diseases at the Crossroads of Virology, Immunology, and Cancer Biology
T2 - 114th General Meeting of the American Society for Microbiology (ASM 2014)
AN - 1518614223; 6284225
JF - 114th General Meeting of the American Society for Microbiology (ASM 2014)
AU - Yarchoan, Robert
Y1 - 2014/05/17/
PY - 2014
DA - 2014 May 17
KW - Virology
KW - Malignancy
KW - Immunology
KW - Cancer
KW - Human immunodeficiency virus
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518614223?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=114th+General+Meeting+of+the+American+Society+for+Microbiology+%28ASM+2014%29&rft.atitle=HIV-Related+Malignancies%3A+Diseases+at+the+Crossroads+of+Virology%2C+Immunology%2C+and+Cancer+Biology&rft.au=Yarchoan%2C+Robert&rft.aulast=Yarchoan&rft.aufirst=Robert&rft.date=2014-05-17&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=114th+General+Meeting+of+the+American+Society+for+Microbiology+%28ASM+2014%29&rft.issn=&rft_id=info:doi/
L2 - http://www.abstractsonline.com/plan/Browse.aspx
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-23
N1 - Last updated - 2014-04-24
ER -
TY - CPAPER
T1 - Spatial Organization Of Transcription Machinery In Fast-growing Bacterial Cells
T2 - 114th General Meeting of the American Society for Microbiology (ASM 2014)
AN - 1518610714; 6284604
JF - 114th General Meeting of the American Society for Microbiology (ASM 2014)
AU - Cagliero, C
AU - Zhou, Y
AU - Schneider, T
AU - Jin, D
Y1 - 2014/05/17/
PY - 2014
DA - 2014 May 17
KW - Transcription
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518610714?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=114th+General+Meeting+of+the+American+Society+for+Microbiology+%28ASM+2014%29&rft.atitle=Spatial+Organization+Of+Transcription+Machinery+In+Fast-growing+Bacterial+Cells&rft.au=Cagliero%2C+C%3BZhou%2C+Y%3BSchneider%2C+T%3BJin%2C+D&rft.aulast=Cagliero&rft.aufirst=C&rft.date=2014-05-17&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=114th+General+Meeting+of+the+American+Society+for+Microbiology+%28ASM+2014%29&rft.issn=&rft_id=info:doi/
L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={673511F0-C86B-432F-A387-058032B8500B}
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-23
N1 - Last updated - 2014-04-24
ER -
TY - CPAPER
T1 - The Search for Permissive Cells in the Gut
T2 - 114th General Meeting of the American Society for Microbiology (ASM 2014)
AN - 1518610094; 6284508
JF - 114th General Meeting of the American Society for Microbiology (ASM 2014)
AU - Green, Kim
Y1 - 2014/05/17/
PY - 2014
DA - 2014 May 17
KW - Digestive tract
KW - Permissive cells
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518610094?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=114th+General+Meeting+of+the+American+Society+for+Microbiology+%28ASM+2014%29&rft.atitle=The+Search+for+Permissive+Cells+in+the+Gut&rft.au=Green%2C+Kim&rft.aulast=Green&rft.aufirst=Kim&rft.date=2014-05-17&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=114th+General+Meeting+of+the+American+Society+for+Microbiology+%28ASM+2014%29&rft.issn=&rft_id=info:doi/
L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={673511F0-C86B-432F-A387-058032B8500B}
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-23
N1 - Last updated - 2014-04-24
ER -
TY - CPAPER
T1 - Small Changes Can Lead to Big Effects: Visualizing How BacteriophageT4 Appropriates Host RNA Polymerase
T2 - 114th General Meeting of the American Society for Microbiology (ASM 2014)
AN - 1518609777; 6284556
JF - 114th General Meeting of the American Society for Microbiology (ASM 2014)
AU - Hinton, Deborah
Y1 - 2014/05/17/
PY - 2014
DA - 2014 May 17
KW - DNA-directed RNA polymerase
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=114th+General+Meeting+of+the+American+Society+for+Microbiology+%28ASM+2014%29&rft.atitle=Small+Changes+Can+Lead+to+Big+Effects%3A+Visualizing+How+BacteriophageT4+Appropriates+Host+RNA+Polymerase&rft.au=Hinton%2C+Deborah&rft.aulast=Hinton&rft.aufirst=Deborah&rft.date=2014-05-17&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=114th+General+Meeting+of+the+American+Society+for+Microbiology+%28ASM+2014%29&rft.issn=&rft_id=info:doi/
L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={673511F0-C86B-432F-A387-058032B8500B}
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-23
N1 - Last updated - 2014-04-24
ER -
TY - JOUR
T1 - Incorrect identification of recent HIV infection in adults in the United States using a limiting-antigen avidity assay
AN - 1765983245; PQ0002610787
AB - Objectives: To evaluate factors associated with misclassification by the limiting-antigen avidity (LAg-avidity) assay among individuals with long-standing HIV infection. Design: Samples were obtained from the Multicenter AIDS Cohort Study and AIDS Linked to the IntraVenous Experience cohort (1089 samples from 667 individuals, 595 samples collected 2-4 years and 494 samples collected 4-8 years after HIV seroconversion). Paired samples from both time points were available for 422 (63.3%) of the 667 individuals. Methods: Samples were considered to be misclassified if the LAg-avidity assay result was 1.5 or less normalized optical density (OD-n) units. Results: Overall, 4.8% (52/1089) of the samples were misclassified, including 1.8% [1 6/884, 95% confidence interval (Cl) 1.09-3.06%] of samples from individuals with viral loads above 400copies/ml and 1.4% (10/705) of samples from individuals with viral loads above 400copies/ml and CD4 super(+) cell counts above 200cells/ mu l (95% Cl 0.68-2.60%). Age, race, sex, and mode of HIV acquisition were not associated with misclassification. In an adjusted analysis, viral load below 400 copies/ml [adjusted odds ratio (aOR) 3.72, 95% Cl 1.61 -8.57], CD4 super(+) cell count below 50cells/ mu l (aOR 5.41, 95% Cl 1.86-15.74), and low LAg-avidity result ([< or =]1.5 OD-n) from the earlier time point (aOR 5.60, 95% Cl 1.55-20.25) were significantly associated with misclassification. Conclusions: The manufacturer of the LAg-avidity assay recommends excluding individuals from incidence surveys who are receiving antiretroviral therapy, are elite suppressors, or have AIDS (CD4 super(+) cell count <200cells/ mu l). The results of this study indicate that those exclusions do not remove all sources of assay misclassification among individuals with long-standing HIV infection.
JF - AIDS
AU - Longosz, Andrew F
AU - Mehta, Shruti H
AU - Kirk, Gregory D
AU - Margolick, Joseph B
AU - Brown, Joelle
AU - Quinn, Thomas C
AU - Eshleman, Susan H
AU - Laeyendecker, Oliver
AD - Laboratory of Immunoregulation, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, NIH, olaeyen1@jhmi.edu
Y1 - 2014/05/15/
PY - 2014
DA - 2014 May 15
SP - 1227
EP - 1232
PB - Lippincott Williams & Wilkins, Inc, 530 Walnut Street Philadelphia PA 19106-3621 United States
VL - 28
IS - 8
SN - 0269-9370, 0269-9370
KW - Health & Safety Science Abstracts; Immunology Abstracts; Virology & AIDS Abstracts
KW - HIV
KW - incidence
KW - limiting-antigen avidity
KW - misclassification
KW - MSM
KW - people who inject drugs
KW - Acquired immune deficiency syndrome
KW - Intravenous administration
KW - Age
KW - antiretroviral therapy
KW - Assays
KW - Infection
KW - Antiretroviral agents
KW - USA
KW - CD4 antigen
KW - Human immunodeficiency virus
KW - Avidity
KW - Optical density
KW - Seroconversion
KW - Races
KW - Sex
KW - V 22360:AIDS and HIV
KW - H 11000:Diseases/Injuries/Trauma
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2016-02-01
N1 - Last updated - 2016-03-17
N1 - SubjectsTermNotLitGenreText - Age; Intravenous administration; CD4 antigen; Acquired immune deficiency syndrome; Avidity; antiretroviral therapy; Optical density; Seroconversion; Infection; Races; Sex; Human immunodeficiency virus; Assays; Antiretroviral agents; USA
DO - http://dx.doi.org/10.1097/QAD.0000000000000221
ER -
TY - JOUR
T1 - Lifespan of effector memory CD4 super(+) T cells determined by replication-incompetent integrated HIV-1 provirus
AN - 1765980495; PQ0002610773
AB - Objective: Determining the precise lifespan of human T-cell is challenging due to the inability of standard techniques to distinguish between dividing and dying cells. Here, we measured the lifespan of a pool of T cells that were derived from a single cell 'naturally' labelled with a single integrated clone of a replication-incompetent HIV-1 provirus. Design/methods: Utilizing a combination of techniques, we were able to sequence/ map an integration site of a unique provirus with a stop codon at position 42 of the HIV-1 protease. In-vitro reconstruction of this provirus into an infectious clone confirmed its inability to replicate. By combining cell separation and integration site-specific PCR, we were able to follow the fate of this single provirus in multiple T-cell subsets over a 20-year period. As controls, a number of additional integrated proviruses were also sequenced. Results: The replication-incompetent HIV-1 provirus was solely contained in the pool of effector memory CD4 super(+) T cells for 17 years. The percentage of the total effector memory CD4 super(+) T cells containing the replication-incompetent provirus peaked at 1% with a functional half-life of 11.1 months. In the process of sequencing multiple proviruses, we also observed high levels of lethal mutations in the peripheral blood pool of proviruses. Conclusion: These data indicate that human effector memory CD4 super(+) T cells are able to persist in vivo for more than 1 7 years without detectably reverting to a central memory phenotype. A secondary observation is that the fraction of the pool of integrated HIV-1 proviruses capable of replicating may be considerably less than the 12% currently noted in the literature.
JF - AIDS
AU - Imamichi, Hiromi
AU - Natarajan
AU - Adelsberger, Joseph W
AU - Rehm, Catherine A
AU - Lempicki, Richard A
AU - Das, Biswajit
AU - Hazen, Allison
AU - Imamichi, Tomozumi
AU - Lane, H Clifford
AD - Clinical and Molecular Retrovirology Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, CLANE@niaid.nih.gov
Y1 - 2014/05/15/
PY - 2014
DA - 2014 May 15
SP - 1091
EP - 1099
PB - Lippincott Williams & Wilkins, Inc, 530 Walnut Street Philadelphia PA 19106-3621 United States
VL - 28
IS - 8
SN - 0269-9370, 0269-9370
KW - Health & Safety Science Abstracts; Immunology Abstracts; Virology & AIDS Abstracts
KW - genetic marker
KW - HIV-1
KW - in-vivo persistence of CD4-positive T lymphocytes
KW - integration
KW - provirus
KW - replication-incompetent
KW - Acquired immune deficiency syndrome
KW - Data processing
KW - Life span
KW - Immunological memory
KW - Memory cells
KW - Peripheral blood
KW - Integration
KW - Stop codon
KW - CD4 antigen
KW - Human immunodeficiency virus 1
KW - Lymphocytes T
KW - Polymerase chain reaction
KW - Proteinase
KW - Mutation
KW - Proviruses
KW - H 6000:Natural Disasters/Civil Defense/Emergency Management
KW - V 22360:AIDS and HIV
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS&rft.atitle=Lifespan+of+effector+memory+CD4+super%28%2B%29+T+cells+determined+by+replication-incompetent+integrated+HIV-1+provirus&rft.au=Imamichi%2C+Hiromi%3BNatarajan%3BAdelsberger%2C+Joseph+W%3BRehm%2C+Catherine+A%3BLempicki%2C+Richard+A%3BDas%2C+Biswajit%3BHazen%2C+Allison%3BImamichi%2C+Tomozumi%3BLane%2C+H+Clifford&rft.aulast=Imamichi&rft.aufirst=Hiromi&rft.date=2014-05-15&rft.volume=28&rft.issue=8&rft.spage=1091&rft.isbn=&rft.btitle=&rft.title=AIDS&rft.issn=02699370&rft_id=info:doi/10.1097%2FQAD.0000000000000223
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2016-02-01
N1 - Last updated - 2016-03-17
N1 - SubjectsTermNotLitGenreText - Data processing; Life span; Memory cells; Immunological memory; Peripheral blood; Integration; CD4 antigen; Stop codon; Lymphocytes T; Polymerase chain reaction; Proteinase; Mutation; Proviruses; Acquired immune deficiency syndrome; Human immunodeficiency virus 1
DO - http://dx.doi.org/10.1097/QAD.0000000000000223
ER -
TY - JOUR
T1 - CLPTM1L promotes growth and enhances aneuploidy in pancreatic cancer cells.
AN - 1525765152; 24648346
AB - Genome-wide association studies (GWAS) of 10 different cancers have identified pleiotropic cancer predisposition loci across a region of chromosome 5p15.33 that includes the TERT and CLPTM1L genes. Of these, susceptibility alleles for pancreatic cancer have mapped to the CLPTM1L gene, thus prompting an investigation of the function of CLPTM1L in the pancreas. Immunofluorescence analysis indicated that CLPTM1L localized to the endoplasmic reticulum where it is likely embedded in the membrane, in accord with multiple predicted transmembrane domains. Overexpression of CLPTM1L enhanced growth of pancreatic cancer cells in vitro (1.3-1.5-fold; PDAY7 < 0.003) and in vivo (3.46-fold; PDAY68 = 0.039), suggesting a role in tumor growth; this effect was abrogated by deletion of two hydrophilic domains. Affinity purification followed by mass spectrometry identified an interaction between CLPTM1L and non-muscle myosin II (NMM-II), a protein involved in maintaining cell shape, migration, and cytokinesis. The two proteins colocalized in the cytoplasm and, after treatment with a DNA-damaging agent, at the centrosomes. Overexpression of CLPTM1L and depletion of NMM-II induced aneuploidy, indicating that CLPTM1L may interfere with normal NMM-II function in regulating cytokinesis. Immunohistochemical analysis revealed enhanced staining of CLPTM1L in human pancreatic ductal adenocarcinoma (n = 378) as compared with normal pancreatic tissue samples (n = 17; P = 1.7 × 10(-4)). Our results suggest that CLPTM1L functions as a growth-promoting gene in the pancreas and that overexpression may lead to an abrogation of normal cytokinesis, indicating that it should be considered as a plausible candidate gene that could explain the effect of pancreatic cancer susceptibility alleles on chr5p15.33.
©2014 American Association for Cancer Research.
JF - Cancer research
AU - Jia, Jinping
AU - Bosley, Allen D
AU - Thompson, Abbey
AU - Hoskins, Jason W
AU - Cheuk, Adam
AU - Collins, Irene
AU - Parikh, Hemang
AU - Xiao, Zhen
AU - Ylaya, Kris
AU - Dzyadyk, Marta
AU - Cozen, Wendy
AU - Hernandez, Brenda Y
AU - Lynch, Charles F
AU - Loncarek, Jadranka
AU - Altekruse, Sean F
AU - Zhang, Lizhi
AU - Westlake, Christopher J
AU - Factor, Valentina M
AU - Thorgeirsson, Snorri
AU - Bamlet, William R
AU - Hewitt, Stephen M
AU - Petersen, Gloria M
AU - Andresson, Thorkell
AU - Amundadottir, Laufey T
AD - Authors' Affiliations: Laboratory of Translational Genomics, Division of Cancer Epidemiology and Genetics; Pediatric Oncology Branch; Laboratory of Pathology; Division of Cancer Control and Population Sciences; Laboratory of Experimental Carcinogenesis, National Cancer Institute, NIH, Department of Health and Human Services, Bethesda; Laboratory of Proteomics and Analytical Technologies, Leidos Biomedical Research, Frederick National Laboratory for Cancer Research; Laboratory of Protein Dynamics and Signaling and Laboratory of Cell & Developmental Signaling, NCI-Frederick, Frederick, Maryland; Keck School of Medicine, University of Southern California, Los Angeles, California; University of Hawaii Cancer Center, Honolulu, Hawaii; Department of Epidemiology, College of Public Health, University of Iowa, Iowa City, Iowa; and Department of Health Sciences Research, Mayo Clinic, Rochester, Minnesota. ; Authors' Affiliations: Laboratory of Translational Genomics, Division of Cancer Epidemiology and Genetics; Pediatric Oncology Branch; Laboratory of Pathology; Division of Cancer Control and Population Sciences; Laboratory of Experimental Carcinogenesis, National Cancer Institute, NIH, Department of Health and Human Services, Bethesda; Laboratory of Proteomics and Analytical Technologies, Leidos Biomedical Research, Frederick National Laboratory for Cancer Research; Laboratory of Protein Dynamics and Signaling and Laboratory of Cell & Developmental Signaling, NCI-Frederick, Frederick, Maryland; Keck School of Medicine, University of Southern California, Los Angeles, California; University of Hawaii Cancer Center, Honolulu, Hawaii; Department of Epidemiology, College of Public Health, University of Iowa, Iowa City, Iowa; and Department of Health Sciences Research, Mayo Clinic, Rochester, Minnesota amundadottirl@mail.nih.gov.
Y1 - 2014/05/15/
PY - 2014
DA - 2014 May 15
SP - 2785
EP - 2795
VL - 74
IS - 10
KW - CLPTM1L protein, human
KW - 0
KW - Membrane Proteins
KW - Neoplasm Proteins
KW - Myosin Type II
KW - EC 3.6.1.-
KW - Index Medicus
KW - Heterografts
KW - Myosin Type II -- metabolism
KW - Animals
KW - Aneuploidy
KW - Cell Growth Processes -- physiology
KW - Humans
KW - HEK293 Cells
KW - Mice, Nude
KW - Mice
KW - Cell Line, Tumor
KW - Subcellular Fractions -- metabolism
KW - Female
KW - Neoplasm Proteins -- biosynthesis
KW - Pancreatic Neoplasms -- pathology
KW - Pancreatic Neoplasms -- metabolism
KW - Carcinoma, Pancreatic Ductal -- metabolism
KW - Membrane Proteins -- metabolism
KW - Neoplasm Proteins -- genetics
KW - Membrane Proteins -- biosynthesis
KW - Carcinoma, Pancreatic Ductal -- pathology
KW - Carcinoma, Pancreatic Ductal -- genetics
KW - Pancreatic Neoplasms -- genetics
KW - Membrane Proteins -- genetics
KW - Neoplasm Proteins -- metabolism
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=CLPTM1L+promotes+growth+and+enhances+aneuploidy+in+pancreatic+cancer+cells.&rft.au=Jia%2C+Jinping%3BBosley%2C+Allen+D%3BThompson%2C+Abbey%3BHoskins%2C+Jason+W%3BCheuk%2C+Adam%3BCollins%2C+Irene%3BParikh%2C+Hemang%3BXiao%2C+Zhen%3BYlaya%2C+Kris%3BDzyadyk%2C+Marta%3BCozen%2C+Wendy%3BHernandez%2C+Brenda+Y%3BLynch%2C+Charles+F%3BLoncarek%2C+Jadranka%3BAltekruse%2C+Sean+F%3BZhang%2C+Lizhi%3BWestlake%2C+Christopher+J%3BFactor%2C+Valentina+M%3BThorgeirsson%2C+Snorri%3BBamlet%2C+William+R%3BHewitt%2C+Stephen+M%3BPetersen%2C+Gloria+M%3BAndresson%2C+Thorkell%3BAmundadottir%2C+Laufey+T&rft.aulast=Jia&rft.aufirst=Jinping&rft.date=2014-05-15&rft.volume=74&rft.issue=10&rft.spage=2785&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=1538-7445&rft_id=info:doi/10.1158%2F0008-5472.CAN-13-3176
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-08-07
N1 - Date created - 2014-05-16
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1158/0008-5472.CAN-13-3176
ER -
TY - JOUR
T1 - Herb-drug interaction prediction based on the high specific inhibition of andrographolide derivatives towards UDP-glucuronosyltransferase (UGT) 2B7.
AN - 1518241986; 24631340
AB - Herb-drug interaction strongly limits the clinical application of herbs and drugs, and the inhibition of herbal components towards important drug-metabolizing enzymes (DMEs) has been regarded as one of the most important reasons. The present study aims to investigate the inhibition potential of andrographolide derivatives towards one of the most important phase II DMEs UDP-glucuronosyltransferases (UGTs). Recombinant UGT isoforms (except UGT1A4)-catalyzed 4-methylumbelliferone (4-MU) glucuronidation reaction and UGT1A4-catalyzed trifluoperazine (TFP) glucuronidation were employed to firstly screen the andrographolide derivatives' inhibition potential. High specific inhibition of andrographolide derivatives towards UGT2B7 was observed. The inhibition type and parameters (Ki) were determined for the compounds exhibiting strong inhibition capability towards UGT2B7, and human liver microsome (HLMs)-catalyzed zidovudine (AZT) glucuronidation probe reaction was used to furtherly confirm the inhibition behavior. In combination of inhibition parameters (Ki) and in vivo concentration of andrographolide and dehydroandrographolide, the potential in vivo inhibition magnitude was predicted. Additionally, both the in vitro inhibition data and computational modeling results provide important information for the modification of andrographolide derivatives as selective inhibitors of UGT2B7. Taken together, data obtained from the present study indicated the potential herb-drug interaction between Andrographis paniculata and the drugs mainly undergoing UGT2B7-catalyzed metabolic elimination, and the andrographolide derivatives as potential candidates for the selective inhibitors of UGT2B7.
Copyright © 2014 Elsevier Inc. All rights reserved.
JF - Toxicology and applied pharmacology
AU - Ma, Hai-Ying
AU - Sun, Dong-Xue
AU - Cao, Yun-Feng
AU - Ai, Chun-Zhi
AU - Qu, Yan-Qing
AU - Hu, Cui-Min
AU - Jiang, Changtao
AU - Dong, Pei-Pei
AU - Sun, Xiao-Yu
AU - Hong, Mo
AU - Tanaka, Naoki
AU - Gonzalez, Frank J
AU - Ma, Xiao-Chi
AU - Fang, Zhong-Ze
AD - The Fourth Affiliated Hospital of China Medical University, Shenyang 110032, China. Electronic address: cmu4h-mhy@126.com. ; School of Traditional Chinese Medicine, Shenyang Pharmaceutical University, No. 103, Wenhua Road, Shenyang 110016, China. ; The First Affiliated Hospital of Liaoning Medical University, Jinzhou 121001, China; Joint Center for Translational Medicine, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Zhongshan Road, Dalian 116023, China. ; Joint Center for Translational Medicine, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Zhongshan Road, Dalian 116023, China. ; Thyroid Surgery, Yantaishan Hospital, Yantai, Shandong, China. ; Joint Center for Translational Medicine, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Zhongshan Road, Dalian 116023, China; Department of Microbiology & Immunology, Georgetown University Medical Center, Washington, DC 20057, USA. ; Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA. ; Academy of Integrative Medicine, Dalian Medical University, Dalian 116044, China. ; The First Affiliated Hospital of Liaoning Medical University, Jinzhou 121001, China; Joint Center for Translational Medicine, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Zhongshan Road, Dalian 116023, China; Academy of Integrative Medicine, Dalian Medical University, Dalian 116044, China; College of Pharmacy, Pharmacokinetic and Drug Transport Key Laboratory, Dalian, Medical University, Dalian, China. Electronic address: maxc1978@163.com. ; The First Affiliated Hospital of Liaoning Medical University, Jinzhou 121001, China; Joint Center for Translational Medicine, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Zhongshan Road, Dalian 116023, China; Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA. Electronic address: zzfang228@gmail.com.
Y1 - 2014/05/15/
PY - 2014
DA - 2014 May 15
SP - 86
EP - 94
VL - 277
IS - 1
KW - Diterpenes
KW - 0
KW - andrographolide
KW - 410105JHGR
KW - UGT2B7 protein, human
KW - EC 2.4.1.-
KW - Glucuronosyltransferase
KW - EC 2.4.1.17
KW - UGT1A5 protein, human
KW - Index Medicus
KW - Andrographolide derivatives
KW - Adverse effects
KW - UDP-glucuronosyltransferases (UGTs)
KW - Herb–drug interaction (HDI)
KW - Enzyme Repression -- drug effects
KW - Humans
KW - Microsomes, Liver -- enzymology
KW - Microsomes, Liver -- drug effects
KW - Glucuronosyltransferase -- metabolism
KW - Glucuronosyltransferase -- drug effects
KW - Herb-Drug Interactions
KW - Andrographis
KW - Diterpenes -- metabolism
KW - Diterpenes -- chemistry
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+and+applied+pharmacology&rft.atitle=Herb-drug+interaction+prediction+based+on+the+high+specific+inhibition+of+andrographolide+derivatives+towards+UDP-glucuronosyltransferase+%28UGT%29+2B7.&rft.au=Ma%2C+Hai-Ying%3BSun%2C+Dong-Xue%3BCao%2C+Yun-Feng%3BAi%2C+Chun-Zhi%3BQu%2C+Yan-Qing%3BHu%2C+Cui-Min%3BJiang%2C+Changtao%3BDong%2C+Pei-Pei%3BSun%2C+Xiao-Yu%3BHong%2C+Mo%3BTanaka%2C+Naoki%3BGonzalez%2C+Frank+J%3BMa%2C+Xiao-Chi%3BFang%2C+Zhong-Ze&rft.aulast=Ma&rft.aufirst=Hai-Ying&rft.date=2014-05-15&rft.volume=277&rft.issue=1&rft.spage=86&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+applied+pharmacology&rft.issn=1096-0333&rft_id=info:doi/10.1016%2Fj.taap.2014.02.021
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-06-15
N1 - Date created - 2014-04-21
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.taap.2014.02.021
ER -
TY - JOUR
T1 - Breast cancer risk after radiotherapy for heritable and non-heritable retinoblastoma: a US-UK study
AN - 1534855121; 19881880
AB - Background: Retinoblastoma is a rare childhood eye cancer caused by germline or somatic mutations in the RB1 gene. Previous studies observed elevated breast cancer risk among retinoblastoma survivors. However, there has been no research on breast cancer risk in relation to radiation (primarily scatter radiation from the primary treatment) and genetic susceptibility of retinoblastoma survivors. Methods: Two groups of retinoblastoma survivors from the US and UK were selected, and breast cancer risk analysed using a case-control methodology, nesting within the respective cohorts, matching on heritability (that is to say, having bilateral retinoblastoma or being unilateral cases with at least one relative with retinoblastoma), and using exact statistical methods. There were a total of 31 cases and 77 controls. Results: Overall there was no significant variation of breast cancer risk with dose (P>0.5). However, there was a pronounced and significant (P=0.047) increase in the risk of breast cancer with increasing radiation dose for non-heritable retinoblastoma patients and a slight and borderline significant (P=0.072) decrease in risk of breast cancer with increasing radiation dose for heritable retinoblastoma patients, implying significant (P=0.024) heterogeneity in radiation risk between the heritable and non-heritable retinoblastoma groups; this was unaffected by the blindness status. There was no significant effect of any type of alkylating-agent chemotherapy on breast cancer risk (P>0.5). Conclusions: There is significant radiation-related risk of breast cancer for non-heritable retinoblastoma survivors but no excess risk for heritable retinoblastoma survivors, and no significant risk overall. However, these results are based on very small numbers of cases; therefore, they must be interpreted with caution.
JF - British Journal of Cancer
AU - Little, M P
AU - Schaeffer, M L
AU - Reulen, R C
AU - Abramson, D H
AU - Stovall, M
AU - Weathers, R
AU - de Vathaire, F
AU - Diallo, I
AU - Seddon, J M
AU - Hawkins, M M
AU - Tucker, M A
AU - Kleinerman, R A
AD - Division of Cancer Epidemiology and Genetics, Department of Health and Human Services, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Y1 - 2014/05/13/
PY - 2014
DA - 2014 May 13
SP - 2623
EP - 2632
PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL - 110
IS - 10
SN - 0007-0920, 0007-0920
KW - Risk Abstracts
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-01
N1 - Last updated - 2014-06-12
DO - http://dx.doi.org/10.1038/bjc.2014.193
ER -
TY - CPAPER
T1 - Antiviral Proteins from Natural Product Extracts: from Discovery to Development
T2 - 27th International Conference on Antiviral Research (ICAR 2014)
AN - 1562646591; 6301808
JF - 27th International Conference on Antiviral Research (ICAR 2014)
AU - O'Keefe, Barry
Y1 - 2014/05/12/
PY - 2014
DA - 2014 May 12
KW - Molecular structure
KW - natural products
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L2 - http://c.ymcdn.com/sites/www.isar-icar.com/resource/resmgr/docs/ICAR_Program2014final.pdf
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-08-31
N1 - Last updated - 2014-09-18
ER -
TY - CPAPER
T1 - Progressive Ratio Responding to Palatable High Sucrose Food in Mice Lacking Adult Hippocampal Neurogenesis
T2 - 2014 Keystone Symposia Conference on Adult Neurogenesis
AN - 1518611697; 6280415
JF - 2014 Keystone Symposia Conference on Adult Neurogenesis
AU - Karlsson, Rose-Marie
Y1 - 2014/05/12/
PY - 2014
DA - 2014 May 12
KW - Neurogenesis
KW - Hippocampus
KW - Food
KW - Sucrose
KW - Mice
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L2 - http://www.keystonesymposia.org/index.cfm?e=Web.Meeting.Flyer&MeetingID=1304
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-23
N1 - Last updated - 2014-04-24
ER -
TY - CPAPER
T1 - Physical Activity and New Neuron Connectivity
T2 - 2014 Keystone Symposia Conference on Adult Neurogenesis
AN - 1518609647; 6280416
JF - 2014 Keystone Symposia Conference on Adult Neurogenesis
AU - Van Praag, Henriette
Y1 - 2014/05/12/
PY - 2014
DA - 2014 May 12
KW - Neural networks
KW - Neurons
KW - Physical activity
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Keystone+Symposia+Conference+on+Adult+Neurogenesis&rft.atitle=Physical+Activity+and+New+Neuron+Connectivity&rft.au=Van+Praag%2C+Henriette&rft.aulast=Van+Praag&rft.aufirst=Henriette&rft.date=2014-05-12&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Keystone+Symposia+Conference+on+Adult+Neurogenesis&rft.issn=&rft_id=info:doi/
L2 - http://www.keystonesymposia.org/index.cfm?e=Web.Meeting.Flyer&MeetingID=1304
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-23
N1 - Last updated - 2014-04-24
ER -
TY - JOUR
T1 - Identification of Biologically Active, HIV TAR RNA-Binding Small Molecules Using Small Molecule Microarrays
AN - 1683350669; PQ0001582112
AB - Identifying small molecules that selectively bind to structured RNA motifs remains an important challenge in developing potent and specific therapeutics. Most strategies to find RNA-binding molecules have identified highly charged compounds or aminoglycosides that commonly have modest selectivity. Here we demonstrate a strategy to screen a large unbiased library of druglike small molecules in a microarray format against an RNA target. This approach has enabled the identification of a novel chemotype that selectively targets the HIV transactivation response (TAR) RNA hairpin in a manner not dependent on cationic charge. Thienopyridine 4 binds to and stabilizes the TAR hairpin with a Kd of 2.4 mu M. Structure-activity relationships demonstrate that this compound achieves activity through hydrophobic and aromatic substituents on a heterocyclic core, rather than cationic groups typically required. Selective 2'-hydroxyl acylation analyzed by primer extension (SHAPE) analysis was performed on a 365-nucleotide sequence derived from the 5' untranslated region (UTR) of the HIV-1 genome to determine global structural changes in the presence of the molecule. Importantly, the interaction of compound 4 can be mapped to the TAR hairpin without broadly disrupting any other structured elements of the 5' UTR. Cell-based anti-HIV assays indicated that 4 inhibits HIV-induced cytopathicity in T lymphocytes with an EC50 of 28 mu M, while cytotoxicity was not observed at concentrations approaching 1 mM.
JF - Journal of the American Chemical Society
AU - Sztuba-Solinska, Joanna
AU - Shenoy, Shilpa R
AU - Gareiss, Peter
AU - Krumpe, Lauren RH
AU - Le Grice, Stuart FJ
AU - O'Keefe, Barry R
AU - Schneekloth, John S
AD - HIV Drug Resistance Program, National Cancer Institute, Frederick, Maryland, United States,
PY - 2014
SP - 8402
EP - 8410
PB - American Chemical Society, P.O. Box 182426 Columbus OH 43218-2426 United States
VL - 136
IS - 23
SN - 0002-7863, 0002-7863
KW - Biochemistry Abstracts 2: Nucleic Acids; Biotechnology and Bioengineering Abstracts
KW - Genomes
KW - Nucleotide sequence
KW - Hydrophobicity
KW - Acylation
KW - Cytotoxicity
KW - RNA
KW - Human immunodeficiency virus
KW - Human immunodeficiency virus 1
KW - Lymphocytes T
KW - Primers
KW - Structure-activity relationships
KW - Aromatics
KW - N 14810:Methods
KW - W 30900:Methods
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1683350669?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+American+Chemical+Society&rft.atitle=Identification+of+Biologically+Active%2C+HIV+TAR+RNA-Binding+Small+Molecules+Using+Small+Molecule+Microarrays&rft.au=Sztuba-Solinska%2C+Joanna%3BShenoy%2C+Shilpa+R%3BGareiss%2C+Peter%3BKrumpe%2C+Lauren+RH%3BLe+Grice%2C+Stuart+FJ%3BO%27Keefe%2C+Barry+R%3BSchneekloth%2C+John+S&rft.aulast=Sztuba-Solinska&rft.aufirst=Joanna&rft.date=2014-05-02&rft.volume=136&rft.issue=23&rft.spage=8402&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+American+Chemical+Society&rft.issn=00027863&rft_id=info:doi/10.1021%2Fja502754f
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-05-01
N1 - Last updated - 2016-01-21
N1 - SubjectsTermNotLitGenreText - Genomes; Cytotoxicity; RNA; Nucleotide sequence; Lymphocytes T; Hydrophobicity; Primers; Acylation; Structure-activity relationships; Aromatics; Human immunodeficiency virus; Human immunodeficiency virus 1
DO - http://dx.doi.org/10.1021/ja502754f
ER -
TY - CPAPER
T1 - The nature of AID off-targeting activity
T2 - 2014 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2014)
AN - 1518611710; 6280542
JF - 2014 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2014)
AU - Casellas, Rafael
Y1 - 2014/05/02/
PY - 2014
DA - 2014 May 02
KW - activation-induced cytidine deaminase
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518611710?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2014%29&rft.atitle=The+nature+of+AID+off-targeting+activity&rft.au=Casellas%2C+Rafael&rft.aulast=Casellas&rft.aufirst=Rafael&rft.date=2014-05-02&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2014%29&rft.issn=&rft_id=info:doi/
L2 - http://www.immunology2014.org/Program/index.html?loc=nav
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-23
N1 - Last updated - 2014-04-24
ER -
TY - CPAPER
T1 - Translational development of a malaria vaccine from bench to bedside: is it prime time for T cells?
T2 - 2014 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2014)
AN - 1518611483; 6280585
JF - 2014 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2014)
AU - Seder, Robert
Y1 - 2014/05/02/
PY - 2014
DA - 2014 May 02
KW - Translation
KW - Lymphocytes T
KW - Disease control
KW - Malaria
KW - Vaccines
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518611483?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2014%29&rft.atitle=Translational+development+of+a+malaria+vaccine+from+bench+to+bedside%3A+is+it+prime+time+for+T+cells%3F&rft.au=Seder%2C+Robert&rft.aulast=Seder&rft.aufirst=Robert&rft.date=2014-05-02&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2014%29&rft.issn=&rft_id=info:doi/
L2 - http://www.immunology2014.org/Program/index.html?loc=nav
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-23
N1 - Last updated - 2014-04-24
ER -
TY - CPAPER
T1 - Adoptive T cell therapy: from biology to practice
T2 - 2014 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2014)
AN - 1518611444; 6280606
JF - 2014 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2014)
AU - Restifo, Nicholas
Y1 - 2014/05/02/
PY - 2014
DA - 2014 May 02
KW - Lymphocytes T
KW - Therapy
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518611444?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2014%29&rft.atitle=Adoptive+T+cell+therapy%3A+from+biology+to+practice&rft.au=Restifo%2C+Nicholas&rft.aulast=Restifo&rft.aufirst=Nicholas&rft.date=2014-05-02&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2014%29&rft.issn=&rft_id=info:doi/
L2 - http://www.immunology2014.org/Program/index.html?loc=nav
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-23
N1 - Last updated - 2014-04-24
ER -
TY - CPAPER
T1 - Cytokine regulation of Staphylococcus aureus infections
T2 - 2014 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2014)
AN - 1518611003; 6280502
JF - 2014 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2014)
AU - Datta, Sandip
Y1 - 2014/05/02/
PY - 2014
DA - 2014 May 02
KW - Cytokines
KW - Infection
KW - Staphylococcus aureus
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518611003?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2014%29&rft.atitle=Cytokine+regulation+of+Staphylococcus+aureus+infections&rft.au=Datta%2C+Sandip&rft.aulast=Datta&rft.aufirst=Sandip&rft.date=2014-05-02&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2014%29&rft.issn=&rft_id=info:doi/
L2 - http://www.immunology2014.org/Program/index.html?loc=nav
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-23
N1 - Last updated - 2014-04-24
ER -
TY - CPAPER
T1 - IL-7 receptor as a new target for immune intervention in inflammation and autoimmunity
T2 - 2014 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2014)
AN - 1518609676; 6280533
JF - 2014 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2014)
AU - Park, Hyun
Y1 - 2014/05/02/
PY - 2014
DA - 2014 May 02
KW - Interleukin 7
KW - Autoimmunity
KW - Intervention
KW - Inflammation
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518609676?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2014%29&rft.atitle=IL-7+receptor+as+a+new+target+for+immune+intervention+in+inflammation+and+autoimmunity&rft.au=Park%2C+Hyun&rft.aulast=Park&rft.aufirst=Hyun&rft.date=2014-05-02&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2014%29&rft.issn=&rft_id=info:doi/
L2 - http://www.immunology2014.org/Program/index.html?loc=nav
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-23
N1 - Last updated - 2014-04-24
ER -
TY - CPAPER
T1 - Visualizing the dynamics and micro-anatomy of the immune system: how this complex machine really works
T2 - 2014 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2014)
AN - 1518609517; 6280601
JF - 2014 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2014)
AU - Germain, Ronald
Y1 - 2014/05/02/
PY - 2014
DA - 2014 May 02
KW - Immune system
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518609517?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2014%29&rft.atitle=Visualizing+the+dynamics+and+micro-anatomy+of+the+immune+system%3A+how+this+complex+machine+really+works&rft.au=Germain%2C+Ronald&rft.aulast=Germain&rft.aufirst=Ronald&rft.date=2014-05-02&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2014%29&rft.issn=&rft_id=info:doi/
L2 - http://www.immunology2014.org/Program/index.html?loc=nav
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-23
N1 - Last updated - 2014-04-24
ER -
TY - CPAPER
T1 - Finding the molecular links between house dust and asthma
T2 - 2014 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2014)
AN - 1518609512; 6280567
JF - 2014 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2014)
AU - Cook, Donald
Y1 - 2014/05/02/
PY - 2014
DA - 2014 May 02
KW - House dust
KW - Asthma
KW - Respiratory diseases
KW - Dust
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518609512?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2014%29&rft.atitle=Finding+the+molecular+links+between+house+dust+and+asthma&rft.au=Cook%2C+Donald&rft.aulast=Cook&rft.aufirst=Donald&rft.date=2014-05-02&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2014%29&rft.issn=&rft_id=info:doi/
L2 - http://www.immunology2014.org/Program/index.html?loc=nav
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-23
N1 - Last updated - 2014-04-24
ER -
TY - JOUR
T1 - Cardiac Reactivity During the Ascending Phase of Acute Intravenous Alcohol Exposure and Association with Subjective Perceptions of Intoxication in Social Drinkers
AN - 1842509609; 19774224
AB - The aim of this study was to characterize cardiac reactivity measures, heart rate (HR), and heart rate variability (HRV), following acute intravenous (IV) alcohol administration and their association with subjective responses in social drinkers. Twenty-four subjects (11 females) received IV alcohol infusions to attain and clamp the breath alcohol concentration (BrAC) at 50 mg% or placebo in separate sessions. Serial 5-minute cardiac recordings at baseline and during the infusion were analyzed to obtain frequency and time domain cardiac measures. Self-reported subjective perceptions were also obtained at the same time points. HR showed significant decreases from baseline, while the HRV measure pNN50 showed steady increases during the ascending phase of alcohol infusion. HR was inversely correlated with pNN50 across time and treatment. There was a significant association of HR with subjective feelings of high, intoxication, feeling drug effects, and liking drug effects across time during the ascending phase. Acute IV alcohol resulted in decreases in HR and increases in HRV consistent with autonomic parasympathetic activation. The association of these changes with subjective responses suggests that cardiac reactivity may serve as a physiological marker of subjective alcohol effects. This study broadens the understanding of acute cardiovascular effects of alcohol and clinically significant cardiac conditions such as arrhythmia and cardiomyopathy associated with chronic alcohol drinking.
JF - Alcoholism: Clinical and Experimental Research
AU - Vatsalya, Vatsalya
AU - Momenan, Reza
AU - Hommer, Daniel W
AU - Ramchandani, Vijay A
AD - Section on Human Psychopharmacology Laboratory of Clinical and Translational Studies. National Institute on Alcohol Abuse and Alcoholism
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 1247
EP - 1254
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 38
IS - 5
SN - 0145-6008, 0145-6008
KW - Toxicology Abstracts
KW - Intoxication
KW - Heart
KW - Arrhythmia
KW - Intravenous administration
KW - Parasympathetic nervous system
KW - Heart rate
KW - Drug abuse
KW - Cardiomyopathy
KW - Perception
KW - Alcoholism
KW - Drinking behavior
KW - Drugs
KW - Ethanol
KW - X 24380:Social Poisons & Drug Abuse
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1842509609?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcoholism%3A+Clinical+and+Experimental+Research&rft.atitle=Cardiac+Reactivity+During+the+Ascending+Phase+of+Acute+Intravenous+Alcohol+Exposure+and+Association+with+Subjective+Perceptions+of+Intoxication+in+Social+Drinkers&rft.au=Vatsalya%2C+Vatsalya%3BMomenan%2C+Reza%3BHommer%2C+Daniel+W%3BRamchandani%2C+Vijay+A&rft.aulast=Vatsalya&rft.aufirst=Vatsalya&rft.date=2014-05-01&rft.volume=38&rft.issue=5&rft.spage=1247&rft.isbn=&rft.btitle=&rft.title=Alcoholism%3A+Clinical+and+Experimental+Research&rft.issn=01456008&rft_id=info:doi/10.1111%2Facer.12377
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2016-11-01
N1 - Last updated - 2016-12-22
N1 - SubjectsTermNotLitGenreText - Heart; Intoxication; Intravenous administration; Arrhythmia; Parasympathetic nervous system; Heart rate; Drug abuse; Cardiomyopathy; Perception; Alcoholism; Drinking behavior; Drugs; Ethanol
DO - http://dx.doi.org/10.1111/acer.12377
ER -
TY - JOUR
T1 - History of Weight Control Attempts Among Adolescent Girls With Loss of Control Eating
AN - 1732808412; PQ0002227716
AB - Objective: Loss of control (LOC) eating and a weight control attempt (WCA) history during adolescence are important behavioral risk factors for eating disorders and obesity. The current study investigated the significance of the presence of a WCA history among adolescent girls with LOC eating. Method: Participants were 114 obesity-prevention-seeking 12-17-year-old (M = 14.5, SD = 1.7 years) girls who were between the 75th and 97th body mass index (BMI) percentile (BMI-z: M = 1.5, SD = 0.3) and reported LOC eating episodes during the previous month (M = 4.0, SD = 4.9 episodes; Median = 2.0). Measures included the Eating Disorder Examination to assess LOC eating, eating pathology, and WCA history, and self-report questionnaires for symptoms of general psychopathology. Eating behavior was observed during a laboratory meal designed to capture a LOC eating episode. Results: 67.5% reported a WCA history. As compared to girls without a WCA history (no-WCA), those with a WCA history (WCA) had greater disordered eating attitudes and depressive symptoms (ps .10). During the laboratory meal, WCA consumed less energy from snack-type foods than no-WCA (M = 245.0, SD = 156.1 vs. M = 341.6, SD = 192.3 kcal; p = .01). Conclusions: Reported WCAs are highly prevalent and are associated with greater psychopathology symptoms among adolescent girls with LOC eating. Prospective data are needed to determine whether these overlapping risk behaviors confer differential vulnerability for developing eating disorders and obesity.
JF - Health Psychology
AU - Vannucci, Anna
AU - Shomaker, Lauren B
AU - Field, Sara E
AU - Sbrocco, Tracy
AU - Stephens, Mark
AU - Kozlosky, Merel
AU - Reynolds, James C
AU - Yanovski, Jack A
AU - Tanofsky-Kraff, Marian
AD - Uniformed Services University of the Health Sciences and Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, mtanofsky@usuhs.edu
PY - 2014
SP - 419
EP - 423
PB - American Psychological Association, 750 First St., N.E. Washington DC 20002-4242 United States
VL - 33
IS - 5
SN - 0278-6133, 0278-6133
KW - Physical Education Index
KW - loss of control eating
KW - dieting
KW - weight control behavior
KW - eating disorders
KW - obesity
KW - Evaluation
KW - Obesity
KW - Attitudes
KW - Weight control
KW - Eating disorders
KW - Girls
KW - Adolescence
KW - Body mass
KW - PE 030:Exercise, Health & Physical Fitness
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1732808412?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aphysicaleducation&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Health+Psychology&rft.atitle=History+of+Weight+Control+Attempts+Among+Adolescent+Girls+With+Loss+of+Control+Eating&rft.au=Vannucci%2C+Anna%3BShomaker%2C+Lauren+B%3BField%2C+Sara+E%3BSbrocco%2C+Tracy%3BStephens%2C+Mark%3BKozlosky%2C+Merel%3BReynolds%2C+James+C%3BYanovski%2C+Jack+A%3BTanofsky-Kraff%2C+Marian&rft.aulast=Vannucci&rft.aufirst=Anna&rft.date=2014-05-01&rft.volume=33&rft.issue=5&rft.spage=419&rft.isbn=&rft.btitle=&rft.title=Health+Psychology&rft.issn=02786133&rft_id=info:doi/10.1037%2Fa0033184
LA - English
DB - Physical Education Index
N1 - Date revised - 2015-11-01
N1 - Last updated - 2015-12-09
N1 - SubjectsTermNotLitGenreText - Evaluation; Obesity; Attitudes; Weight control; Eating disorders; Body mass; Adolescence; Girls
DO - http://dx.doi.org/10.1037/a0033184
ER -
TY - JOUR
T1 - Learning by doing: observing an interprofessional process as an interprofessional team
AN - 1665161484
AB - New competencies exist for interprofessional education, which are centered on the goal of improving quality of care and patient safety through improved interprofessional collaboration. Interprofessional education and effective interprofessional collaboration are cornerstones of the Veterans Affairs Quality Scholars fellowship program. The purpose of this project was to evaluate an innovative interprofessional education strategy in which teams of physicians and nurses were "learning by doing" as they observed and analyzed the functioning of an interprofessional process, specifically, inpatient discharge. Fellows completed voluntary, anonymous surveys seeking their perspectives about the project. Fellowsʼ feedback revealed several themes, with both positive and negative characteristics related to team functioning, interprofessional understanding, microsystem knowledge, pooled knowledge and assignment challenges. The strength of this strategy is exemplified by the fact that fellows not only learned from each otherʼs separate professional observations, but also observed the emergence of a shared interprofessional perspective through working together.
JF - Journal of Interprofessional Care
AU - Brennan, Caitlin W
AU - Olds, Danielle M
AU - Dolansky, Mary
AU - Estrada, Carlos A
AU - Patrician, Patricia A
AD - National Institutes of Health Clinical Center, Nursing Department, Research and Practice Development, 10 Center Drive, Room 2B08, Bethesda, MD 20892, USA ; National Database of Nursing Quality Indicators (NDNQI(R)), University of Kansas Medical Center, Kansas City, KS, USA ; Frances Payne Bolton School of Nursing, Case Western Reserve University, Cleveland, OH, USA ; Birmingham VA Medical Center, University of Alabama at Birmingham, Birmingham, AL, USA ; University of Alabama at Birmingham, Birmingham, AL, USA ; National Institutes of Health Clinical Center, Nursing Department, Research and Practice Development, 10 Center Drive, Room 2B08, Bethesda, MD 20892, USA
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 249
EP - 251
CY - Abingdon
PB - Taylor & Francis Ltd.
VL - 28
IS - 3
SN - 1356-1820
KW - Medical Sciences
KW - Interprofessional collaboration
KW - interprofessional education
KW - interprofessional evaluation
KW - teams
KW - Doctors
KW - Veterans
KW - Feedback
KW - Hospitalization
KW - Interagency collaboration
KW - Interdisciplinary approach
KW - Interdisciplinary education
KW - Interdisciplinary team work
KW - Learning
KW - Nurses
KW - Patient care
KW - Professional knowledge
KW - Quality of care
KW - Safety
KW - Safety measures
KW - Teams
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665161484?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Interprofessional+Care&rft.atitle=Learning+by+doing%3A+observing+an+interprofessional+process+as+an+interprofessional+team&rft.au=Brennan%2C+Caitlin+W%3BOlds%2C+Danielle+M%3BDolansky%2C+Mary%3BEstrada%2C+Carlos+A%3BPatrician%2C+Patricia+A&rft.aulast=Brennan&rft.aufirst=Caitlin&rft.date=2014-05-01&rft.volume=28&rft.issue=3&rft.spage=249&rft.isbn=&rft.btitle=&rft.title=Journal+of+Interprofessional+Care&rft.issn=13561820&rft_id=info:doi/10.3109%2F13561820.2013.838750
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Date revised - 2015-01-09
N1 - Last updated - 2016-05-13
DO - http://dx.doi.org/10.3109/13561820.2013.838750
ER -
TY - JOUR
T1 - Neglected Parasitic Infections in the United States: Cysticercosis
AN - 1647024281; 21184014
AB - Cysticercosis is a potentially fatal and preventable neglected parasitic infection caused by the larval form of Taenia solium. Patients with symptomatic disease usually have signs and symptoms of neurocysticercosis, which commonly manifest as seizures or increased intracranial pressure. Although there are many persons living in the United States who emigrated from highly disease-endemic countries and there are foci of autochthonous transmission of the parasite in the United States, little is known about burden and epidemiology of the disease in this country. In addition, despite advances in the diagnosis and management of neurocysticercosis, there remain many unanswered questions. Improving our understanding and management of neurocysticercosis in the United States will require improved surveillance or focused prospective studies in appropriate areas and allocation of resources towards answering some of the key questions discussed in this report.
JF - American Journal of Tropical Medicine and Hygiene
AU - Cantey, Paul T
AU - Coyle, Christina M
AU - Sorvillo, Frank J
AU - Wilkins, Patricia P
AU - Starr, Michelle C
AU - Nash, Theodore E
AD - Division of Parasitic Diseases and Malaria, Centers for Disease Control and Prevention, 1600 Clifton Road NE, Mailstop A-06, Atlanta, GA 30333; Department of Medicine, Albert Einstein College of Medicine, Bronx, New York; Department of Pediatrics, University of Washington, Seattle, Washington; Department of Epidemiology, School of Public Health, University of California-Los Angeles, Los Angeles, California; Gastrointestinal Parasites Section, Laboratory of Parasitic Diseases, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, pcantey@cdc.gov
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 805
EP - 809
PB - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States
VL - 90
IS - 5
SN - 0002-9637, 0002-9637
KW - Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts B: Bacteriology; ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality
KW - Parasites
KW - Symptoms
KW - Resource management
KW - Seizures
KW - Surveillance and enforcement
KW - Infection
KW - Disease transmission
KW - USA
KW - Neurotransmission
KW - Epidemiology
KW - Cysticercosis
KW - Taenia
KW - Taenia solium
KW - Pressure
KW - Hygiene
KW - Q1 08484:Species interactions: parasites and diseases
KW - Q5 08502:Methods and instruments
KW - J 02400:Human Diseases
KW - K 03420:Plant Diseases
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.atitle=Neglected+Parasitic+Infections+in+the+United+States%3A+Cysticercosis&rft.au=Cantey%2C+Paul+T%3BCoyle%2C+Christina+M%3BSorvillo%2C+Frank+J%3BWilkins%2C+Patricia+P%3BStarr%2C+Michelle+C%3BNash%2C+Theodore+E&rft.aulast=Cantey&rft.aufirst=Paul&rft.date=2014-05-01&rft.volume=90&rft.issue=5&rft.spage=805&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.13-0724
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-01-01
N1 - Last updated - 2016-02-18
N1 - SubjectsTermNotLitGenreText - Symptoms; Parasites; Resource management; Epidemiology; Surveillance and enforcement; Hygiene; Disease transmission; Neurotransmission; Seizures; Cysticercosis; Pressure; Infection; Taenia solium; Taenia; USA
DO - http://dx.doi.org/10.4269/ajtmh.13-0724
ER -
TY - JOUR
T1 - G6PD A- Deficiency and Severe Malaria in The Gambia: Heterozygote Advantage and Possible Homozygote Disadvantage
AN - 1647024172; 21184024
AB - Glucose-6-phosphate dehydrogenase (G6PD) deficiency is frequent in Africa, because it confers resistance to Plasmodium falciparum malaria; however, the nature of the protection and the genotypes associated with it have been controversial. In 1972, Bienzle and others described protection from malaria in West African females heterozygous for G6PD A-. They determined that G6PD A- heterozygotes had lower parasite counts than A- homozygotes, hemizygous males, and normal individuals. However, other studies have reached different conclusions about the protective genotypes. DNA samples from 135 children with severe malaria and 146 children with mild malaria from The Gambia were genotyped for the G6PD A- mutation that is most frequent among Gambians (G6PD 968 T->C); there was a marked deficiency of heterozygotes and an excess of homozygotes with severe malaria, producing a strong deviation from Hardy-Weinberg equilibrium. Our results support the protective effect in G6PD A- heterozygous females and suggest that homozygotes might be more susceptible to severe malaria attacks.
JF - American Journal of Tropical Medicine and Hygiene
AU - Sirugo, Giorgio
AU - Predazzi, Irene M
AU - Bartlett, Jacquelaine
AU - Tacconelli, Alessandra
AU - Walther, Michael
AU - Williams, Scott M
AD - Centro di Ricerca, Ospedale San Pietro Fatebenefratelli, Via Cassia, 600, 00189 Rome, Italy; Center for Human Genetics Research, Vanderbilt University Medical Center, Nashville, Tennessee; Department of Genetics, Geisel School of Medicine, Dartmouth College, Hanover, New Hampshire; National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland; Medical Research Council Laboratories, Fajara, Banjul, The Gambia, sirugo.giorgio@fbfrm.it
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 856
EP - 859
PB - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States
VL - 90
IS - 5
SN - 0002-9637, 0002-9637
KW - Microbiology Abstracts B: Bacteriology; Microbiology Abstracts C: Algology, Mycology & Protozoology; ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality
KW - Parasites
KW - Human diseases
KW - Gambia
KW - Mutations
KW - Malaria
KW - Plasmodium falciparum
KW - Genotypes
KW - Children
KW - Homozygotes
KW - Glucosephosphate dehydrogenase
KW - Public health
KW - Heterozygote advantage
KW - DNA
KW - Africa
KW - Hygiene
KW - Mutation
KW - Dehydrogenases
KW - K 03400:Human Diseases
KW - Q1 08484:Species interactions: parasites and diseases
KW - Q5 08502:Methods and instruments
KW - J 02400:Human Diseases
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.atitle=G6PD+A-+Deficiency+and+Severe+Malaria+in+The+Gambia%3A+Heterozygote+Advantage+and+Possible+Homozygote+Disadvantage&rft.au=Sirugo%2C+Giorgio%3BPredazzi%2C+Irene+M%3BBartlett%2C+Jacquelaine%3BTacconelli%2C+Alessandra%3BWalther%2C+Michael%3BWilliams%2C+Scott+M&rft.aulast=Sirugo&rft.aufirst=Giorgio&rft.date=2014-05-01&rft.volume=90&rft.issue=5&rft.spage=856&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.13-0622
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-01-01
N1 - Last updated - 2016-02-04
N1 - SubjectsTermNotLitGenreText - Parasites; Human diseases; Mutations; DNA; Malaria; Genotypes; Hygiene; Dehydrogenases; Public health; Heterozygote advantage; Children; Mutation; Homozygotes; Glucosephosphate dehydrogenase; Plasmodium falciparum; Gambia; Africa
DO - http://dx.doi.org/10.4269/ajtmh.13-0622
ER -
TY - JOUR
T1 - Investigation of Dengue and Japanese Encephalitis Virus Transmission in Hanam, Viet Nam
AN - 1647022956; 21184029
AB - This study investigated whether a large dengue epidemic that struck Hanaoi in 2009 also affected a nearby semirural area. Seroconversion (dengue virus-reactive immunoglobulin G enzyme-linked immunosorbent assay) was high during 2009 compared with 2008, but neutralization assays showed that it was caused by both dengue virus and Japanese encephalitis virus infections. The findings highlight the importance of continued Japanese encephalitis virus vaccination and dengue surveillance.
JF - American Journal of Tropical Medicine and Hygiene
AU - Fox, Annette
AU - Whitehead, Stephen
AU - Anders, Katherine L
AU - Hoa, Le Nguyen Minh
AU - Mai, Le Quynh
AU - Thai, Pham Quang
AU - Yen, Nguyen Thu
AU - Duong, Tran Nhu
AU - Thoang, Dang Dinh
AU - Farrar, Jeremy
AU - Wertheim, Heiman
AU - Simmons, Cameron
AU - Hien, Nguyen Tran
AU - Horby, Peter
AD - Oxford University Clinical Research Unit and Wellcome Trust Major Overseas Programme, Viet Nam; Centre for Tropical Medicine, Nuffield Department of Clinical Medicine, University of Oxford, Oxford, United Kingdom; National Institute of Allergy and Infectious Diseases, Bethesda, Maryland; National Institute of Hygiene and Epidemiology, Hanaoi, Viet Nam; Hanam Centre for Preventive Medicine, Hanam, Viet Nam, afox@pacific.net.au
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 892
EP - 896
PB - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States
VL - 90
IS - 5
SN - 0002-9637, 0002-9637
KW - Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts B: Bacteriology; CSA Neurosciences Abstracts; Virology & AIDS Abstracts; ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality
KW - Dengue virus
KW - Enzyme-linked immunosorbent assay
KW - Epidemics
KW - Surveillance and enforcement
KW - Infection
KW - Vaccination
KW - Encephalitis
KW - Vietnam
KW - Dengue
KW - Immunoglobulin G
KW - Seroconversion
KW - Japanese encephalitis virus
KW - Hygiene
KW - V 22490:Miscellaneous
KW - K 03400:Human Diseases
KW - Q1 08484:Species interactions: parasites and diseases
KW - Q5 08502:Methods and instruments
KW - J 02350:Immunology
KW - N3 11027:Neurology & neuropathology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.atitle=Investigation+of+Dengue+and+Japanese+Encephalitis+Virus+Transmission+in+Hanam%2C+Viet+Nam&rft.au=Fox%2C+Annette%3BWhitehead%2C+Stephen%3BAnders%2C+Katherine+L%3BHoa%2C+Le+Nguyen+Minh%3BMai%2C+Le+Quynh%3BThai%2C+Pham+Quang%3BYen%2C+Nguyen+Thu%3BDuong%2C+Tran+Nhu%3BThoang%2C+Dang+Dinh%3BFarrar%2C+Jeremy%3BWertheim%2C+Heiman%3BSimmons%2C+Cameron%3BHien%2C+Nguyen+Tran%3BHorby%2C+Peter&rft.aulast=Fox&rft.aufirst=Annette&rft.date=2014-05-01&rft.volume=90&rft.issue=5&rft.spage=892&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.13-0077
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-01-01
N1 - Last updated - 2016-10-12
N1 - SubjectsTermNotLitGenreText - Epidemics; Surveillance and enforcement; Hygiene; Vaccination; Enzyme-linked immunosorbent assay; Dengue; Immunoglobulin G; Seroconversion; Infection; Encephalitis; Dengue virus; Japanese encephalitis virus; Vietnam
DO - http://dx.doi.org/10.4269/ajtmh.13-0077
ER -
TY - JOUR
T1 - Immune Responses to O-Specific Polysaccharide and Lipopolysaccharide of Vibrio cholerae O1 Ogawa in Adult Bangladeshi Recipients of an Oral Killed Cholera Vaccine and Comparison to Responses in Patients with Cholera
AN - 1647017392; 21184027
AB - Protective immunity to cholera is serogroup specific, and serogrouping is defined by the O-specific polysaccharide (OSP) of lipopolysaccharide (LPS). We characterized OSP-specific immune responses in adult recipients of an oral killed cholera vaccine (OCV WC-rBS) and compared these with responses in patients with cholera caused by Vibrio cholerae O1 Ogawa. Although vaccinees developed plasma immunoglobulin G (IgG), IgM, IgA antibody and antibody secreting cell (ASC, marker of mucosal response) to Ogawa OSP and LPS 7 days after vaccination, responses were significantly lower than that which occurred after cholera. Similarly, patients recovering from cholera had detectable IgA, IgM, and IgG memory B cell (MBC) responses against OSP and LPS on Day 30 and Day 90, whereas vaccinees only developed IgG responses to OSP 30 days after the second immunization. The markedly lower ASC and MBC responses to OSP and LPS observed among vaccinees might explain, in part, the lower protection of an OCV compared with natural infection.
JF - American Journal of Tropical Medicine and Hygiene
AU - Uddin, Taher
AU - Aktar, Amena
AU - Xu, Peng
AU - Johnson, Russell A
AU - Rahman, M Arifur
AU - Leung, Daniel T
AU - Afrin, Sadia
AU - Akter, Aklima
AU - Alam, Mohammad Murshid
AU - Rahman, Atiqur
AD - Centre for Vaccine Sciences, International Centre for Diarrhoeal Disease Research, Bangladesh (icddr,b), Dhaka, Bangladesh; NIDDK, LBC, National Institutes of Health, Bethesda, Maryland; Division of Infectious Diseases, Massachusetts General Hospital, Boston, Massachusetts; Departments of Medicine and Pediatrics, Harvard Medical School, Boston, Massachusetts; Department of Biochemistry and Molecular Biology, University of Dhaka, Bangladesh; Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts; Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 873
EP - 881
PB - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States
VL - 90
IS - 5
SN - 0002-9637, 0002-9637
KW - Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts B: Bacteriology; Immunology Abstracts; ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality
KW - Mucosa
KW - Immunological memory
KW - Disease control
KW - Infection
KW - Polysaccharides
KW - Lipopolysaccharides
KW - Cholera
KW - Pathogenic bacteria
KW - Lymphocytes B
KW - Bacterial diseases
KW - Memory cells
KW - Immunity
KW - Vaccination
KW - Vibrio cholerae
KW - Immunoglobulin A
KW - Antibodies
KW - Immunoglobulin G
KW - Immune response
KW - Vaccines
KW - Hygiene
KW - Immunoglobulin M
KW - F 06905:Vaccines
KW - K 03400:Human Diseases
KW - Q1 08484:Species interactions: parasites and diseases
KW - J 02350:Immunology
KW - Q5 08524:Public health, medicines, dangerous organisms
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.atitle=Immune+Responses+to+O-Specific+Polysaccharide+and+Lipopolysaccharide+of+Vibrio+cholerae+O1+Ogawa+in+Adult+Bangladeshi+Recipients+of+an+Oral+Killed+Cholera+Vaccine+and+Comparison+to+Responses+in+Patients+with+Cholera&rft.au=Uddin%2C+Taher%3BAktar%2C+Amena%3BXu%2C+Peng%3BJohnson%2C+Russell+A%3BRahman%2C+M+Arifur%3BLeung%2C+Daniel+T%3BAfrin%2C+Sadia%3BAkter%2C+Aklima%3BAlam%2C+Mohammad+Murshid%3BRahman%2C+Atiqur&rft.aulast=Uddin&rft.aufirst=Taher&rft.date=2014-05-01&rft.volume=90&rft.issue=5&rft.spage=873&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.13-0498
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-01-01
N1 - Last updated - 2016-03-17
N1 - SubjectsTermNotLitGenreText - Antibodies; Pathogenic bacteria; Bacterial diseases; Disease control; Immunity; Vaccines; Hygiene; Polysaccharides; Vaccination; Lymphocytes B; Mucosa; Immunological memory; Memory cells; Infection; Immunoglobulin A; Immunoglobulin G; Lipopolysaccharides; Cholera; Immune response; Immunoglobulin M; Vibrio cholerae
DO - http://dx.doi.org/10.4269/ajtmh.13-0498
ER -
TY - JOUR
T1 - Cannabis withdrawal in chronic, frequent cannabis smokers during sustained abstinence within a closed residential environment
AN - 1560134539; 19654335
AB - Objectives Chronic, frequent cannabis smokers may experience residual and offset effects, withdrawal, and craving when abstaining from the drug. We characterized the prevalence, duration, and intensity of these effects in chronic frequent cannabis smokers during abstinence on a closed research unit. Methods Non-treatment-seeking participants (N=29 on admission, 66% and 34% remaining after 2 and 4 weeks) provided subjective effects data. A battery of five instruments was computer-administered daily to measure psychological, sensory, and physical symptoms associated with cannabinoid intoxication and withdrawal. Plasma and oral fluid specimens were concurrently collected and analyzed for cannabinoids. Outcome variables were evaluated as change from admission (Day 0) with regression models. Results Most abstinence effects, including irritability and anxiety were greatest on Days 0-3 and decreased thereafter. Cannabis craving significantly decreased over time, whereas decreased appetite began to normalize on Day 4. Strange dreams and difficulty getting to sleep increased over time, suggesting intrinsic sleep problems in chronic cannabis smokers. Symptoms likely induced by residual drug effects were at maximum intensity on admission and positively correlated with plasma and oral fluid cannabinoid concentrations on admission but not afterward; these symptoms showed overall prevalence higher than cannabis withdrawal symptoms. Conclusions The combined influence of residual/offset drug effects, withdrawal, and craving was observed in chronic cannabis smokers during monitored abstinence. Abstinence symptoms were generally more intense in the initial phase, implying importance of early intervention in cannabis quit attempts. Sleep disturbance persisting for an extended period suggests that hypnotic medications could be beneficial in treating cannabis dependence. (Am J Addict 2014; 23:234-242)
JF - American Journal on Addictions
AU - Lee, Dayong
AU - Schroeder, Jennifer R
AU - Karschner, Erin L
AU - Goodwin, Robert S
AU - Hirvonen, Jussi
AU - Gorelick, David A
AU - Huestis, Marilyn A
AD - Chemistry and Drug Metabolism, National Institute on Drug Abuse, National Institute of Health, Baltimore, Maryland.
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 234
EP - 242
PB - Wiley Subscription Services, Inc., 1105 N Market St Wilmington DE 19801
VL - 23
IS - 3
SN - 1055-0496, 1055-0496
KW - Toxicology Abstracts
KW - Intoxication
KW - Dreams
KW - Data processing
KW - Addicts
KW - Anxiety
KW - Sleep disorders
KW - Withdrawal
KW - Hypnotics
KW - Drug abuse
KW - Appetite
KW - Models
KW - Cannabinoids
KW - Sleep
KW - Regression analysis
KW - Cannabis
KW - Addiction
KW - Drug addiction
KW - oral fluids
KW - X 24380:Social Poisons & Drug Abuse
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+on+Addictions&rft.atitle=Cannabis+withdrawal+in+chronic%2C+frequent+cannabis+smokers+during+sustained+abstinence+within+a+closed+residential+environment&rft.au=Lee%2C+Dayong%3BSchroeder%2C+Jennifer+R%3BKarschner%2C+Erin+L%3BGoodwin%2C+Robert+S%3BHirvonen%2C+Jussi%3BGorelick%2C+David+A%3BHuestis%2C+Marilyn+A&rft.aulast=Lee&rft.aufirst=Dayong&rft.date=2014-05-01&rft.volume=23&rft.issue=3&rft.spage=234&rft.isbn=&rft.btitle=&rft.title=American+Journal+on+Addictions&rft.issn=10550496&rft_id=info:doi/10.1111%2Fj.1521-0391.2014.12088.x
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-09-01
N1 - Last updated - 2014-10-02
N1 - SubjectsTermNotLitGenreText - Intoxication; Dreams; Data processing; Sleep disorders; Anxiety; Addicts; Withdrawal; Hypnotics; Appetite; Drug abuse; Models; Cannabinoids; Sleep; Cannabis; Regression analysis; Addiction; Drug addiction; oral fluids
DO - http://dx.doi.org/10.1111/j.1521-0391.2014.12088.x
ER -
TY - JOUR
T1 - Reduced fatalism and increased prevention behavior after two high-profile lung cancer events
AN - 1536010727; 4569283
AB - The positive impact of media coverage of high-profile cancer events on cancer prevention behaviors is well-established. However, less work has focused on potential adverse psychological reactions to such events, such as fatalism. Conducting 3 studies, the authors explored how the lung cancer death of Peter Jennings and diagnosis of Dana Reeve in 2005 related to fatalism. Analysis of a national media sample in Study 1 found that media coverage of these events often focused on reiterating the typical profile of those diagnosed with lung cancer; 38% of the media mentioned at least 1 known risk factor for lung cancer, most often smoking. Data from a nationally representative survey in Study 2 found that respondents reported lower lung cancer fatalism, after, compared with before, the events (OR = 0.16, 95% CI [0.03, 0.93]). A sustained increase in call volume to the national tobacco Quitline after these events was found in Study 3. These results suggest that there is a temporal association between high-profile cancer events, the subsequent media coverage, psychological outcomes, and cancer prevention behaviors. These results suggest that high-profile cancer events could be leveraged as an opportunity for large-scale public heath communication campaigns through the dissemination of cancer prevention messages and services. Reprinted by permission of Taylor & Francis Ltd.
JF - Journal of health communication
AU - Portnoy, David B
AU - Leach, Corinne R
AU - Kaufman, Annette R
AU - Moser, Richard P
AU - Alfano, Catherine M
AD - US National Institutes of Health
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 577
EP - 592
VL - 19
IS - 5
SN - 1081-0730, 1081-0730
KW - Sociology
KW - Death
KW - Prevention
KW - Fatalism
KW - Cancer
KW - Public health
KW - Media coverage
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1536010727?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+health+communication&rft.atitle=Reduced+fatalism+and+increased+prevention+behavior+after+two+high-profile+lung+cancer+events&rft.au=Portnoy%2C+David+B%3BLeach%2C+Corinne+R%3BKaufman%2C+Annette+R%3BMoser%2C+Richard+P%3BAlfano%2C+Catherine+M&rft.aulast=Portnoy&rft.aufirst=David&rft.date=2014-05-01&rft.volume=19&rft.issue=5&rft.spage=577&rft.isbn=&rft.btitle=&rft.title=Journal+of+health+communication&rft.issn=10810730&rft_id=info:doi/10.1080%2F10810730.2013.821553
LA - English
DB - International Bibliography of the Social Sciences (IBSS)
N1 - Date revised - 2014-06-16
N1 - Last updated - 2014-06-17
N1 - SubjectsTermNotLitGenreText - Media coverage; 10449 5772; 1939 3617 6220; 10072; 3303; 4825 10777 1547 10792
DO - http://dx.doi.org/10.1080/10810730.2013.821553
ER -
TY - JOUR
T1 - Prediagnostic lifestyle factors and survival after colon and rectal cancer diagnosis in the National Institutes of Health (NIH)-AARP Diet and Health Study
AN - 1534857187; 19822178
AB - BACKGROUND Few studies have examined the relationship of lifestyle factors with mortality among patients with colorectal cancer. METHODS Among NIH-AARP Diet and Health study participants, 4213 colon and 1514 rectal cancer cases were identified through linkage to state cancer registries and determined date and cause of death using the National Death Index. Lifestyle factors were assessed at baseline and included: healthy diet (measured by Healthy Eating Index 2005 [HEI-2005]), body mass index (BMI), physical activity, alcohol consumption and smoking. The association of factors was examined individually and combined into a lifestyle score with 5-year mortality from all-causes, colorectal cancer, and cardiovascular disease (CVD). Relative risks (RRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazards models. RESULTS Among colon cancer survivors, smokers had increased risk of total mortality (RR=1.74; 95% CI=1.45-2.08) and colorectal cancer mortality (RR=1.46; 95% CI=1.17-1.82), compared to never smokers. Obese (BMI, greater than or equal to 30) individuals had increased risk of all death (RR=1.19; 95% CI=1.02-1.39) and CVD death (RR=1.84; 95% CI=1.05-3.23), compared to normal weight (BMI, 18.5 to<25) individuals. Compared to those with the lowest lifestyle score, those with the highest score had a 34% lower risk of all-cause mortality (RR=0.66; 95% CI=0.50-0.87). Among rectal cancer survivors, individuals in the highest quintile of HEI-2005 scores had reduced all-cause mortality (RR=0.60; 95% CI=0.42-0.86) compared to those in the lowest. Higher combined lifestyle scores were associated with a 46% lower risk of total mortality (0.54; 0.32-0.91). CONCLUSIONS Healthier lifestyle before cancer diagnosis was associated with improved overall survival after diagnosis with colorectal cancer. Cancer 2014; 120:1540-1547 2014. Several modifiable lifestyle factors measured prediagnosis were related to survival among patients with colorectal cancer. A combined lifestyle score consisting of meeting recommendations for diet, body weight, physical activity, alcohol intake, and smoking was also associated with reduced all-cause mortality.
JF - Cancer
AU - Pelser, Colleen
AU - Arem, Hannah
AU - Pfeiffer, Ruth M
AU - Elena, Joanne W
AU - Alfano, Catherine M
AU - Hollenbeck, Albert R
AU - Park, Yikyung
AD - Cancer Prevention Fellowship Program, Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland.
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 1540
EP - 1547
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 120
IS - 10
SN - 0008-543X, 0008-543X
KW - Health & Safety Science Abstracts; Risk Abstracts
KW - Diets
KW - Risk assessment
KW - Obesity
KW - Alcohol
KW - Mortality
KW - Physical activity
KW - Survival
KW - Cancer
KW - Smoking
KW - Health risks
KW - Body weight
KW - Risk factors
KW - Colorectal carcinoma
KW - Cardiovascular diseases
KW - H 11000:Diseases/Injuries/Trauma
KW - R2 23060:Medical and environmental health
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer&rft.atitle=Prediagnostic+lifestyle+factors+and+survival+after+colon+and+rectal+cancer+diagnosis+in+the+National+Institutes+of+Health+%28NIH%29-AARP+Diet+and+Health+Study&rft.au=Pelser%2C+Colleen%3BArem%2C+Hannah%3BPfeiffer%2C+Ruth+M%3BElena%2C+Joanne+W%3BAlfano%2C+Catherine+M%3BHollenbeck%2C+Albert+R%3BPark%2C+Yikyung&rft.aulast=Pelser&rft.aufirst=Colleen&rft.date=2014-05-01&rft.volume=120&rft.issue=10&rft.spage=1540&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/10.1002%2Fcncr.28573
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-01
N1 - Last updated - 2014-06-26
N1 - SubjectsTermNotLitGenreText - Risk assessment; Diets; Mortality; Alcohol; Obesity; Physical activity; Survival; Cancer; Health risks; Smoking; Body weight; Risk factors; Colorectal carcinoma; Cardiovascular diseases
DO - http://dx.doi.org/10.1002/cncr.28573
ER -
TY - JOUR
T1 - Visiting Again? Subjective Well-Being of Children in Elementary School and Repeated Visits to School Health Nurses
AN - 1531918783; 201413853
AB - Children with vague complaints are without chronic illness, and who repeatedly visit the school nurse may be at risk for limited academic success. This study compares student reports of subjective well-being between children who do and do not repeatedly visit the school nurse with vague complaints. Children in grades 4 through 6 completed the School Well-Being Profile-American English (SWBP-AE), a questionnaire with 4 well-being subscales: health status, school environment, social relationships, and school as a means of self-fulfillment. School nurses extracted data on clinic visits from clinic records. Logistic regression explored associations between well-being subscales and repeated visits to the school nurse. Of the 320 students participating in the study, 33 (12.04%) students made repeated visits to the school nurse. Perception of health status (OR = 2.072; 95% CI = 1.037, 4.163) was the only significant (p < .05) predictor of repeated visits to the nurse. Children with poor perception of their health status are more likely to repeatedly visit the school nurse. Children's perceptions of their school environment, social relationships, or school as a means of self-fulfillment are not statistically significant predictors of repeated visits to the school nurse. Adapted from the source document.
JF - Journal of School Health
AU - Leaver, Cynthia A
AD - National Institute of Nursing Research, National Institutes of Health, Division of Intramural Research
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 294
EP - 301
PB - Wiley-Blackwell, UK
VL - 84
IS - 5
SN - 0022-4391, 0022-4391
KW - Social relationships
KW - Wellbeing
KW - Health status
KW - School nurses
KW - Clinics
KW - Children
KW - article
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1531918783?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+School+Health&rft.atitle=Visiting+Again%3F+Subjective+Well-Being+of+Children+in+Elementary+School+and+Repeated+Visits+to+School+Health+Nurses&rft.au=Leaver%2C+Cynthia+A&rft.aulast=Leaver&rft.aufirst=Cynthia&rft.date=2014-05-01&rft.volume=84&rft.issue=5&rft.spage=294&rft.isbn=&rft.btitle=&rft.title=Journal+of+School+Health&rft.issn=00224391&rft_id=info:doi/10.1111%2Fjosh.12150
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Date revised - 2014-06-01
N1 - Last updated - 2016-09-27
N1 - SubjectsTermNotLitGenreText - School nurses; Children; Wellbeing; Health status; Clinics; Social relationships
DO - http://dx.doi.org/10.1111/josh.12150
ER -
TY - JOUR
T1 - A problem-solving education intervention in caregivers and patients during allogeneic hematopoietic stem cell transplantation
AN - 1531431165; 4565572
AB - The aim of this study was to determine the effect of problem-solving education on self-efficacy and distress in informal caregivers of allogeneic hematopoietic stem cell transplantation patients. Patient/caregiver teams attended three 1-hour problem-solving education sessions to help cope with problems during hematopoietic stem cell transplantation. Primary measures included the Cancer Self-Efficacy Scale-transplant and Brief Symptom Inventory-18. Active caregivers reported improvements in self-efficacy (p Reprinted by permission of Sage Publications Ltd
JF - Journal of health psychology
AU - Bevans, Margaret
AU - Wehrlen, Leslie
AU - Castro, Kathleen
AU - Prince, Patricia
AU - Shelburne, Nonniekaye
AU - Soeken, Karen
AU - Zabora, James
AU - Wallen, Gwenyth R
AD - National Institutes of Health Clinical Center ; National Cancer Institute ; University of Maryland ; Inova Health System
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 602
EP - 617
VL - 19
IS - 5
SN - 1359-1053, 1359-1053
KW - Sociology
KW - Anxiety
KW - Survival strategy
KW - Caring
KW - Problem solving
KW - Family
KW - Patients
KW - Cancer
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+health+psychology&rft.atitle=A+problem-solving+education+intervention+in+caregivers+and+patients+during+allogeneic+hematopoietic+stem+cell+transplantation&rft.au=Bevans%2C+Margaret%3BWehrlen%2C+Leslie%3BCastro%2C+Kathleen%3BPrince%2C+Patricia%3BShelburne%2C+Nonniekaye%3BSoeken%2C+Karen%3BZabora%2C+James%3BWallen%2C+Gwenyth+R&rft.aulast=Bevans&rft.aufirst=Margaret&rft.date=2014-05-01&rft.volume=19&rft.issue=5&rft.spage=602&rft.isbn=&rft.btitle=&rft.title=Journal+of+health+psychology&rft.issn=13591053&rft_id=info:doi/10.1177%2F1359105313475902
LA - English
DB - International Bibliography of the Social Sciences (IBSS)
N1 - Date revised - 2014-06-02
N1 - Last updated - 2014-06-03
N1 - SubjectsTermNotLitGenreText - 1147 4196; 1939 3617 6220; 12432; 4748; 10220; 9271 7890 5792 10484; 2039 13521
DO - http://dx.doi.org/10.1177/1359105313475902
ER -
TY - JOUR
T1 - Assurance of neuroattenuation of a live vaccine against West Nile virus: A comprehensive study of neuropathogenesis after infection with chimeric WN/DEN4 Delta 30 vaccine in comparison to two parental viruses and a surrogate flavivirus reference vaccine
AN - 1529943856; 19862597
AB - The upsurge of West Nile virus (WNV) human infections in 2012 suggests that the US can expect periodic WNV outbreaks in the future. Availability of safe and effective vaccines against WNV in endemic areas, particularly for aging populations that are at high risk of West Nile neuroinvasive disease (WNND), could be beneficial. WN/DEN4 Delta 30 is a live, attenuated chimeric vaccine against WNV produced by replacement of the genes encoding the pre-membrane and envelope protein genes of the vaccine virus against dengue virus type 4 (DEN4 Delta 30) with corresponding sequences derived from a wild type WNV. Following intrathalamic inoculation of nonhuman primates (NHPs), a comprehensive neuropathogenesis study was performed and neurovirulence of WN/DEN4 Delta 30 vaccine candidate was compared to that of two parental viruses (i.e., WNV and DEN4 Delta 30), as well as to that of an attenuated flavivirus surrogate reference (i.e., yellow fever YF 17D). Clinical and virological data, as well as results of a semi-quantitative histopathological analysis, demonstrated that WN/DEN4 Delta 30 vaccine is highly attenuated for the central nervous system (CNS) of NHPs in comparison to a wild type WNV. Importantly, based on the virus replicative ability in the CNS of NHPs and the degree of induced histopathological changes, the level of neuroattenuation of WN/DEN4 Delta 30 vaccine was similar to that of YF 17D, and therefore within an acceptable range. In addition, we show that the DEN4 Delta 30 vaccine tested in this study also has a low neurovirulence profile. In summary, our results demonstrate a high level of neuroattenuation of two vaccine candidates, WN/DEN4 Delta 30 and DEN4 Delta 30. We also show here a remarkable sensitivity of our WNV-NY99 NHP model, as well as striking resemblance of the observed neuropathology to that seen in human WNND. These results support the use of this NHP model for translational studies of WNV neuropathogenesis and/or testing the effectiveness of vaccines and therapeutic approaches.
JF - Vaccine
AU - Maximova, Olga A
AU - Speicher, James M
AU - Skinner, Jeff R
AU - Murphy, Brian R
AU - St Claire, Marisa C
AU - Ragland, Danny R
AU - Herbert, Richard L
AU - Pare, Dan R
AU - Moore, Rashida M
AU - Pletnev, Alexander G
AD - Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, United States
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 3187
EP - 3197
PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom
VL - 32
IS - 26
SN - 0264-410X, 0264-410X
KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Virology & AIDS Abstracts; Immunology Abstracts
KW - West Nile virus (WNV)
KW - Live attenuated WNV vaccine
KW - Neuropathogenesis
KW - Neurovirulence
KW - Nonhuman primates
KW - Translation
KW - Central nervous system
KW - Invasiveness
KW - Viruses
KW - Aging
KW - Animal models
KW - Disease control
KW - Histopathology
KW - Infection
KW - Flavivirus
KW - Public health
KW - Endemic species
KW - Risk factors
KW - Yellow fever
KW - Envelope protein
KW - Neuropathology
KW - Dengue virus type 4
KW - Data processing
KW - Environmental impact
KW - Inoculation
KW - Vaccines
KW - West Nile virus
KW - F 06905:Vaccines
KW - Q1 08423:Behaviour
KW - Q5 08524:Public health, medicines, dangerous organisms
KW - V 22310:Genetics, Taxonomy & Structure
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Vaccine&rft.atitle=Assurance+of+neuroattenuation+of+a+live+vaccine+against+West+Nile+virus%3A+A+comprehensive+study+of+neuropathogenesis+after+infection+with+chimeric+WN%2FDEN4+Delta+30+vaccine+in+comparison+to+two+parental+viruses+and+a+surrogate+flavivirus+reference+vaccine&rft.au=Maximova%2C+Olga+A%3BSpeicher%2C+James+M%3BSkinner%2C+Jeff+R%3BMurphy%2C+Brian+R%3BSt+Claire%2C+Marisa+C%3BRagland%2C+Danny+R%3BHerbert%2C+Richard+L%3BPare%2C+Dan+R%3BMoore%2C+Rashida+M%3BPletnev%2C+Alexander+G&rft.aulast=Maximova&rft.aufirst=Olga&rft.date=2014-05-01&rft.volume=32&rft.issue=26&rft.spage=3187&rft.isbn=&rft.btitle=&rft.title=Vaccine&rft.issn=0264410X&rft_id=info:doi/10.1016%2Fj.vaccine.2014.04.002
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-05-01
N1 - Last updated - 2016-12-22
N1 - SubjectsTermNotLitGenreText - Central nervous system; Endemic species; Aging; Viruses; Environmental impact; Disease control; Histopathology; Vaccines; Public health; Translation; Invasiveness; Data processing; Neuropathogenesis; Animal models; Neurovirulence; Infection; Yellow fever; Risk factors; Envelope protein; Inoculation; Neuropathology; West Nile virus; Flavivirus; Dengue virus type 4
DO - http://dx.doi.org/10.1016/j.vaccine.2014.04.002
ER -
TY - JOUR
T1 - Humans and Ferrets with Prior H1N1 Influenza Virus Infections Do Not Exhibit Evidence of Original Antigenic Sin after Infection or Vaccination with the 2009 Pandemic H1N1 Influenza Virus
AN - 1529934374; 19846340
AB - The hypothesis of original antigenic sin (OAS) states that the imprint established by an individual's first influenza virus infection governs the antibody response thereafter. Subsequent influenza virus infection results in an antibody response against the original infecting virus and an impaired immune response against the newer influenza virus. The purpose of our study was to seek evidence of OAS after infection or vaccination with the 2009 pandemic H1N1 (2009 pH1N1) virus in ferrets and humans previously infected with H1N1 viruses with various antigenic distances from the 2009 pH1N1 virus, including viruses from 1935 through 1999. In ferrets, seasonal H1N1 priming did not diminish the antibody response to infection or vaccination with the 2009 pH1N1 virus, nor did it diminish the T-cell response, indicating the absence of OAS in seasonal H1N1 virus-primed ferrets. Analysis of paired samples of human serum taken before and after vaccination with a monovalent inactivated 2009 pH1N1 vaccine showed a significantly greater-fold rise in the titer of antibody against the 2009 pH1N1 virus than against H1N1 viruses that circulated during the childhood of each subject. Thus, prior experience with H1N1 viruses did not result in an impairment of the antibody response against the 2009 pH1N1 vaccine. Our data from ferrets and humans suggest that prior exposure to H1N1 viruses did not impair the immune response against the 2009 pH1N1 virus.
JF - Clinical and Vaccine Immunology
AU - O'Donnell, Christopher D
AU - Wright, Amber
AU - Vogel, Leatrice
AU - Boonnak, Kobporn
AU - Treanor, John J
AU - Subbarao, Kanta
AD - Laboratory of Infectious Diseases, NIAID, Bethesda, Maryland, USA, ksubbarao@niaid.nih.gov.
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 737
EP - 746
PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL - 21
IS - 5
SN - 1556-679X, 1556-679X
KW - Health & Safety Science Abstracts; Virology & AIDS Abstracts; Immunology Abstracts
KW - Data processing
KW - Immunology
KW - Viruses
KW - Antibody response
KW - Infection
KW - Children
KW - Vaccination
KW - Influenza
KW - pandemics
KW - Influenza virus
KW - Sulfur dioxide
KW - Mustela
KW - Lymphocytes T
KW - Vaccines
KW - Immune response
KW - Seasonal variations
KW - V 22350:Immunology
KW - F 06905:Vaccines
KW - H 4000:Food and Drugs
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-05-01
N1 - Number of references - 55
N1 - Last updated - 2014-08-21
N1 - SubjectsTermNotLitGenreText - Influenza; pandemics; Data processing; Lymphocytes T; Immune response; Vaccines; Antibody response; Children; Infection; Vaccination; Sulfur dioxide; Immunology; Viruses; Seasonal variations; Influenza virus; Mustela
DO - http://dx.doi.org/10.1128/CVI.00790-13
ER -
TY - JOUR
T1 - Consultation on dengue vaccines: Progress in understanding protection, 26-28 June 2013, Rockville, Maryland
AN - 1529927661; 19862614
AB - There is an unmet need for a dengue vaccine to further prevent the spread of this disease and contain the growing pandemic. To this end several vaccine companies and academic groups are actively pursuing the development of a tetravalent vaccine to prevent dengue. In the last few years progress has been made in this area, including the first results of a vaccine efficacy trial and improved understanding of the immune responses to the infection. Despite this progress, development of dengue vaccines faces important challenges including the need for a vaccine that induces balanced immune responses against all dengue strains and an incomplete understanding of the mechanism(s) of protection against infection and disease. This is a summary of a Consultation on dengue vaccines held in June 26-28, 2013 by the National Institute of Allergy and Infectious Diseases (part of the US National Institutes of Health) and the Dengue Vaccine Initiative (part of the International Vaccine Institute). The primary goal of this consultation was to review the progress in dengue vaccine development, evaluate the known mechanism of protection of dengue vaccines and discuss avenues for future research.
JF - Vaccine
AU - Cassetti, MCristina
AU - Halstead, Scott B
AD - National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 3115
EP - 3121
PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom
VL - 32
IS - 26
SN - 0264-410X, 0264-410X
KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Health & Safety Science Abstracts; Virology & AIDS Abstracts; Immunology Abstracts
KW - Dengue
KW - Dengue virus
KW - Dengue hemorrhagic fever
KW - Severe dengue
KW - Vaccine
KW - Immunopathogenesis
KW - Acquired immunity
KW - T cell immunity
KW - Innate immunity
KW - Human diseases
KW - Disease control
KW - Infection
KW - Allergies
KW - Public health
KW - Disease transmission
KW - Allergic reactions
KW - Hypersensitivity
KW - pandemics
KW - Infectious diseases
KW - USA, Maryland, Rockville
KW - USA, Maryland
KW - Strains
KW - ANW, USA, Maryland
KW - Reviews
KW - Immune response
KW - Vaccines
KW - V 22350:Immunology
KW - Q1 08423:Behaviour
KW - F 06910:Microorganisms & Parasites
KW - Q5 08524:Public health, medicines, dangerous organisms
KW - H 4000:Food and Drugs
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-05-01
N1 - Last updated - 2016-12-22
N1 - SubjectsTermNotLitGenreText - Allergic reactions; Human diseases; Infectious diseases; Disease control; Vaccines; Strains; Disease transmission; Public health; pandemics; Hypersensitivity; Dengue; Reviews; Immune response; Infection; Allergies; USA, Maryland, Rockville; USA, Maryland; ANW, USA, Maryland
DO - http://dx.doi.org/10.1016/j.vaccine.2014.04.017
ER -
TY - JOUR
T1 - Nucleophosmin modulates stability, activity, and nucleolar accumulation of base excision repair proteins.
AN - 1524821577; 24648491
AB - Nucleophosmin (NPM1) is a multifunctional protein that controls cell growth and genome stability via a mechanism that involves nucleolar-cytoplasmic shuttling. It is clear that NPM1 also contributes to the DNA damage response, yet its exact function is poorly understood. We recently linked NPM1 expression to the functional activation of the major abasic endonuclease in mammalian base excision repair (BER), apurinic/apyrimidinic endonuclease 1 (APE1). Here we unveil a novel role for NPM1 as a modulator of the whole BER pathway by 1) controlling BER protein levels, 2) regulating total BER capacity, and 3) modulating the nucleolar localization of several BER enzymes. We find that cell treatment with the genotoxin cisplatin leads to concurrent relocalization of NPM1 and BER components from nucleoli to the nucleoplasm, and cellular experiments targeting APE1 suggest a role for the redistribution of nucleolar BER factors in determining cisplatin toxicity. Finally, based on the use of APE1 as a representative protein of the BER pathway, our data suggest a function for BER proteins in the regulation of ribogenesis.
© 2014 Poletto et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).
JF - Molecular biology of the cell
AU - Poletto, Mattia
AU - Lirussi, Lisa
AU - Wilson, David M
AU - Tell, Gianluca
AD - Department of Medical and Biological Sciences, University of Udine, Udine 33100, Italy. ; Laboratory of Molecular Gerontology, National Institute on Aging, Intramural Research Program, National Institutes of Health, Baltimore, MD 21224. ; Department of Medical and Biological Sciences, University of Udine, Udine 33100, Italy gianluca.tell@uniud.it.
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 1641
EP - 1652
VL - 25
IS - 10
KW - Cross-Linking Reagents
KW - 0
KW - Nuclear Proteins
KW - RNA, Small Interfering
KW - Tumor Suppressor Protein p53
KW - nucleophosmin
KW - 117896-08-9
KW - Fen1 protein, mouse
KW - EC 3.1.-
KW - Flap Endonucleases
KW - Apex1 protein, mouse
KW - EC 4.2.99.18
KW - DNA-(Apurinic or Apyrimidinic Site) Lyase
KW - DNA Ligases
KW - EC 6.5.1.-
KW - DNA Ligase ATP
KW - EC 6.5.1.1
KW - Doxycycline
KW - N12000U13O
KW - Cisplatin
KW - Q20Q21Q62J
KW - Index Medicus
KW - Animals
KW - Flap Endonucleases -- biosynthesis
KW - HeLa Cells
KW - Humans
KW - Cell Nucleolus -- genetics
KW - Cross-Linking Reagents -- pharmacology
KW - Doxycycline -- pharmacology
KW - Mice
KW - DNA Damage -- genetics
KW - DNA Ligases -- biosynthesis
KW - Ribosomes -- genetics
KW - Protein Transport -- genetics
KW - Cisplatin -- pharmacology
KW - DNA Ligases -- metabolism
KW - Tumor Suppressor Protein p53 -- genetics
KW - RNA Interference
KW - Flap Endonucleases -- metabolism
KW - DNA Repair -- genetics
KW - DNA-(Apurinic or Apyrimidinic Site) Lyase -- genetics
KW - Nuclear Proteins -- genetics
KW - DNA-(Apurinic or Apyrimidinic Site) Lyase -- metabolism
KW - DNA-(Apurinic or Apyrimidinic Site) Lyase -- biosynthesis
KW - Nuclear Proteins -- biosynthesis
KW - Nuclear Proteins -- metabolism
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+biology+of+the+cell&rft.atitle=Nucleophosmin+modulates+stability%2C+activity%2C+and+nucleolar+accumulation+of+base+excision+repair+proteins.&rft.au=Poletto%2C+Mattia%3BLirussi%2C+Lisa%3BWilson%2C+David+M%3BTell%2C+Gianluca&rft.aulast=Poletto&rft.aufirst=Mattia&rft.date=2014-05-01&rft.volume=25&rft.issue=10&rft.spage=1641&rft.isbn=&rft.btitle=&rft.title=Molecular+biology+of+the+cell&rft.issn=1939-4586&rft_id=info:doi/10.1091%2Fmbc.E13-12-0717
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-01-13
N1 - Date created - 2014-05-14
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1091/mbc.E13-12-0717
ER -
TY - JOUR
T1 - Fine-tuning of epigenetic regulation with respect to promoter CpG content in a cell type-specific manner.
AN - 1524817136; 24521667
AB - Epigenetic regulation of gene expression is fundamental for cell type-specific gene expression. However, integrated comparative transcriptomic and epigenomic analyses in various adult primary differentiated cells remain underrepresented. We generated promoter landscapes of DNA methylation and three important histone methylation marks (H3K4me3, H3K9me2, and H3K27me3) in two primary cell types (B lymphocytes and liver) from adult mice. In line with previous studies, we also observed distinct H3K4me3 patterns at promoters dictated by CpG content in differentiated primary cells. We further explored the distribution of initiating RNA polymerase II and elongating RNA polymerase II across genes within different promoter classes, suggesting different rate-limiting steps at CpG-rich vs. CpG-poor genes. Examination of differentially expressed genes revealed that regulation of tissue-specific genes is closely related to gene function regardless of promoter type. Although repressive chromatin marks displayed differential preference to promoters based on CpG content, we observed fine-tuning of the pattern of association of these marks with specific promoter types in a cell type-specific manner. The distribution of H3K9me2 and H3K27me3, relative to CpG content, differed substantially between the two cell types. Cell-type specific accumulation of repressive chromatin marks was also observed at silent genes in both cell types, suggesting that differentiated primary cells may exhibit cell-type specificity in the distribution of repressive chromatin marks. Epigenetic regulation of gene expression and the association of specific histone marks with promoter sequence classes are fine-tuned in a cell type-specific manner. This unexpected finding underscores the value of extensive study of epigenetic marks across cell and tissue types.
JF - Epigenetics
AU - Li, Ruifang
AU - Mav, Deepak
AU - Grimm, Sara A
AU - Jothi, Raja
AU - Shah, Ruchir
AU - Wade, Paul A
AD - Laboratory of Molecular Carcinogenesis; National Institute of Environmental Health Sciences; Research Triangle Park, NC USA. ; SRA International; Research Triangle Park, NC USA. ; Integrative Bioinformatics; National Institute of Environmental Health Sciences; Research Triangle Park, NC USA. ; Laboratory of Molecular Carcinogenesis; National Institute of Environmental Health Sciences; Research Triangle Park, NC USA; Biostatistics Branch; National Institute of Environmental Health Sciences; Research Triangle Park, NC USA.
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 747
EP - 759
VL - 9
IS - 5
KW - Histones
KW - 0
KW - RNA Polymerase II
KW - EC 2.7.7.-
KW - Index Medicus
KW - CpG content
KW - promoter
KW - epigenetics
KW - transcription regulation
KW - CpG island
KW - RNA Polymerase II -- metabolism
KW - Animals
KW - DNA Methylation
KW - Histones -- metabolism
KW - Mice, Inbred C57BL
KW - Organ Specificity
KW - Gene Expression Regulation
KW - Male
KW - Histones -- genetics
KW - Promoter Regions, Genetic
KW - Liver -- cytology
KW - B-Lymphocytes -- cytology
KW - CpG Islands
KW - Liver -- metabolism
KW - B-Lymphocytes -- metabolism
KW - Epigenesis, Genetic
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Epigenetics&rft.atitle=Fine-tuning+of+epigenetic+regulation+with+respect+to+promoter+CpG+content+in+a+cell+type-specific+manner.&rft.au=Li%2C+Ruifang%3BMav%2C+Deepak%3BGrimm%2C+Sara+A%3BJothi%2C+Raja%3BShah%2C+Ruchir%3BWade%2C+Paul+A&rft.aulast=Li&rft.aufirst=Ruifang&rft.date=2014-05-01&rft.volume=9&rft.issue=5&rft.spage=747&rft.isbn=&rft.btitle=&rft.title=Epigenetics&rft.issn=1559-2308&rft_id=info:doi/10.4161%2Fepi.28075
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-01-10
N1 - Date created - 2014-05-14
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Genes Dev. 2011 May 15;25(10):1010-22 [21576262]
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Cell. 1999 Oct 29;99(3):247-57 [10555141]
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Cell. 1992 Jun 12;69(6):915-26 [1606615]
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Cancer Res. 2006 Aug 15;66(16):7939-47 [16912168]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.4161/epi.28075
ER -
TY - JOUR
T1 - Single-dose live-attenuated Nipah virus vaccines confer complete protection by eliciting antibodies directed against surface glycoproteins
AN - 1524434240; 19753917
AB - Background Nipah virus (NiV), a zoonotic pathogen causing severe respiratory illness and encephalitis in humans, emerged in Malaysia in 1998 with subsequent outbreaks on an almost annual basis since 2001 in parts of the Indian subcontinent. The high case fatality rate, human-to-human transmission, wide-ranging reservoir distribution and lack of licensed intervention options are making NiV a serious regional and potential global public health problem. The objective of this study was to develop a fast-acting, single-dose NiV vaccine that could be implemented in a ring vaccination approach during outbreaks. Methods In this study we have designed new live-attenuated vaccine vectors based on recombinant vesicular stomatitis viruses (rVSV) expressing NiV glycoproteins (G or F) or nucleoprotein (N) and evaluated their protective efficacy in Syrian hamsters, an established NiV animal disease model. We further characterized the humoral immune response to vaccination in hamsters using ELISA and neutralization assays and performed serum transfer studies. Results Vaccination of Syrian hamsters with a single dose of the rVSV vaccine vectors resulted in strong humoral immune responses with neutralizing activities found only in those animals vaccinated with rVSV expressing NiV G or F proteins. Vaccinated animals with neutralizing antibody responses were completely protected from lethal NiV disease, whereas animals vaccinated with rVSV expressing NiV N showed only partial protection. Protection of NiV G or F vaccinated animals was conferred by antibodies, most likely the neutralizing fraction, as demonstrated by serum transfer studies. Protection of N-vaccinated hamsters was not antibody-dependent indicating a role of adaptive cellular responses for protection. Conclusions The rVSV vectors expressing Nipah virus G or F are prime candidates for new 'emergency vaccines' to be utilized for NiV outbreak management.
JF - Vaccine
AU - DeBuysscher, Blair L
AU - Scott, Dana
AU - Marzi, Andrea
AU - Prescott, Joseph
AU - Feldmann, Heinz
AD - Laboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rocky Mountain Laboratories, Hamilton, MT, USA
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 2637
EP - 2644
PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom
VL - 32
IS - 22
SN - 0264-410X, 0264-410X
KW - Health & Safety Science Abstracts; Virology & AIDS Abstracts; Immunology Abstracts
KW - glycoprotein G
KW - Viruses
KW - Nucleoproteins
KW - Animal models
KW - Intervention
KW - Disease transmission
KW - Public health
KW - Vesicular stomatitis
KW - Glycoproteins
KW - Immune response (humoral)
KW - Neutralization
KW - Reservoirs
KW - Mortality
KW - Enzyme-linked immunosorbent assay
KW - F protein
KW - Vectors
KW - Pathogens
KW - ISEW, Malaysia
KW - Encephalitis
KW - Antibodies
KW - Nipah virus
KW - Proteins
KW - Immune response
KW - Outbreaks
KW - Vaccines
KW - Animal diseases
KW - V 22350:Immunology
KW - F 06905:Vaccines
KW - H 1000:Occupational Safety and Health
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Vaccine&rft.atitle=Single-dose+live-attenuated+Nipah+virus+vaccines+confer+complete+protection+by+eliciting+antibodies+directed+against+surface+glycoproteins&rft.au=DeBuysscher%2C+Blair+L%3BScott%2C+Dana%3BMarzi%2C+Andrea%3BPrescott%2C+Joseph%3BFeldmann%2C+Heinz&rft.aulast=DeBuysscher&rft.aufirst=Blair&rft.date=2014-05-01&rft.volume=32&rft.issue=22&rft.spage=2637&rft.isbn=&rft.btitle=&rft.title=Vaccine&rft.issn=0264410X&rft_id=info:doi/10.1016%2Fj.vaccine.2014.02.087
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-05-01
N1 - Last updated - 2014-08-21
N1 - SubjectsTermNotLitGenreText - glycoprotein G; Enzyme-linked immunosorbent assay; Nucleoproteins; F protein; Animal models; Vectors; Pathogens; Encephalitis; Public health; Disease transmission; Vesicular stomatitis; Antibodies; Glycoproteins; Vaccines; Immune response (humoral); Mortality; Viruses; Intervention; Proteins; Outbreaks; Immune response; Reservoirs; Neutralization; Animal diseases; Nipah virus; ISEW, Malaysia
DO - http://dx.doi.org/10.1016/j.vaccine.2014.02.087
ER -
TY - JOUR
T1 - Brief Report: Loss of p15Ink4b Accelerates Development of Myeloid Neoplasms in Nup98-HoxD13 Transgenic Mice
AN - 1524416715; 19752648
AB - Homeostasis of hematopoietic stem and progenitor cells is a tightly regulated process. The disturbance of the balance in the hematopoietic progenitor pool can result in favorable conditions for development of diseases such as myelodysplastic syndromes and leukemia. It has been shown recently that mice lacking p15Ink4b have skewed differentiation of common myeloid progenitors toward the myeloid lineage at the expense of erythroid progenitors. The lack of p15INK4B expression in human leukemic blasts has been linked to poor prognosis and increased risk of myelodysplastic syndromes transformation to acute myeloid leukemia. However, the role of p15Ink4b in disease development is just beginning to be elucidated. This study examines the collaboration of the loss of p15Ink4b with Nup98-HoxD13 translocation in the development of hematological malignancies in a mouse model. Here, we report that loss of p15Ink4b collaborates with Nup98-HoxD13 transgene in the development of predominantly myeloid neoplasms, namely acute myeloid leukemia, myeloproliferative disease, and myelodysplastic syndromes. This mouse model could be a very valuable tool for studying p15Ink4b function in tumorigenesis as well as preclinical drug testing. Stem Cells 2014; 32:1361-1366
JF - Stem Cells
AU - Humeniuk, Rita
AU - Koller, Richard
AU - Bies, Juraj
AU - Aplan, Peter
AU - Wolff, Linda
AD - National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 1361
EP - 1366
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 32
IS - 5
SN - 1066-5099, 1066-5099
KW - Genetics Abstracts; Biotechnology and Bioengineering Abstracts
KW - Transformation
KW - Acute myeloid leukemia
KW - Tumorigenesis
KW - Transgenes
KW - Animal models
KW - Prognosis
KW - Homeostasis
KW - Transgenic mice
KW - Differentiation
KW - Myelodysplastic syndrome
KW - Malignancy
KW - Stem cells
KW - Hemopoiesis
KW - Myeloproliferative diseases
KW - Blast
KW - Translocation
KW - Drugs
KW - W 30910:Imaging
KW - G 07730:Development & Cell Cycle
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Stem+Cells&rft.atitle=Brief+Report%3A+Loss+of+p15Ink4b+Accelerates+Development+of+Myeloid+Neoplasms+in+Nup98-HoxD13+Transgenic+Mice&rft.au=Humeniuk%2C+Rita%3BKoller%2C+Richard%3BBies%2C+Juraj%3BAplan%2C+Peter%3BWolff%2C+Linda&rft.aulast=Humeniuk&rft.aufirst=Rita&rft.date=2014-05-01&rft.volume=32&rft.issue=5&rft.spage=1361&rft.isbn=&rft.btitle=&rft.title=Stem+Cells&rft.issn=10665099&rft_id=info:doi/10.1002%2Fstem.1635
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-05-01
N1 - Last updated - 2014-05-29
N1 - SubjectsTermNotLitGenreText - Transformation; Acute myeloid leukemia; Transgenes; Tumorigenesis; Prognosis; Animal models; Homeostasis; Transgenic mice; Myelodysplastic syndrome; Differentiation; Stem cells; Malignancy; Hemopoiesis; Myeloproliferative diseases; Blast; Drugs; Translocation
DO - http://dx.doi.org/10.1002/stem.1635
ER -
TY - JOUR
T1 - Pesticides, chemical and industrial exposures in relation to systemic Lupus erythematosus
AN - 1524414831; 19778858
AB - Growing evidence suggests exposure to chemicals and industrial pollutants may increase risk of systemic Lupus erythematosus (SLE). Here we review research on SLE associations with occupational and industrial exposures, primarily drawing on studies in human populations and summarizing epidemiologic research published in the past decade. The association of occupational silica exposure with SLE is well established, but key questions remain, including the required dose and susceptibility factors, and SLE risk due to other silicate exposures. Research on SLE and other exposures is less well developed, though several potential associations merit further consideration because of the consistency of preliminary human findings, experimental animal research, and biologic plausibility. These include pesticides and solvents, for which experimental findings also support investigation of specific agents, including organochlorines and trichloroethylene. Experimental findings and biologic plausibility suggest research on SLE and occupational exposure to hydrocarbons (i.e. mineral oils) is warranted, especially given the widespread exposures in the population. Experimental and limited human findings support further investigation of SLE related to mercury exposure, especially in dental occupations. Research on environmental risk factors in risk-enriched cohorts (family-based) is recommended, as is further investigation of exposures in relation to intermediate markers of effect (e.g. antinuclear antibodies), clinical features (e.g. nephritis), and outcomes.
JF - Lupus
AU - Parks, C G
AU - De Roos, AJ
AD - Epidemiology Branch, National Institute of Environmental Health Sciences, NC, USA, Parks1@mail.nih.gov
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 527
EP - 536
PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom
VL - 23
IS - 6
SN - 0961-2033, 0961-2033
KW - Risk Abstracts; Health & Safety Science Abstracts; Pollution Abstracts; Immunology Abstracts
KW - Antinuclear antibodies
KW - mineral oil
KW - Organochlorine compounds
KW - Oil
KW - Pollutants
KW - Risk factors
KW - Trichloroethylene
KW - Systemic lupus erythematosus
KW - Occupational exposure
KW - Hydrocarbons
KW - Human populations
KW - Silicic acid
KW - Solvents
KW - Population studies
KW - Silica
KW - Reviews
KW - Nephritis
KW - Pesticides
KW - Mercury
KW - Minerals
KW - F 06930:Autoimmunity
KW - R2 23060:Medical and environmental health
KW - H 1000:Occupational Safety and Health
KW - P 6000:TOXICOLOGY AND HEALTH
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Lupus&rft.atitle=Pesticides%2C+chemical+and+industrial+exposures+in+relation+to+systemic+Lupus+erythematosus&rft.au=Parks%2C+C+G%3BDe+Roos%2C+AJ&rft.aulast=Parks&rft.aufirst=C&rft.date=2014-05-01&rft.volume=23&rft.issue=6&rft.spage=527&rft.isbn=&rft.btitle=&rft.title=Lupus&rft.issn=09612033&rft_id=info:doi/10.1177%2F0961203313511680
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-05-01
N1 - Number of references - 58
N1 - Last updated - 2014-08-21
N1 - SubjectsTermNotLitGenreText - mineral oil; Antinuclear antibodies; Organochlorine compounds; Hydrocarbons; Silicic acid; Solvents; Population studies; Silica; Pollutants; Nephritis; Risk factors; Reviews; Pesticides; Mercury; Systemic lupus erythematosus; Trichloroethylene; Occupational exposure; Oil; Human populations; Minerals
DO - http://dx.doi.org/10.1177/0961203313511680
ER -
TY - JOUR
T1 - International Society for the Advancement of Cytometry cell sorter biosafety standards
AN - 1524399826; 19752542
AB - Flow cytometric cell sorting of biological specimens has become prevalent in basic and clinical research laboratories. These specimens may contain known or unknown infectious agents, necessitating precautions to protect instrument operators and the environment from biohazards arising from the use of sorters. To this end the International Society of Analytical Cytology (ISAC) was proactive in establishing biosafety guidelines in 1997 (Schmid et al., Cytometry 1997; 28:99-117) and subsequently published revised biosafety standards for cell sorting of unfixed samples in 2007 (Schmid et al., Cytometry Part A J Int Soc Anal Cytol 2007; 71A:414-437). Since their publication, these documents have become recognized worldwide as the standard of practice and safety precautions for laboratories performing cell sorting experiments. However, the field of cytometry has progressed since 2007, and the document requires an update. The new Standards provides guidance: (1) for laboratory design for cell sorter laboratories; (2) for the creation of laboratory or instrument specific Standard Operating Procedures (SOP); and (3) on procedures for the safe operation of cell sorters, including personal protective equipment (PPE) and validation of aerosol containment. Published copyright 2013 Wiley Periodicals Inc. super()
JF - Cytometry Part A
AU - Holmes, Kevin L
AU - Fontes, Benjamin
AU - Hogarth, Philip
AU - Konz, Richard
AU - Monard, Simon
AU - Pletcher, Charles H
AU - Wadley, Robert B
AU - Schmid, Ingrid
AU - Perfetto, Stephen P
AD - Flow Cytometry Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland.
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 434
EP - 453
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 85
IS - 5
SN - 1552-4922, 1552-4922
KW - Biotechnology and Bioengineering Abstracts
KW - Flow cytometry
KW - Aerosols
KW - Cytometry
KW - W 30965:Miscellaneous, Reviews
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1524399826?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cytometry+Part+A&rft.atitle=International+Society+for+the+Advancement+of+Cytometry+cell+sorter+biosafety+standards&rft.au=Holmes%2C+Kevin+L%3BFontes%2C+Benjamin%3BHogarth%2C+Philip%3BKonz%2C+Richard%3BMonard%2C+Simon%3BPletcher%2C+Charles+H%3BWadley%2C+Robert+B%3BSchmid%2C+Ingrid%3BPerfetto%2C+Stephen+P&rft.aulast=Holmes&rft.aufirst=Kevin&rft.date=2014-05-01&rft.volume=85&rft.issue=5&rft.spage=434&rft.isbn=&rft.btitle=&rft.title=Cytometry+Part+A&rft.issn=15524922&rft_id=info:doi/10.1002%2Fcyto.a.22454
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-05-01
N1 - Last updated - 2014-05-29
N1 - SubjectsTermNotLitGenreText - Flow cytometry; Aerosols; Cytometry
DO - http://dx.doi.org/10.1002/cyto.a.22454
ER -
TY - JOUR
T1 - Role of ventral subiculum in context-induced reinstatement of heroin seeking in rats
AN - 1524395888; 19744645
AB - In rats, reexposure to heroin-paired contexts after extinction of lever responding in a different context reinstates heroin seeking. Previous reports indicate that ventral hippocampus/Ca1 region plays a critical role in cocaine-, cue- and context-induced reinstatement of cocaine seeking. Here, we examined whether ventral subiculum, the output region of ventral hippocampus, is involved in context-induced reinstatement of heroin seeking. We found that reversible inactivation of ventral subiculum, but not posterior Ca1, with the gamma-aminobutyric acid agonists muscimol+baclofen decreased context-induced reinstatement of heroin seeking. Our findings, together with previous studies on cocaine seeking, indicate a critical role of ventral subiculum in context-induced relapse across drug classes. In rats, re-exposure to heroin-paired contexts after extinction of lever-pressing in a different context reinstates heroin seeking. Previous reports indicate that ventral hippocampus plays a critical role in cocaine-, cue-, and context-induced reinstatement of cocaine seeking. Here, we found that reversible inactivation of ventral subiculum, the output region of ventral hippocampus, decreased context-induced reinstatement of heroin seeking. Our findings, together with previous studies on cocaine seeking, indicate a critical role of ventral subiculum in context-induced relapse across drug classes.
JF - Addiction Biology
AU - Bossert, Jennifer M
AU - Stern, Anna L
AD - Behavioral Neuroscience Branch, Intramural Research Program, National Institute on Drug Abuse, NIH/DHHS, Baltimore, MD, USA.
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 338
EP - 342
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 19
IS - 3
SN - 1355-6215, 1355-6215
KW - Toxicology Abstracts; CSA Neurosciences Abstracts
KW - Conditioned cues
KW - drug environment
KW - heroin self-administration
KW - hippocampus
KW - muscimol+baclofen
KW - reinstatement
KW - relapse
KW - Extinction
KW - Hippocampus
KW - Heroin
KW - gamma -Aminobutyric acid
KW - Addiction
KW - Cocaine
KW - Drug abuse
KW - Reinstatement
KW - X 24380:Social Poisons & Drug Abuse
KW - N3 11001:Behavioral and Cognitive Neuroscience
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-05-01
N1 - Last updated - 2014-10-30
N1 - SubjectsTermNotLitGenreText - Extinction; Heroin; Hippocampus; gamma -Aminobutyric acid; Addiction; Drug abuse; Cocaine; Reinstatement
DO - http://dx.doi.org/10.1111/adb.12015
ER -
TY - JOUR
T1 - Virus nomenclature below the species level: a standardized nomenclature for filovirus strains and variants rescued from cDNA.
AN - 1521909806; 24190508
AB - Specific alterations (mutations, deletions, insertions) of virus genomes are crucial for the functional characterization of their regulatory elements and their expression products, as well as a prerequisite for the creation of attenuated viruses that could serve as vaccine candidates. Virus genome tailoring can be performed either by using traditionally cloned genomes as starting materials, followed by site-directed mutagenesis, or by de novo synthesis of modified virus genomes or parts thereof. A systematic nomenclature for such recombinant viruses is necessary to set them apart from wild-type and laboratory-adapted viruses, and to improve communication and collaborations among researchers who may want to use recombinant viruses or create novel viruses based on them. A large group of filovirus experts has recently proposed nomenclatures for natural and laboratory animal-adapted filoviruses that aim to simplify the retrieval of sequence data from electronic databases. Here, this work is extended to include nomenclature for filoviruses obtained in the laboratory via reverse genetics systems. The previously developed template for natural filovirus genetic variant naming, (/)///-, is retained, but we propose to adapt the type of information added to each field for cDNA clone-derived filoviruses. For instance, the full-length designation of an Ebola virus Kikwit variant rescued from a plasmid developed at the US Centers for Disease Control and Prevention could be akin to "Ebola virus H.sapiens-rec/COD/1995/Kikwit-abc1" (with the suffix "rec" identifying the recombinant nature of the virus and "abc1" being a placeholder for any meaningful isolate designator). Such a full-length designation should be used in databases and the methods section of publications. Shortened designations (such as "EBOV H.sap/COD/95/Kik-abc1") and abbreviations (such as "EBOV/Kik-abc1") could be used in the remainder of the text, depending on how critical it is to convey information contained in the full-length name. "EBOV" would suffice if only one EBOV strain/variant/isolate is addressed.
JF - Archives of virology
AU - Kuhn, Jens H
AU - Bào, Yīmíng
AU - Bavari, Sina
AU - Becker, Stephan
AU - Bradfute, Steven
AU - Brauburger, Kristina
AU - Rodney Brister, J
AU - Bukreyev, Alexander A
AU - Caì, Yíngyún
AU - Chandran, Kartik
AU - Davey, Robert A
AU - Dolnik, Olga
AU - Dye, John M
AU - Enterlein, Sven
AU - Gonzalez, Jean-Paul
AU - Formenty, Pierre
AU - Freiberg, Alexander N
AU - Hensley, Lisa E
AU - Hoenen, Thomas
AU - Honko, Anna N
AU - Ignatyev, Georgy M
AU - Jahrling, Peter B
AU - Johnson, Karl M
AU - Klenk, Hans-Dieter
AU - Kobinger, Gary
AU - Lackemeyer, Matthew G
AU - Leroy, Eric M
AU - Lever, Mark S
AU - Mühlberger, Elke
AU - Netesov, Sergey V
AU - Olinger, Gene G
AU - Palacios, Gustavo
AU - Patterson, Jean L
AU - Paweska, Janusz T
AU - Pitt, Louise
AU - Radoshitzky, Sheli R
AU - Ryabchikova, Elena I
AU - Saphire, Erica Ollmann
AU - Shestopalov, Aleksandr M
AU - Smither, Sophie J
AU - Sullivan, Nancy J
AU - Swanepoel, Robert
AU - Takada, Ayato
AU - Towner, Jonathan S
AU - van der Groen, Guido
AU - Volchkov, Viktor E
AU - Volchkova, Valentina A
AU - Wahl-Jensen, Victoria
AU - Warren, Travis K
AU - Warfield, Kelly L
AU - Weidmann, Manfred
AU - Nichol, Stuart T
AD - Integrated Research Facility at Fort Detrick (IRF-Frederick), Division of Clinical Research (DCR), National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), B-8200 Research Plaza, Fort Detrick, Frederick, MD, 21702, USA, kuhnjens@mail.nih.gov.
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 1229
EP - 1237
VL - 159
IS - 5
KW - Index Medicus
KW - Genome, Viral
KW - Filoviridae -- classification
KW - Reassortant Viruses -- classification
KW - Filoviridae -- genetics
KW - Reassortant Viruses -- genetics
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+virology&rft.atitle=Virus+nomenclature+below+the+species+level%3A+a+standardized+nomenclature+for+filovirus+strains+and+variants+rescued+from+cDNA.&rft.au=Kuhn%2C+Jens+H%3BB%C3%A0o%2C+Y%C4%ABm%C3%ADng%3BBavari%2C+Sina%3BBecker%2C+Stephan%3BBradfute%2C+Steven%3BBrauburger%2C+Kristina%3BRodney+Brister%2C+J%3BBukreyev%2C+Alexander+A%3BCa%C3%AC%2C+Y%C3%ADngy%C3%BAn%3BChandran%2C+Kartik%3BDavey%2C+Robert+A%3BDolnik%2C+Olga%3BDye%2C+John+M%3BEnterlein%2C+Sven%3BGonzalez%2C+Jean-Paul%3BFormenty%2C+Pierre%3BFreiberg%2C+Alexander+N%3BHensley%2C+Lisa+E%3BHoenen%2C+Thomas%3BHonko%2C+Anna+N%3BIgnatyev%2C+Georgy+M%3BJahrling%2C+Peter+B%3BJohnson%2C+Karl+M%3BKlenk%2C+Hans-Dieter%3BKobinger%2C+Gary%3BLackemeyer%2C+Matthew+G%3BLeroy%2C+Eric+M%3BLever%2C+Mark+S%3BM%C3%BChlberger%2C+Elke%3BNetesov%2C+Sergey+V%3BOlinger%2C+Gene+G%3BPalacios%2C+Gustavo%3BPatterson%2C+Jean+L%3BPaweska%2C+Janusz+T%3BPitt%2C+Louise%3BRadoshitzky%2C+Sheli+R%3BRyabchikova%2C+Elena+I%3BSaphire%2C+Erica+Ollmann%3BShestopalov%2C+Aleksandr+M%3BSmither%2C+Sophie+J%3BSullivan%2C+Nancy+J%3BSwanepoel%2C+Robert%3BTakada%2C+Ayato%3BTowner%2C+Jonathan+S%3Bvan+der+Groen%2C+Guido%3BVolchkov%2C+Viktor+E%3BVolchkova%2C+Valentina+A%3BWahl-Jensen%2C+Victoria%3BWarren%2C+Travis+K%3BWarfield%2C+Kelly+L%3BWeidmann%2C+Manfred%3BNichol%2C+Stuart+T&rft.aulast=Kuhn&rft.aufirst=Jens&rft.date=2014-05-01&rft.volume=159&rft.issue=5&rft.spage=1229&rft.isbn=&rft.btitle=&rft.title=Archives+of+virology&rft.issn=1432-8798&rft_id=info:doi/10.1007%2Fs00705-013-1877-2
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-06-24
N1 - Date created - 2014-05-06
N1 - Date revised - 2017-01-13
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1007/s00705-013-1877-2
ER -
TY - JOUR
T1 - Lower NLRP3 inflammasome activity in NAG-1 transgenic mice is linked to a resistance to obesity and increased insulin sensitivity.
AN - 1521338508; 24124102
AB - The NLRP3 inflammasome plays an important regulatory role in obesity-induced insulin resistance. NSAID activated gene-1 (NAG-1) is a divergent member of the TGF-β superfamily. NAG-1 Tg mice are resistant to dietary- and genetic-induced obesity and have improved insulin sensitivity. The objective was to examine whether NLRP3 inflammasome activity is associated with this observed phenotype in NAG-1 Tg mice.
Key components of the NLRP3 inflammasome were examined in NAG-1 Tg mice on both regular and high fat diet (HFD) conditions. The expression of caspase-1 and ASC, key components of the NLRP3 inflammasome, is significantly reduced at mRNA and protein levels in white adipose tissue (WAT) of NAG-1 Tg mice. HFD increases the expression of caspase-1 and ASC in WT mice, but their expression is reduced in NAG-1 Tg mice. Furthermore, there is reduced IL-18, IL-1β, and TNF-α expression in the WAT of NAG-1 Tg mice. NAG-1 Tg mice have significantly lower serum leptin and insulin levels and reduced expression of macrophage infiltration markers (F4/80, CD11b, and CD11c) in WAT.
The study suggests the lower NLRP3 inflammasome activity may play a role in the resistance of NAG-1 Tg mice to diet-induced obesity and improved insulin sensitivity. Copyright © 2013 The Obesity Society.
JF - Obesity (Silver Spring, Md.)
AU - Wang, Xingya
AU - Chrysovergis, Kali
AU - Kosak, Justin
AU - Eling, Thomas E
AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences (NIEHS), 111. T.W. Alexander Dr, Research Triangle Park, North Carolina, USA.
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 1256
EP - 1263
VL - 22
IS - 5
KW - Antigens, CD11b
KW - 0
KW - Antigens, CD11c
KW - Carrier Proteins
KW - Inflammasomes
KW - Insulin
KW - Interleukin-18
KW - Interleukin-1beta
KW - Leptin
KW - NLR Family, Pyrin Domain-Containing 3 Protein
KW - Nlrp3 protein, mouse
KW - RNA, Messenger
KW - Transforming Growth Factor beta
KW - Tumor Necrosis Factor-alpha
KW - Caspase 1
KW - EC 3.4.22.36
KW - Index Medicus
KW - Animals
KW - Caspase 1 -- metabolism
KW - Interleukin-1beta -- genetics
KW - Antigens, CD11b -- metabolism
KW - Diet, High-Fat
KW - Mice, Transgenic
KW - RNA, Messenger -- genetics
KW - Tumor Necrosis Factor-alpha -- genetics
KW - Leptin -- blood
KW - Adipose Tissue, White -- metabolism
KW - Caspase 1 -- genetics
KW - Antigens, CD11c -- genetics
KW - Transforming Growth Factor beta -- genetics
KW - Interleukin-18 -- genetics
KW - Male
KW - Antigens, CD11b -- genetics
KW - Insulin -- blood
KW - Mice
KW - Interleukin-18 -- metabolism
KW - Antigens, CD11c -- metabolism
KW - RNA, Messenger -- metabolism
KW - Interleukin-1beta -- metabolism
KW - Mice, Inbred C57BL
KW - Tumor Necrosis Factor-alpha -- metabolism
KW - Transforming Growth Factor beta -- metabolism
KW - Female
KW - Obesity -- metabolism
KW - Carrier Proteins -- metabolism
KW - Obesity -- genetics
KW - Carrier Proteins -- genetics
KW - Insulin Resistance -- genetics
KW - Inflammasomes -- metabolism
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-01-02
N1 - Date created - 2014-05-05
N1 - Date revised - 2017-01-13
N1 - SuppNotes - Cited By:
Am J Physiol Endocrinol Metab. 2010 Sep;299(3):E486-96 [20570821]
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Diabetes. 2011 Jun;60(6):1688-98 [21515850]
Proc Natl Acad Sci U S A. 2011 Sep 13;108(37):15324-9 [21876127]
Endocrinology. 2011 Oct;152(10):3769-78 [21862623]
Clin Endocrinol (Oxf). 2012 Jan;76(1):46-50 [21645023]
Prostate. 2012 May 1;72(6):677-89 [21809352]
Mediators Inflamm. 2013;2013:641851 [23737651]
Diabetes. 2013 Sep;62(9):3064-74 [23670974]
J Clin Invest. 2003 Dec;112(12):1796-808 [14679176]
Diabetes Obes Metab. 2005 Jul;7(4):406-13 [15955127]
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Cell Metab. 2010 Dec 1;12(6):593-605 [21109192]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1002/oby.20638
ER -
TY - JOUR
T1 - The histone-fold complex MHF is remodeled by FANCM to recognize branched DNA and protect genome stability.
AN - 1521330494; 24699063
AB - Histone-fold proteins typically assemble in multiprotein complexes to bind duplex DNA. However, one histone-fold complex, MHF, associates with Fanconi anemia (FA) protein FANCM to form a branched DNA remodeling complex that senses and repairs stalled replication forks and activates FA DNA damage response network. How the FANCM-MHF complex recognizes branched DNA is unclear. Here, we solved the crystal structure of MHF and its complex with the MHF-interaction domain (referred to as MID) of FANCM, and performed structure-guided mutagenesis. We found that the MID-MHF complex consists of one histone H3-H4-like MHF heterotetramer wrapped by a single polypeptide of MID. We identified a zinc atom-liganding structure at the central interface between MID and MHF that is critical for stabilization of the complex. Notably, the DNA-binding surface of MHF was altered by MID in both electrostatic charges and allosteric conformation. This leads to a switch in the DNA-binding preference - from duplex DNA by MHF alone, to branched DNA by the MID-MHF complex. Mutations that disrupt either the composite DNA-binding surface or the protein-protein interface of the MID-MHF complex impaired activation of the FA network and genome stability. Our data provide the structural basis of how FANCM and MHF work together to recognize branched DNA, and suggest a novel mechanism by which histone-fold complexes can be remodeled by their partners to bind special DNA structures generated during DNA metabolism.
JF - Cell research
AU - Fox, David
AU - Yan, Zhijiang
AU - Ling, Chen
AU - Zhao, Ye
AU - Lee, Duck-Yeon
AU - Fukagawa, Tatsuo
AU - Yang, Wei
AU - Wang, Weidong
AD - Laboratory of Genetics, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA. ; Laboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institute of Health, Bethesda, MD 20892, USA. ; Biochemistry Core Facility, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA. ; Department of Molecular Genetics, National Institute of Genetics and the Graduate University for Advanced Studies, Mishima 411-8540, Japan.
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 560
EP - 575
VL - 24
IS - 5
KW - APITD1 protein, human
KW - 0
KW - Apoptosis Regulatory Proteins
KW - DNA, Cruciform
KW - DNA-Binding Proteins
KW - Histones
KW - Multiprotein Complexes
KW - Nuclear Proteins
KW - STRA13 protein, human
KW - Tumor Suppressor Proteins
KW - DNA
KW - 9007-49-2
KW - FANCM protein, human
KW - EC 3.6.1.-
KW - DNA Helicases
KW - EC 3.6.4.-
KW - Index Medicus
KW - Models, Molecular
KW - HeLa Cells
KW - Humans
KW - Histones -- metabolism
KW - HEK293 Cells
KW - Protein Multimerization
KW - Protein Interaction Domains and Motifs
KW - Nucleic Acid Conformation
KW - Fanconi Anemia -- metabolism
KW - DNA Helicases -- chemistry
KW - DNA Repair
KW - DNA Helicases -- metabolism
KW - DNA-Binding Proteins -- chemistry
KW - DNA Damage
KW - Apoptosis Regulatory Proteins -- chemistry
KW - DNA -- metabolism
KW - Tumor Suppressor Proteins -- chemistry
KW - Genomic Instability
KW - Tumor Suppressor Proteins -- metabolism
KW - Apoptosis Regulatory Proteins -- metabolism
KW - DNA -- genetics
KW - DNA -- chemistry
KW - Nuclear Proteins -- chemistry
KW - Nuclear Proteins -- metabolism
KW - Fanconi Anemia -- genetics
KW - DNA-Binding Proteins -- metabolism
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1521330494?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cell+research&rft.atitle=The+histone-fold+complex+MHF+is+remodeled+by+FANCM+to+recognize+branched+DNA+and+protect+genome+stability.&rft.au=Fox%2C+David%3BYan%2C+Zhijiang%3BLing%2C+Chen%3BZhao%2C+Ye%3BLee%2C+Duck-Yeon%3BFukagawa%2C+Tatsuo%3BYang%2C+Wei%3BWang%2C+Weidong&rft.aulast=Fox&rft.aufirst=David&rft.date=2014-05-01&rft.volume=24&rft.issue=5&rft.spage=560&rft.isbn=&rft.btitle=&rft.title=Cell+research&rft.issn=1748-7838&rft_id=info:doi/10.1038%2Fcr.2014.42
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-12-23
N1 - Date created - 2014-05-05
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Genes Dev. 2012 Jul 1;26(13):1393-408 [22751496]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1038/cr.2014.42
ER -
TY - JOUR
T1 - Suppressive oligodeoxynucleotides reduce lung cancer susceptibility in mice with silicosis.
AN - 1520347928; 24403310
AB - Silicosis is an inflammatory lung disease induced by the inhalation of silica-containing dust particles. There is conflicting data on whether patients with silicosis are more susceptible to lung cancer induced by cigarette smoke. To examine this issue experimentally, a model was developed in which one of the most abundant and potent carcinogens present in cigarette smoke [4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK)] was administered to mice at the peak of silica-induced pulmonary inflammation. Results show that the incidence of lung tumors in silicotic mice treated with NNK was significantly increased compared with mice exposed to silica or NNK alone. Synthetic oligonucleotides (ODN) containing repetitive TTAGGG motifs can block pathologic inflammation. We therefore examined whether treatment with these suppressive (Sup) ODN could block silica-induced pulmonary inflammation and thereby reduce susceptibility to lung cancer. Results show that Sup (but not control) ODN inhibit pulmonary fibrosis and other inflammatory manifestations of chronic silicosis. Of greater import, Sup ODN reduced lung tumor incidence and multiplicity in silicotic mice exposed to NNK. These findings establish an experimental model for examining the role of silicotic inflammation in cancer susceptibility and demonstrate that Sup ODN represent a novel therapy for chronic silicosis.
JF - Carcinogenesis
AU - Bode, Christian
AU - Kinjo, Takeshi
AU - Alvord, W Gregory
AU - Klinman, Dennis M
AD - Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702, USA.
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 1078
EP - 1083
VL - 35
IS - 5
KW - Anti-Inflammatory Agents
KW - 0
KW - Biomarkers
KW - Interleukin-1beta
KW - Nitrosamines
KW - Oligodeoxyribonucleotides
KW - RNA, Messenger
KW - Silicon Dioxide
KW - 7631-86-9
KW - 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone
KW - 7S395EDO61
KW - Index Medicus
KW - Animals
KW - Interleukin-1beta -- genetics
KW - Humans
KW - Gene Expression
KW - Nitrosamines -- adverse effects
KW - Disease Models, Animal
KW - Mice
KW - RNA, Messenger -- genetics
KW - Pneumonia -- drug therapy
KW - Pneumonia -- pathology
KW - Pneumonia -- etiology
KW - Silicon Dioxide -- adverse effects
KW - RNA, Messenger -- metabolism
KW - Interleukin-1beta -- metabolism
KW - Female
KW - Pneumonia -- complications
KW - Lung Neoplasms -- prevention & control
KW - Lung Neoplasms -- etiology
KW - Silicosis -- pathology
KW - Disease Susceptibility
KW - Silicosis -- complications
KW - Oligodeoxyribonucleotides -- pharmacology
KW - Anti-Inflammatory Agents -- administration & dosage
KW - Oligodeoxyribonucleotides -- administration & dosage
KW - Lung Neoplasms -- pathology
KW - Anti-Inflammatory Agents -- pharmacology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Suppressive+oligodeoxynucleotides+reduce+lung+cancer+susceptibility+in+mice+with+silicosis.&rft.au=Bode%2C+Christian%3BKinjo%2C+Takeshi%3BAlvord%2C+W+Gregory%3BKlinman%2C+Dennis+M&rft.aulast=Bode&rft.aufirst=Christian&rft.date=2014-05-01&rft.volume=35&rft.issue=5&rft.spage=1078&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgu005
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-06-24
N1 - Date created - 2014-04-30
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Dis Mon. 2007 Aug;53(8):394-416 [17976433]
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J Immunol. 2008 Jun 1;180(11):7648-54 [18490767]
Nature. 2008 Jul 24;454(7203):436-44 [18650914]
J Mol Cell Cardiol. 2008 Aug;45(2):168-75 [18502445]
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Occup Med (Lond). 2009 Mar;59(2):89-95 [19233828]
Clin Exp Immunol. 2009 Jun;156(3):528-34 [19438607]
Cancer Causes Control. 2009 Aug;20(6):925-33 [19184475]
Nat Protoc. 2009;4(9):1350-62 [19713956]
Cell. 2011 Mar 4;144(5):646-74 [21376230]
Anticancer Res. 2011 Sep;31(9):2877-82 [21868532]
Risk Anal. 2011 Oct;31(10):1543-60 [21477084]
Lancet. 2012 May 26;379(9830):2008-18 [22534002]
Int J Epidemiol. 2012 Jun;41(3):711-21 [22467291]
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Arthritis Rheum. 2004 May;50(5):1686-9 [15146440]
Inhal Toxicol. 2004 Mar;16(3):133-9 [15204774]
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Carcinogenesis. 1989 Jan;10(1):91-6 [2910536]
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Mol Carcinog. 1998 Sep;23(1):36-44 [9766436]
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Mol Carcinog. 1999 Aug;25(4):231-40 [10449029]
Carcinogenesis. 1999 Oct;20(10):1939-44 [10506108]
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Arthritis Rheum. 2005 Feb;52(2):651-8 [15692999]
J Immunol. 2005 Apr 15;174(8):4579-83 [15814679]
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Epidemiology. 2001 Jan;12(1):88-93 [11138826]
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Occup Environ Med. 2002 Mar;59(3):205-13; quiz 214 [11886955]
J Immunol. 2002 Sep 1;169(5):2653-61 [12193738]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/carcin/bgu005
ER -
TY - JOUR
T1 - Tamoxifen-DNA adduct formation in monkey and human reproductive organs.
AN - 1520347749; 24501327
AB - The estrogen analog tamoxifen (TAM), used for adjuvant therapy of breast cancer, induces endometrial and uterine tumors in breast cancer patients. Proliferation stimulus of the uterine endometrium is likely involved in tumor induction, but genotoxicity may also play a role. Formation of TAM-DNA adducts in human tissues has been reported but remains controversial. To address this issue, we examined TAM-DNA adducts in uteri from two species of monkeys, Erythrocebus patas (patas) and Macaca fascicularis (macaque), and in human endometrium and myometrium. Monkeys were given 3-4 months of chronic TAM dosing scaled to be equivalent to the daily human dose. In the uteri, livers and brains from the patas (n = 3), and endometrium from the macaques (n = 4), TAM-DNA adducts were measurable by TAM-DNA chemiluminescence immunoassay. Average TAM-DNA adduct values for the patas uteri (23 adducts/10(8) nucleotides) were similar to those found in endometrium of the macaques (19 adducts/10(8) nucleotides). Endometrium of macaques exposed to both TAM and low-dose estradiol (n = 5) averaged 34 adducts/10(8) nucleotides. To examine TAM-DNA persistence in the patas, females (n = 3) were exposed to TAM for 3 months and to no drug for an additional month, resulting in low or non-detectable TAM-DNA in livers and uteri. Human endometrial and myometrial samples from women receiving (n = 8) and not receiving (n = 8) TAM therapy were also evaluated. Women receiving TAM therapy averaged 10.3 TAM-DNA adducts/10(8) nucleotides, whereas unexposed women showed no detectable TAM-DNA. The data indicate that genotoxicity, in addition to estrogen agonist effects, may contribute to TAM-induced human endometrial cancer.
JF - Carcinogenesis
AU - Hernandez-Ramon, Elena E
AU - Sandoval, Nicole A
AU - John, Kaarthik
AU - Cline, J Mark
AU - Wood, Charles E
AU - Woodward, Ruth A
AU - Poirier, Miriam C
AD - Carcinogen-DNA Interactions Section, LCBG, CCR, National Cancer Institute, NIH, Building 37, Room 4032, NIH 37 Convent Drive, MSC-4255, Bethesda, MD 20892, USA.
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 1172
EP - 1176
VL - 35
IS - 5
KW - DNA Adducts
KW - 0
KW - Tamoxifen
KW - 094ZI81Y45
KW - DNA
KW - 9007-49-2
KW - Index Medicus
KW - Animals
KW - Humans
KW - Erythrocebus patas
KW - Myometrium -- metabolism
KW - Female
KW - Endometrium -- metabolism
KW - Uterus -- metabolism
KW - DNA Adducts -- chemistry
KW - DNA -- metabolism
KW - Tamoxifen -- chemistry
KW - DNA Adducts -- adverse effects
KW - Tamoxifen -- metabolism
KW - DNA -- chemistry
KW - DNA Adducts -- metabolism
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Tamoxifen-DNA+adduct+formation+in+monkey+and+human+reproductive+organs.&rft.au=Hernandez-Ramon%2C+Elena+E%3BSandoval%2C+Nicole+A%3BJohn%2C+Kaarthik%3BCline%2C+J+Mark%3BWood%2C+Charles+E%3BWoodward%2C+Ruth+A%3BPoirier%2C+Miriam+C&rft.aulast=Hernandez-Ramon&rft.aufirst=Elena&rft.date=2014-05-01&rft.volume=35&rft.issue=5&rft.spage=1172&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgu029
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-06-24
N1 - Date created - 2014-04-30
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Carcinogenesis. 2000 Aug;21(8):1461-7 [10910945]
Lancet. 2013 Mar 9;381(9869):805-16 [23219286]
Arch Toxicol. 2001 Aug;75(6):375-80 [11570696]
J Natl Cancer Inst. 2002 Aug 7;94(15):1122 [12165635]
Annu Rev Pharmacol Toxicol. 2003;43:149-73 [12171978]
Mutagenesis. 2003 Jul;18(4):395-9 [12840114]
Cancer Res. 2003 Sep 15;63(18):5999-6003 [14522927]
Cancer Res. 2003 Dec 1;63(23):8461-5 [14679010]
J Natl Cancer Inst. 2004 Jul 21;96(14):1099-104 [15265972]
Cancer Res. 1993 Sep 1;53(17):3919-24 [8358718]
Carcinogenesis. 1995 Jun;16(6):1299-304 [7788846]
Cancer Res. 1996 Apr 1;56(7):1475-9 [8603387]
Cancer Res. 1996 Oct 1;56(19):4374-7 [8813128]
Br J Clin Pharmacol. 2014 Apr;77(4):673-83 [24033670]
Lancet. 1998 May 16;351(9114):1451-67 [9605801]
J Natl Cancer Inst. 1998 Sep 16;90(18):1371-88 [9747868]
Carcinogenesis. 1999 Feb;20(2):339-42 [10069474]
Chem Res Toxicol. 1999 Jul;12(7):646-53 [10409405]
Cancer Res. 1999 Oct 1;59(19):4829-33 [10519392]
Mutagenesis. 2005 Mar;20(2):115-24 [15755801]
Cardiovasc Toxicol. 2005;5(3):333-46 [16244378]
Cancer Res. 2007 Jul 15;67(14):6995-7002 [17638912]
Toxicol Sci. 2007 Sep;99(1):203-13 [17545213]
Pharmacogenet Genomics. 2007 Sep;17(9):731-42 [17700362]
Mutagenesis. 2008 Jan;23(1):1-18 [17989146]
Mutagenesis. 2009 Sep;24(5):391-404 [19505894]
Drug Metab Dispos. 2010 Jan;38(1):200-7 [19812351]
Clin Cancer Res. 2010 Feb 1;16(3):946-56 [20103679]
Toxicol Sci. 2010 Nov;118(1):191-201 [20702595]
Drug Metab Dispos. 2013 Jun;41(6):1187-94 [23491640]
Carcinogenesis. 2001 Jun;22(6):839-49 [11375888]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/carcin/bgu029
ER -
TY - JOUR
T1 - A nested case-control study of leukocyte mitochondrial DNA copy number and renal cell carcinoma in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial.
AN - 1520345985; 24398668
AB - Mitochondrial DNA (mtDNA) is vulnerable to mutations, and the number of copies of mtDNA per cell may increase to compensate for DNA damage. Case-control studies have reported associations between altered mtDNA copy number and risk of renal cell carcinoma (RCC); however, this association has not been investigated prospectively. We conducted a nested case-control study (252 cases and 504 controls) of RCC risk in relation to pre-diagnostic leukocyte mtDNA copy number in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. mtDNA copy number was measured in triplicate using a fluorescence-based quantitative PCR assay; samples from 22 cases and 36 controls could not be assayed, leaving 230 cases and 468 controls for analysis. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using unconditional logistic regression. High mtDNA copy number was associated with an increased risk of RCC, both overall (highest quartile versus lowest: OR = 2.0, 95% CI = 1.2-3.2; P trend = 0.002) and among cases diagnosed ≥6 years after blood collection (OR = 2.6, 95% CI = 1.4-5.0; P trend = 0.003). These findings did not differ significantly by sex, body mass index, history of hypertension or smoking status (P interaction ≥ 0.3). Results of this study suggest that high pre-diagnostic leukocyte mtDNA copy number, a suspected marker of oxidative DNA damage and mitochondrial dysfunction, is associated with increased future RCC risk.
JF - Carcinogenesis
AU - Hofmann, Jonathan N
AU - Hosgood, H Dean
AU - Liu, Chin-San
AU - Chow, Wong-Ho
AU - Shuch, Brian
AU - Cheng, Wen-Ling
AU - Lin, Ta-Tsung
AU - Moore, Lee E
AU - Lan, Qing
AU - Rothman, Nathaniel
AU - Purdue, Mark P
AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD 20892, USA.
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 1028
EP - 1031
VL - 35
IS - 5
KW - DNA, Mitochondrial
KW - 0
KW - Index Medicus
KW - Odds Ratio
KW - Risk Factors
KW - Humans
KW - Case-Control Studies
KW - Aged
KW - Middle Aged
KW - Male
KW - Female
KW - Leukocytes -- metabolism
KW - Kidney Neoplasms -- genetics
KW - DNA Copy Number Variations
KW - Kidney Neoplasms -- diagnosis
KW - Carcinoma, Renal Cell -- diagnosis
KW - Carcinoma, Renal Cell -- genetics
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=A+nested+case-control+study+of+leukocyte+mitochondrial+DNA+copy+number+and+renal+cell+carcinoma+in+the+Prostate%2C+Lung%2C+Colorectal+and+Ovarian+Cancer+Screening+Trial.&rft.au=Hofmann%2C+Jonathan+N%3BHosgood%2C+H+Dean%3BLiu%2C+Chin-San%3BChow%2C+Wong-Ho%3BShuch%2C+Brian%3BCheng%2C+Wen-Ling%3BLin%2C+Ta-Tsung%3BMoore%2C+Lee+E%3BLan%2C+Qing%3BRothman%2C+Nathaniel%3BPurdue%2C+Mark+P&rft.aulast=Hofmann&rft.aufirst=Jonathan&rft.date=2014-05-01&rft.volume=35&rft.issue=5&rft.spage=1028&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgt495
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-06-24
N1 - Date created - 2014-04-30
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
J Biomed Sci. 2000 Jan-Feb;7(1):2-15 [10644884]
Cancer Epidemiol Biomarkers Prev. 2012 Sep;21(9):1574-81 [22787200]
Control Clin Trials. 2000 Dec;21(6 Suppl):349S-355S [11189687]
Mutat Res. 2001 May;488(2):119-33 [11344040]
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Free Radic Res. 2003 Dec;37(12):1307-17 [14753755]
Int J Cancer. 1994 Apr 1;57(1):123-8 [8150530]
Proc Natl Acad Sci U S A. 1994 Sep 13;91(19):8739-46 [8090716]
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J Natl Cancer Inst. 2008 Aug 6;100(15):1104-12 [18664653]
Blood. 2008 Nov 15;112(10):4247-9 [18711000]
Carcinogenesis. 2010 May;31(5):847-9 [20176654]
Cancer Prev Res (Phila). 2011 May;4(5):638-54 [21543342]
Cancer Epidemiol Biomarkers Prev. 2011 Sep;20(9):1944-9 [21784958]
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Biochem J. 2000 Jun 1;348 Pt 2:425-32 [10816438]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/carcin/bgt495
ER -
TY - JOUR
T1 - Photoimmunotherapy: comparative effectiveness of two monoclonal antibodies targeting the epidermal growth factor receptor.
AN - 1519846665; 24508062
AB - Photoimmunotherapy (PIT) is a new cancer treatment that combines the specificity of antibodies for targeting tumors with the toxicity induced by photosensitizers after exposure to near infrared (NIR) light. Herein we compare two commonly available anti-EGFR monoclonal antibodies, cetuximab and panitumumab, for their effectiveness as PIT agents in EGFR positive tumor models. A photosensitizer, IR-700, conjugated to either cetuximab (cet-IR700) or panitumumab (pan-IR700), was evaluated using EGFR-expressing A431 and MDAMB468-luc cells in 2D- and 3D-culture. PIT was conducted with irradiation of NIR light after exposure of the sample or animal to each conjugate. In vivo PIT was performed with fractionated exposure of NIR light after injection of each agent into A431 xenografts or a MDAMB468-luc orthotopic tumor bearing model. Cet-IR700 and pan-IR700 bound with equal affinity to the cells in 2D-culture and penetrated equally into the 3D-spheroid, resulting in identical PIT cytotoxic effects in vitro. In contrast, in vivo anti-tumor effects of PIT with cet-IR700 were inferior to that of pan-IR700. Assessment of the biodistribution showed lower accumulation into the tumors and more rapid hepatic catabolism of cet-IR700 compared to pan-IR700. Although cet-IR700 and pan-IR700 showed identical in vitro characteristics, pan-IR700 showed better therapeutic tumor responses than cet-IR700 in in vivo mice models due to the prolonged retention of the conjugate in the circulation, suggesting that retention in the circulation is advantageous for tumor responses to PIT. These results suggest that the choice of monoclonal antibody in photosensitizer conjugates may influence the effectiveness of PIT.
Published by Elsevier B.V.
JF - Molecular oncology
AU - Sato, Kazuhide
AU - Watanabe, Rira
AU - Hanaoka, Hirofumi
AU - Harada, Toshiko
AU - Nakajima, Takahito
AU - Kim, Insook
AU - Paik, Chang H
AU - Choyke, Peter L
AU - Kobayashi, Hisataka
AD - Molecular Imaging Program, Center for Cancer Research, National Cancer Institute, MD 20892, United States. ; Applied/Developmental Research Directorate, Leidos Biomedical Research Inc., Frederick, MD 20892, United States. ; Nuclear Medicine Department, Warren Grant Magnuson Clinical Center, MD 20892, United States. ; Molecular Imaging Program, Center for Cancer Research, National Cancer Institute, MD 20892, United States. Electronic address: Kobayash@mail.nih.gov.
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 620
EP - 632
VL - 8
IS - 3
KW - Antibodies, Monoclonal
KW - 0
KW - Antibodies, Monoclonal, Humanized
KW - Photosensitizing Agents
KW - panitumumab
KW - 6A901E312A
KW - Receptor, Epidermal Growth Factor
KW - EC 2.7.10.1
KW - Cetuximab
KW - PQX0D8J21J
KW - Index Medicus
KW - NIR-fluorescence
KW - Monoclonal antibody
KW - Epidermal growth factor receptor
KW - Photoimmunotherapy
KW - Pharmacokinetics
KW - Animals
KW - Humans
KW - Xenograft Model Antitumor Assays
KW - Mice
KW - Cell Line, Tumor
KW - Female
KW - Antibodies, Monoclonal, Humanized -- pharmacokinetics
KW - Receptor, Epidermal Growth Factor -- antagonists & inhibitors
KW - Photosensitizing Agents -- therapeutic use
KW - Antibodies, Monoclonal -- chemistry
KW - Neoplasms -- therapy
KW - Antibodies, Monoclonal, Humanized -- chemistry
KW - Photosensitizing Agents -- pharmacokinetics
KW - Antibodies, Monoclonal -- therapeutic use
KW - Immunotherapy -- methods
KW - Antibodies, Monoclonal, Humanized -- therapeutic use
KW - Photosensitizing Agents -- chemistry
KW - Neoplasms -- pathology
KW - Antibodies, Monoclonal -- pharmacokinetics
KW - Phototherapy -- methods
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+oncology&rft.atitle=Photoimmunotherapy%3A+comparative+effectiveness+of+two+monoclonal+antibodies+targeting+the+epidermal+growth+factor+receptor.&rft.au=Sato%2C+Kazuhide%3BWatanabe%2C+Rira%3BHanaoka%2C+Hirofumi%3BHarada%2C+Toshiko%3BNakajima%2C+Takahito%3BKim%2C+Insook%3BPaik%2C+Chang+H%3BChoyke%2C+Peter+L%3BKobayashi%2C+Hisataka&rft.aulast=Sato&rft.aufirst=Kazuhide&rft.date=2014-05-01&rft.volume=8&rft.issue=3&rft.spage=620&rft.isbn=&rft.btitle=&rft.title=Molecular+oncology&rft.issn=1878-0261&rft_id=info:doi/10.1016%2Fj.molonc.2014.01.006
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-12-17
N1 - Date created - 2014-04-28
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Crit Rev Oncol Hematol. 2000 Nov-Dec;36(2-3):179-92 [11033305]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.molonc.2014.01.006
ER -
TY - JOUR
T1 - Impact on survival and toxicity by duration of weight extremes during treatment for pediatric acute lymphoblastic leukemia: A report from the Children's Oncology Group.
AN - 1519838217; 24687836
AB - Previous studies regarding the influence of weight on event-free survival (EFS) and treatment-related toxicity (TRT) in childhood acute lymphoblastic leukemia (ALL) considered only weight at diagnosis. Inasmuch as weight varies substantially over treatment, we hypothesized its impact on EFS is instead determined by cumulative time spent at an extreme weight during therapy and on TRT by weight at the time of toxicity.
In a cohort of 2,008 children treated for high-risk ALL in Children's Oncology Group study CCG-1961, we determined the effect on EFS of cumulative time receiving therapy at an extreme weight (either obese or underweight) between end of induction and start of maintenance therapy. We also evaluated the association between weight category and incidence and patterns of TRT during 13,946 treatment courses. Being obese or underweight at diagnosis and for ≥ 50% of the time between end of induction and start of maintenance therapy resulted in inferior EFS (hazard ratios, 1.43 and 2.30, respectively; global P < .001). Normalization of weight during that period resulted in mitigation of this risk comparable to never being obese or underweight. Obese or underweight status at start of each treatment course was significantly associated with specific patterns of TRT.
Influence of weight extremes on EFS and TRT is not set at diagnosis as previously reported but is moderated by subsequent weight status during intensive postinduction treatment phases. These observations suggest that weight is a potentially addressable risk factor to improve EFS and morbidity in pediatric ALL.
JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology
AU - Orgel, Etan
AU - Sposto, Richard
AU - Malvar, Jemily
AU - Seibel, Nita L
AU - Ladas, Elena
AU - Gaynon, Paul S
AU - Freyer, David R
AD - Etan Orgel, Jonathan Jaques Children's Cancer Center, Miller Children's Hospital, Long Beach; Etan Orgel, Paul S. Gaynon, and David R. Freyer, Keck School of Medicine, University of Southern California; Etan Orgel, Richard Sposto, Jemily Malvar, Paul S. Gaynon, and David R. Freyer, Children's Center for Cancer and Blood Diseases, Children's Hospital Los Angeles; Richard Sposto, University of Southern California, Los Angeles, CA; Nita L. Seibel, Cancer Therapy Evaluation Program, National Cancer Institute, Bethesda, MD; and Elena Ladas, Center for Comprehensive Wellness, Columbia University, New York, NY.
Y1 - 2014/05/01/
PY - 2014
DA - 2014 May 01
SP - 1331
EP - 1337
VL - 32
IS - 13
KW - Vincristine
KW - 5J49Q6B70F
KW - Asparaginase
KW - EC 3.5.1.1
KW - Prednisone
KW - VB0R961HZT
KW - Daunorubicin
KW - ZS7284E0ZP
KW - Index Medicus
KW - Young Adult
KW - Daunorubicin -- administration & dosage
KW - Randomized Controlled Trials as Topic
KW - Disease-Free Survival
KW - Vincristine -- adverse effects
KW - Humans
KW - Daunorubicin -- adverse effects
KW - Vincristine -- administration & dosage
KW - Asparaginase -- administration & dosage
KW - Child
KW - Child, Preschool
KW - Infant
KW - Asparaginase -- adverse effects
KW - Prednisone -- adverse effects
KW - Cohort Studies
KW - Adolescent
KW - Time Factors
KW - Prednisone -- administration & dosage
KW - Male
KW - Female
KW - Thinness -- complications
KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects
KW - Thinness -- physiopathology
KW - Obesity -- physiopathology
KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use
KW - Precursor Cell Lymphoblastic Leukemia-Lymphoma -- drug therapy
KW - Precursor Cell Lymphoblastic Leukemia-Lymphoma -- complications
KW - Obesity -- complications
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.atitle=Impact+on+survival+and+toxicity+by+duration+of+weight+extremes+during+treatment+for+pediatric+acute+lymphoblastic+leukemia%3A+A+report+from+the+Children%27s+Oncology+Group.&rft.au=Orgel%2C+Etan%3BSposto%2C+Richard%3BMalvar%2C+Jemily%3BSeibel%2C+Nita+L%3BLadas%2C+Elena%3BGaynon%2C+Paul+S%3BFreyer%2C+David+R&rft.aulast=Orgel&rft.aufirst=Etan&rft.date=2014-05-01&rft.volume=32&rft.issue=13&rft.spage=1331&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.issn=1527-7755&rft_id=info:doi/10.1200%2FJCO.2013.52.6962
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-06-18
N1 - Date created - 2014-04-28
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Adv Data. 2000 Jun 8;(314):1-27 [11183293]
Am J Clin Nutr. 2002 Jun;75(6):978-85 [12036802]
Blood. 2002 Sep 15;100(6):1957-64 [12200352]
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Cancer. 1983 Aug 15;52(4):587-98 [6407749]
Cancer. 1984 Nov 15;54(10):2268-71 [6488146]
Clin Pharmacol Ther. 1991 May;49(5):536-49 [1827621]
Ther Drug Monit. 1991 Jan;13(1):37-41 [2057989]
Basic Life Sci. 1993;60:71-4 [8110167]
Am J Pediatr Hematol Oncol. 1994 Aug;16(3):225-30 [8037340]
Arch Dis Child. 1994 Oct;71(4):304-10 [7979521]
Ann Hum Biol. 1997 May-Jun;24(3):209-15 [9158840]
J Pediatr Hematol Oncol. 1998 Nov-Dec;20(6):534-8 [9856673]
JAMA. 2005 Jan 12;293(2):203-11 [15644547]
Nutr Clin Pract. 2005 Aug;20(4):377-93 [16207678]
J Pediatr Hematol Oncol. 2006 Sep;28(9):575-8 [17006263]
Blood. 2006 Dec 15;108(13):3997-4002 [16917005]
Blood. 2007 Feb 1;109(3):926-35 [17003380]
J Clin Oncol. 2007 May 20;25(15):2063-9 [17513811]
Blood. 2008 Mar 1;111(5):2548-55 [18039957]
Head Neck. 2008 Apr;30(4):503-8 [18098310]
Clin Infect Dis. 2008 May 15;46(10):1582-8 [18419494]
Diabetes Care. 2008 Nov;31(11):2211-21 [18955718]
J Clin Endocrinol Metab. 2008 Nov;93(11 Suppl 1):S74-80 [18987273]
Cancer Chemother Pharmacol. 2009 Jul;64(2):243-51 [19020877]
N Engl J Med. 2009 Jun 25;360(26):2730-41 [19553647]
Cancer Res. 2009 Oct 1;69(19):7867-74 [19773440]
Pediatr Blood Cancer. 2009 Dec 15;53(7):1249-54 [19688832]
Leukemia. 2010 Feb;24(2):285-97 [20016531]
Pharmacol Res. 2010 May;61(5):385-90 [20083201]
Obesity (Silver Spring). 2011 Sep;19(9):1908-11 [21720424]
JAMA. 2012 Feb 1;307(5):483-90 [22253364]
J Clin Oncol. 2012 May 10;30(14):1663-9 [22412151]
J Pediatr Gastroenterol Nutr. 2012 Jun;54(6):720-6 [22157928]
Leuk Lymphoma. 2012 Sep;53(9):1677-81 [22390648]
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Comment In:
J Clin Oncol. 2014 May 1;32(13):1293-4 [24687820]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1200/JCO.2013.52.6962
ER -
TY - JOUR
T1 - Phase II trial on cisplatin-adriamycin-paclitaxel combination as neoadjuvant chemotherapy for locally advanced cervical adenocarcinoma.
AN - 1518817289; 24662130
AB - Neoadjuvant chemotherapy (NACT) followed by surgery is a different therapeutic approach to locally advanced cervical adenocarcinoma (LACA) and seems to offer specific advantages over chemoradiation. This phase II trial was designed to evaluate the toxicity and activity of NACT with cisplatin-adriamycin-paclitaxel (TAP) in patients with LACA.
Patients with International Federation of Gynecology and Obstetrics stage IB2-IIB uterine adenocarcinoma were treated with NACT TAP for 3 cycles. After the last cycle, patients underwent radical surgery with lymph node dissection. Pathological response was classified as no residual tumor (pCR), residual disease with less than 3-mm stromal invasion (pR1), or residual disease with more than 3-mm stromal invasion (pR2). Between 2003 and 2010, 30 women were enrolled. Fourteen complete clinical responses, 10 partial responses, and 6 stabilizations of disease were registered. Three patients achieved a pCR, 6 a pR1 response, and 21 a pR2 response. At a median follow-up of 45 months, progression-free survival and overall survival were 37 and 48 months, respectively. Hematologic toxicity was the most relevant adverse effect.
The TAP combination seems to be feasible with an acceptable toxicity profile and a promising response rate for the treatment of LACA.
JF - International journal of gynecological cancer : official journal of the International Gynecological Cancer Society
AU - Lorusso, Domenica
AU - Ramondino, Stefano
AU - Mancini, Maria
AU - Zanaboni, Flavia
AU - Ditto, Antonino
AU - Raspagliesi, Francesco
AD - Department of Gynecologic Oncology, Fondazione "IRCCS" National Cancer Institute, Milan, Italy.
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 729
EP - 734
VL - 24
IS - 4
KW - Doxorubicin
KW - 80168379AG
KW - Paclitaxel
KW - P88XT4IS4D
KW - Cisplatin
KW - Q20Q21Q62J
KW - Index Medicus
KW - Paclitaxel -- administration & dosage
KW - Young Adult
KW - Neoplasm Staging
KW - Lymphatic Metastasis
KW - Humans
KW - Prognosis
KW - Aged
KW - Doxorubicin -- administration & dosage
KW - Cisplatin -- administration & dosage
KW - Survival Rate
KW - Adult
KW - Neoplasm Grading
KW - Follow-Up Studies
KW - Middle Aged
KW - Adolescent
KW - Female
KW - Adenocarcinoma, Mucinous -- mortality
KW - Uterine Cervical Neoplasms -- mortality
KW - Neoadjuvant Therapy
KW - Adenocarcinoma -- mortality
KW - Adenocarcinoma, Clear Cell -- drug therapy
KW - Cystadenocarcinoma, Serous -- mortality
KW - Adenocarcinoma, Clear Cell -- mortality
KW - Adenocarcinoma -- pathology
KW - Cystadenocarcinoma, Serous -- secondary
KW - Adenocarcinoma, Mucinous -- secondary
KW - Adenocarcinoma, Clear Cell -- secondary
KW - Cystadenocarcinoma, Serous -- drug therapy
KW - Uterine Cervical Neoplasms -- drug therapy
KW - Adenocarcinoma, Mucinous -- drug therapy
KW - Adenocarcinoma -- drug therapy
KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use
KW - Uterine Cervical Neoplasms -- pathology
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-02-13
N1 - Date created - 2014-04-23
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1097/IGC.0000000000000115
ER -
TY - JOUR
T1 - Efficacy of glucarpidase (carboxypeptidase g2) in patients with acute kidney injury after high-dose methotrexate therapy.
AN - 1518814536; 24132809
AB - Because the incidence rate of renal impairment is 2-10% for patients treated with high-dose methotrexate and renal impairment develops in 0-12.4% of patients treated for osteosarcoma, we sought to evaluate the efficacy of glucarpidase, a recently approved drug that rapidly hydrolyzes methotrexate to inactive metabolites, which allows for nonrenal clearance in patients with delayed renal methotrexate elimination.
Pooled analysis of efficacy data from four multicenter single-arm compassionate-use clinical trials using protocols from 1993 to 2007. Of 476 patients with renal toxicity and delayed methotrexate elimination who were treated with intravenous glucarpidase for rescue after high-dose methotrexate, 169 patients had at least one preglucarpidase (baseline) plasma methotrexate concentration greater than 1 μmol/L and one postglucarpidase methotrexate concentration measurement by high-performance liquid chromatography and were included in the efficacy analysis; renal recovery was assessed in 436 patients who had at least one recorded preglucarpidase and postglucarpidase serum creatinine concentration measurement.
Efficacy was defined as rapid and sustained clinically important reduction (RSCIR) in plasma methotrexate concentration, with a concentration of 1 μmol/L or lower at all postglucarpidase determinations. Median age of efficacy-evaluable patients was 20 years (range 5 weeks-84 years). Osteosarcoma (36%), non-Hodgkin lymphoma (27%), and acute lymphoblastic leukemia (20%) were the most frequent underlying diagnoses. Median preglucarpidase serum methotrexate was 11.7 μmol/L. At the first (median 15 minutes) through the last (median 40 hours) postglucarpidase measurement, plasma methotrexate concentrations demonstrated consistent 99% median reduction. RSCIR was achieved by 83 (59%) of 140 patients. A total of 64% of patients with renal impairment greater than or equal to Common Terminology Criteria for Adverse Events grade 2 recovered to grade 0 or 1 at a median of 12.5 days after glucarpidase administration. Glucarpidase caused a clinically important 99% or greater sustained reduction of serum methotrexate levels and provided noninvasive rescue from methotrexate toxicity in renally impaired patients.
© 2013 Pharmacotherapy Publications, Inc.
JF - Pharmacotherapy
AU - Widemann, Brigitte C
AU - Schwartz, Stefan
AU - Jayaprakash, Nalini
AU - Christensen, Robbin
AU - Pui, Ching-Hon
AU - Chauhan, Nikhil
AU - Daugherty, Claire
AU - King, Thomas R
AU - Rush, Janet E
AU - Howard, Scott C
AD - National Cancer Institute, Bethesda, Maryland.
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 427
EP - 439
VL - 34
IS - 5
KW - Antimetabolites, Antineoplastic
KW - 0
KW - gamma-Glutamyl Hydrolase
KW - EC 3.4.19.9
KW - Leucovorin
KW - Q573I9DVLP
KW - Methotrexate
KW - YL5FZ2Y5U1
KW - Index Medicus
KW - acute kidney injury
KW - glucarpidase
KW - methotrexate
KW - carboxypeptidase
KW - Osteosarcoma -- drug therapy
KW - Drug Administration Schedule
KW - Bone Neoplasms -- blood
KW - Leucovorin -- administration & dosage
KW - Humans
KW - Bone Neoplasms -- drug therapy
KW - Treatment Outcome
KW - Osteosarcoma -- blood
KW - Compassionate Use Trials
KW - Osteosarcoma -- complications
KW - Bone Neoplasms -- complications
KW - Leucovorin -- therapeutic use
KW - gamma-Glutamyl Hydrolase -- administration & dosage
KW - Antimetabolites, Antineoplastic -- administration & dosage
KW - Methotrexate -- blood
KW - Methotrexate -- adverse effects
KW - Antimetabolites, Antineoplastic -- adverse effects
KW - Acute Kidney Injury -- chemically induced
KW - Methotrexate -- therapeutic use
KW - Antimetabolites, Antineoplastic -- blood
KW - Acute Kidney Injury -- prevention & control
KW - gamma-Glutamyl Hydrolase -- therapeutic use
KW - Methotrexate -- administration & dosage
KW - Antimetabolites, Antineoplastic -- therapeutic use
KW - Acute Kidney Injury -- blood
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacotherapy&rft.atitle=Efficacy+of+glucarpidase+%28carboxypeptidase+g2%29+in+patients+with+acute+kidney+injury+after+high-dose+methotrexate+therapy.&rft.au=Widemann%2C+Brigitte+C%3BSchwartz%2C+Stefan%3BJayaprakash%2C+Nalini%3BChristensen%2C+Robbin%3BPui%2C+Ching-Hon%3BChauhan%2C+Nikhil%3BDaugherty%2C+Claire%3BKing%2C+Thomas+R%3BRush%2C+Janet+E%3BHoward%2C+Scott+C&rft.aulast=Widemann&rft.aufirst=Brigitte&rft.date=2014-05-01&rft.volume=34&rft.issue=5&rft.spage=427&rft.isbn=&rft.btitle=&rft.title=Pharmacotherapy&rft.issn=1875-9114&rft_id=info:doi/10.1002%2Fphar.1360
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-12-09
N1 - Date created - 2014-04-23
N1 - Date revised - 2017-01-13
N1 - SuppNotes - Cited By:
Cancer. 1969 Jan;23(1):126-31 [5763245]
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Cancer Treat Rep. 1977 Jul;61(4):695-701 [18282]
Cancer Treat Rep. 1977 Jul;61(4):745-8 [301783]
Cancer Treat Rep. 1977 Aug;61(5):779-83 [302143]
Cancer. 1978 Jan;41(1):36-51 [342086]
J Bacteriol. 1978 May;134(2):506-13 [26657]
Clin Pharmacol Ther. 1979 Jul;26(1):63-72 [445963]
Am J Med. 1980 Mar;68(3):370-6 [6965819]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1002/phar.1360
ER -
TY - JOUR
T1 - Tempol protects cardiomyocytes from nucleoside reverse transcriptase inhibitor-induced mitochondrial toxicity.
AN - 1518242332; 24591154
AB - Nucleoside reverse transcriptase inhibitors (NRTIs), essential components of combinational therapies used for treatment of human immunodeficiency virus-1, damage heart mitochondria. Here, we have shown mitochondrial compromise in H9c2 rat cardiomyocytes exposed for 16 passages (P) to the NRTIs zidovudine (AZT, 50μM) and didanosine (ddI, 50μM), and we have demonstrated protection from mitochondrial compromise in cells treated with 200μM 1-oxyl-2,2,6,6-tetramethyl-4-hydroxypiperidine (Tempol) or 200μM 1-hydroxy-4-[2-triphenylphosphonio)-acetamido]-2,2,6,6-tetramethylpiperidine (Tempol-H), along with AZT/ddI, for 16P. Exposure to AZT/ddI caused a moderate growth inhibition at P3, P5, P7, and P13, which was not altered by addition of Tempol or Tempol-H. Mitochondrial oxidative phosphorylation capacity was determined as uncoupled oxygen consumption rate (OCR) by Seahorse XF24 Analyzer. At P5, P7, and P13, AZT/ddI-exposed cells showed an OCR reduction of 8.8-57.2% in AZT/ddI-exposed cells, compared with unexposed cells. Addition of Tempol or Tempol-H, along with AZT/ddI, resulted in OCR levels increased by about 300% above the values seen with AZT/ddI alone. The Seahorse data were further supported by electron microscopy (EM) studies in which P16 cells exposed to AZT/ddI/Tempol had less mitochondrial pathology than P16 cells exposed to AZT/ddI. Western blots of P5 cells showed that Tempol and Tempol-H upregulated expression of mitochondrial uncoupling protein-2 (UCP-2). However, Complex I activity that was reduced by AZT/ddI, was not restored in the presence of AZT/ddI/Tempol. Superoxide levels were increased in the presence of AZT/ddI and significantly decreased in cells exposed to AZT/3TC/Tempol at P3, P7, and P10. In conclusion, Tempol protects against NRTI-induced mitochondrial compromise, and UCP-2 plays a role through mild uncoupling.
JF - Toxicological sciences : an official journal of the Society of Toxicology
AU - Liu, Yongmin
AU - Shim, Eunwoo
AU - Nguyen, Phuonggiang
AU - Gibbons, Alexander T
AU - Mitchell, James B
AU - Poirier, Miriam C
AD - Carcinogen-DNA Interactions Section, Laboratory of Cancer Biology and Genetics, CCR, National Cancer Institute, NIH, Bethesda, Maryland 20892-4255.
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 133
EP - 141
VL - 139
IS - 1
KW - Cyclic N-Oxides
KW - 0
KW - Reverse Transcriptase Inhibitors
KW - Spin Labels
KW - Superoxides
KW - 11062-77-4
KW - Zidovudine
KW - 4B9XT59T7S
KW - Didanosine
KW - K3GDH6OH08
KW - tempol
KW - U78ZX2F65X
KW - Index Medicus
KW - mitochondria
KW - superoxide
KW - Seahorse extracellular flux analyzer
KW - antiretroviral therapy
KW - electron microscopy
KW - oxidative phosphorylation
KW - Rats
KW - Didanosine -- toxicity
KW - Animals
KW - Superoxides -- metabolism
KW - Zidovudine -- toxicity
KW - Microscopy, Electron
KW - Cell Line
KW - Myocytes, Cardiac -- drug effects
KW - Mitochondria -- drug effects
KW - Cyclic N-Oxides -- pharmacology
KW - Myocytes, Cardiac -- ultrastructure
KW - Reverse Transcriptase Inhibitors -- toxicity
KW - Myocytes, Cardiac -- metabolism
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicological+sciences+%3A+an+official+journal+of+the+Society+of+Toxicology&rft.atitle=Tempol+protects+cardiomyocytes+from+nucleoside+reverse+transcriptase+inhibitor-induced+mitochondrial+toxicity.&rft.au=Liu%2C+Yongmin%3BShim%2C+Eunwoo%3BNguyen%2C+Phuonggiang%3BGibbons%2C+Alexander+T%3BMitchell%2C+James+B%3BPoirier%2C+Miriam+C&rft.aulast=Liu&rft.aufirst=Yongmin&rft.date=2014-05-01&rft.volume=139&rft.issue=1&rft.spage=133&rft.isbn=&rft.btitle=&rft.title=Toxicological+sciences+%3A+an+official+journal+of+the+Society+of+Toxicology&rft.issn=1096-0929&rft_id=info:doi/10.1093%2Ftoxsci%2Fkfu034
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-12-28
N1 - Date created - 2014-04-21
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Cardiovasc Toxicol. 2012 Dec;12(4):326-40 [22744233]
Mol Cell. 2012 Oct 26;48(2):158-67 [23102266]
Free Radic Biol Med. 2003 Jun 1;34(11):1359-68 [12757846]
AIDS. 2003 Aug 15;17(12):1769-85 [12891063]
Nat Rev Drug Discov. 2003 Oct;2(10):812-22 [14526384]
Clin Infect Dis. 2004 Mar 1;38(5):743-53 [14986261]
AIDS. 2004 Jan 23;18(2):137-51 [15075530]
Cancer Res. 1991 Dec 15;51(24):6622-8 [1660344]
Lancet. 1999 Sep 25;354(9184):1084-9 [10509500]
Antivir Ther. 2005;10 Suppl 2:M13-27 [16152703]
Cardiovasc Toxicol. 2005;5(3):333-46 [16244378]
Toxicol In Vitro. 2006 Aug;20(5):535-46 [16406476]
AIDS. 2006 Aug 22;20(13):1685-90 [16931932]
Free Radic Biol Med. 2007 Jun 1;42(11):1632-50 [17462532]
Oncogene. 2008 Dec 4;27(53):6729-37 [18794809]
J Bioenerg Biomembr. 2009 Apr;41(2):133-6 [19365715]
Mitochondrion. 2010 Apr;10(3):243-52 [20005987]
Pharmacol Ther. 2010 May;126(2):119-45 [20153367]
Biochim Biophys Acta. 2010 Jun-Jul;1797(6-7):785-91 [20211596]
Expert Opin Drug Metab Toxicol. 2010 Dec;6(12):1493-504 [20929279]
Curr Drug Targets. 2011 Jun;12(6):783-9 [21275885]
Br J Cancer. 2011 Aug 9;105(4):469-74 [21712825]
J Cardiovasc Pharmacol. 2011 Oct;58(4):380-91 [21697725]
Cardiovasc Toxicol. 2012 Jun;12(2):123-34 [22170576]
Adv Exp Med Biol. 2012;748:145-69 [22729857]
Free Radic Biol Med. 2003 Jan 1;34(1):93-102 [12498984]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/toxsci/kfu034
ER -
TY - JOUR
T1 - Biomarkers of coordinate metabolic reprogramming in colorectal tumors in mice and humans.
AN - 1517883853; 24440673
AB - There are no robust noninvasive methods for colorectal cancer screening and diagnosis. Metabolomic and gene expression analyses of urine and tissue samples from mice and humans were used to identify markers of colorectal carcinogenesis.
Mass spectrometry-based metabolomic analysis of urine and tissues from wild-type C57BL/6J and Apc(Min/+) mice, as well as from mice with azoxymethane-induced tumors, was employed in tandem with gene expression analysis. Metabolic profiling was also performed on colon tumor and adjacent nontumor tissues from 39 patients. The effects of β-catenin activity on metabolic profiles were assessed in mice with colon-specific disruption of Apc. Thirteen markers were found in urine associated with development of colorectal tumors in Apc(Min/+) mice. Metabolites related to polyamine metabolism, nucleic acid metabolism, and methylation, identified tumor-bearing mice with 100% accuracy, and also accurately identified mice with polyps. Changes in gene expression in tumor samples from mice revealed that derangement of metabolites were a reflection of coordinate metabolic reprogramming in tumor tissue. Similar changes in urinary metabolites were observed in mice with azoxymethane-induced tumors and in mice with colon-specific activation of β-catenin. The metabolic alterations indicated by markers in urine, therefore, appear to occur during early stages of tumorigenesis, when cancer cells are proliferating. In tissues from patients, tumors had stage-dependent increases in 17 metabolites associated with the same metabolic pathways identified in mice. Ten metabolites that were increased in tumor tissues, compared with nontumor tissues (proline, threonine, glutamic acid, arginine, N1-acetylspermidine, xanthine, uracil, betaine, symmetric dimethylarginine, and asymmetric-dimethylarginine), were also increased in urine from tumor-bearing mice.
Gene expression and metabolomic profiles of urine and tissue samples from mice with colorectal tumors and of colorectal tumor samples from patients revealed pathways associated with derangement of specific metabolic pathways that are indicative of early-stage tumor development. These urine and tissue markers might be used in early detection of colorectal cancer.
Copyright © 2014 AGA Institute. Published by Elsevier Inc. All rights reserved.
JF - Gastroenterology
AU - Manna, Soumen K
AU - Tanaka, Naoki
AU - Krausz, Kristopher W
AU - Haznadar, Majda
AU - Xue, Xiang
AU - Matsubara, Tsutomu
AU - Bowman, Elise D
AU - Fearon, Eric R
AU - Harris, Curtis C
AU - Shah, Yatrik M
AU - Gonzalez, Frank J
AD - Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland. ; Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland. ; Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, Michigan. ; Departments of Internal Medicine, Pathology and Human Genetics, University of Michigan, Ann Arbor, Michigan. ; Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland. Electronic address: gonzalef@mail.nih.gov.
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 1313
EP - 1324
VL - 146
IS - 5
KW - Biomarkers, Tumor
KW - 0
KW - Azoxymethane
KW - MO0N1J0SEN
KW - Abridged Index Medicus
KW - Index Medicus
KW - Metabolic Reprogramming
KW - Colorectal Cancer
KW - Cancer Biomarker
KW - Metabolomics
KW - Apc(Min/+)
KW - Real-Time Polymerase Chain Reaction
KW - Spectrometry, Mass, Electrospray Ionization
KW - Animals
KW - High-Throughput Screening Assays
KW - Reproducibility of Results
KW - Neoplasm Staging
KW - Protein Interaction Maps
KW - Humans
KW - Disease Models, Animal
KW - Predictive Value of Tests
KW - Mice
KW - Cell Proliferation
KW - Mice, Transgenic
KW - Genes, APC
KW - Gene Expression Regulation, Neoplastic
KW - Protein Interaction Mapping
KW - Mice, Inbred C57BL
KW - Chromatography, Reverse-Phase
KW - Biomarkers, Tumor -- metabolism
KW - Metabolomics -- methods
KW - Biomarkers, Tumor -- genetics
KW - Colorectal Neoplasms -- pathology
KW - Colorectal Neoplasms -- metabolism
KW - Colorectal Neoplasms -- urine
KW - Biomarkers, Tumor -- urine
KW - Colorectal Neoplasms -- genetics
KW - Colorectal Neoplasms -- chemically induced
KW - Gene Expression Profiling -- methods
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gastroenterology&rft.atitle=Biomarkers+of+coordinate+metabolic+reprogramming+in+colorectal+tumors+in+mice+and+humans.&rft.au=Manna%2C+Soumen+K%3BTanaka%2C+Naoki%3BKrausz%2C+Kristopher+W%3BHaznadar%2C+Majda%3BXue%2C+Xiang%3BMatsubara%2C+Tsutomu%3BBowman%2C+Elise+D%3BFearon%2C+Eric+R%3BHarris%2C+Curtis+C%3BShah%2C+Yatrik+M%3BGonzalez%2C+Frank+J&rft.aulast=Manna&rft.aufirst=Soumen&rft.date=2014-05-01&rft.volume=146&rft.issue=5&rft.spage=1313&rft.isbn=&rft.btitle=&rft.title=Gastroenterology&rft.issn=1528-0012&rft_id=info:doi/10.1053%2Fj.gastro.2014.01.017
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-06-05
N1 - Date created - 2014-04-18
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Gut. 2007 Jan;56(1):140-8 [16840508]
Prostate Cancer Prostatic Dis. 2006;9(3):230-4 [16683009]
Cancer Res. 2007 Oct 15;67(20):9721-30 [17942902]
Cell Metab. 2008 Jan;7(1):11-20 [18177721]
Mol Cancer. 2008;7:72 [18799019]
Proc Natl Acad Sci U S A. 2008 Dec 2;105(48):18782-7 [19033189]
J Proteome Res. 2009 Oct;8(10):4844-50 [19678709]
Cancer Biol Ther. 2009 Jul;8(14):1313-7 [19502780]
J Proteome Res. 2010 Mar 5;9(3):1627-34 [20121166]
Anticancer Res. 2010 Feb;30(2):369-74 [20332441]
Genes Dev. 2010 Jul 15;24(14):1507-18 [20634317]
Future Oncol. 2010 Sep;6(9):1395-406 [20919825]
J Biol Chem. 2010 Nov 19;285(47):36267-74 [20813845]
Nucleic Acids Res. 2011 Jan;39(Database issue):D561-8 [21045058]
Oncogene. 2011 May 19;30(20):2379-89 [21242974]
J Proteome Res. 2011 Sep 2;10(9):4120-33 [21749142]
CA Cancer J Clin. 2012 Jan-Feb;62(1):10-29 [22237781]
Cancer Cell. 2012 Mar 20;21(3):297-308 [22439925]
N Engl J Med. 2012 Jun 21;366(25):2345-57 [22612596]
Lancet. 2012 Nov 24;380(9856):1840-50 [23079588]
J Natl Cancer Inst. 2001 Jun 6;93(11):858-65 [11390535]
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Cancer Metastasis Rev. 2004 Jan-Jun;23(1-2):29-39 [15000147]
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Metabolism. 1979 Aug;28(8):801-4 [454517]
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Cell. 1996 Oct 18;87(2):159-70 [8861899]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1053/j.gastro.2014.01.017
ER -
TY - JOUR
T1 - Antiangiogenesis beyond VEGF inhibition: a journey from antiangiogenic single-target to broad-spectrum agents.
AN - 1517883597; 24360358
AB - Although the inhibition of angiogenesis is an established modality of cancer treatment, concerns regarding toxicity and drug resistance still constitute barriers to be overcome. For almost a decade since the approval of bevacizumab in 2004, the efforts on antiangiogenic therapeutics have been mainly focused in inhibiting the VEGF pathway. The ongoing understanding of the complexity of the angiogenic process has broadened the spotlight to include concurrent and downstream players to the list of targeted inhibitors. In this review, we summarize the currently existing and the promising antiangiogenic treatments, envisioning an apparent evolutionary trend towards the development of angiogenesis inhibitors of three modalities: single-target, multi-target, and broad-spectrum agents. The clinical efficacy and some structural aspects of monoclonal antibodies, small molecules, endogenous and synthetic angiogenesis inhibitors and their molecular targets are discussed, and the targeting of endothelial cells with the use of cytotoxic drugs in a metronomic schedule is appraised. The reader is invited to revisit current expectations about antiangiogenic therapy in an attempt to set consistent clinical endpoints from which patients could gain real and lasting clinical benefits.
Copyright © 2013 Elsevier Ltd. All rights reserved.
JF - Cancer treatment reviews
AU - Limaverde-Sousa, Gabriel
AU - Sternberg, Cinthya
AU - Ferreira, Carlos Gil
AD - Coordination of Clinical Research and Technology Incorporation, National Cancer Institute of Brazil (INCA), Rio de Janeiro, Brazil. Electronic address: gabriel.sousa@inca.gov.br. ; Coordination of Clinical Research and Technology Incorporation, National Cancer Institute of Brazil (INCA), Rio de Janeiro, Brazil.
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 548
EP - 557
VL - 40
IS - 4
KW - Angiogenesis Inhibitors
KW - 0
KW - Vascular Endothelial Growth Factor A
KW - Index Medicus
KW - Vascular endothelial growth factor
KW - Protein-tyrosine kinases
KW - Endostatin
KW - Sunitinib
KW - Monoclonal antibodies
KW - Drug therapy
KW - Angiogenesis inhibitors
KW - Bevacizumab
KW - Animals
KW - Neovascularization, Pathologic -- drug therapy
KW - Humans
KW - Vascular Endothelial Growth Factor A -- antagonists & inhibitors
KW - Angiogenesis Inhibitors -- therapeutic use
KW - Neoplasms -- drug therapy
KW - Angiogenesis Inhibitors -- pharmacology
KW - Neoplasms -- blood supply
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1517883597?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+treatment+reviews&rft.atitle=Antiangiogenesis+beyond+VEGF+inhibition%3A+a+journey+from+antiangiogenic+single-target+to+broad-spectrum+agents.&rft.au=Limaverde-Sousa%2C+Gabriel%3BSternberg%2C+Cinthya%3BFerreira%2C+Carlos+Gil&rft.aulast=Limaverde-Sousa&rft.aufirst=Gabriel&rft.date=2014-05-01&rft.volume=40&rft.issue=4&rft.spage=548&rft.isbn=&rft.btitle=&rft.title=Cancer+treatment+reviews&rft.issn=1532-1967&rft_id=info:doi/10.1016%2Fj.ctrv.2013.11.009
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-04-21
N1 - Date created - 2014-03-10
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.ctrv.2013.11.009
ER -
TY - JOUR
T1 - Bone marrow mesenchymal stromal cells to treat tissue damage in allogeneic stem cell transplant recipients: correlation of biological markers with clinical responses.
AN - 1517880573; 24452962
AB - Bone marrow mesenchymal stromal cells (BMSCs) have been used to treat acute graft-versus-host disease (GVHD) and other complications following allogeneic hematopoietic stem cell transplantation (SCT). We conducted a phase I trial using third party, early passage BMSCs for patients with steroid-refractory GVHD, tissue injury, or marrow failure following SCT to investigate safety and efficacy. To identify mechanisms of BMSC immunomodulation and tissue repair, patients were serially monitored for plasma GVHD biomarkers, cytokines, and lymphocyte phenotype. Ten subjects were infused a fixed dose of 2 × 10(6) BMSCs/kg intravenously weekly for three doses. There was no treatment-related toxicity (primary endpoint). Eight subjects were evaluable for response at 4 weeks after the last infusion. Five of the seven patients with steroid-refractory acute GVHD achieved a complete response, two of two patients with tissue injury (pneumomediastinum/pneumothorax) achieved resolution but there was no response in two subjects with delayed marrow failure. Rapid reductions in inflammatory cytokines were observed. Clinical responses correlated with a fall in biomarkers (Reg 3α, CK18, and Elafin) relevant for the site of GVHD or tissue injury. The GVHD complete responders survived significantly longer and had higher baseline absolute lymphocyte and central memory CD4 and CD8 counts. Cytokine changes also segregated with survival. These results confirm that BMSCs are associated with rapid clinical and biomarker responses in GVHD and tissue injury. However, BMSCs were ineffective in patients with prolonged GVHD with lower lymphocyte counts, which suggest that effective GVHD control by BMSCs requires a relatively intact immune system.
© 2014 AlphaMed Press.
JF - Stem cells (Dayton, Ohio)
AU - Yin, Fang
AU - Battiwalla, Minoo
AU - Ito, Sawa
AU - Feng, Xingmin
AU - Chinian, Fariba
AU - Melenhorst, Jan Joseph
AU - Koklanaris, Eleftheria
AU - Sabatino, Marianna
AU - Stroncek, David
AU - Samsel, Leigh
AU - Klotz, Jeffrey
AU - Hensel, Nancy F
AU - Robey, Pamela G
AU - Barrett, A John
AD - Hematology Branch, NHLBI, National Institutes of Health, Bethesda, Maryland, USA.
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 1278
EP - 1288
VL - 32
IS - 5
KW - Antigens, Neoplasm
KW - 0
KW - Biomarkers, Tumor
KW - Cytokines
KW - Elafin
KW - Keratin-18
KW - Lectins, C-Type
KW - pancreatitis-associated protein
KW - Index Medicus
KW - Mesenchymal stromal cell
KW - Allogeneic stem cell transplantation
KW - Graft-versus-host disease
KW - Biomarkers
KW - Cytokines -- blood
KW - Young Adult
KW - CD4-Positive T-Lymphocytes -- cytology
KW - Pneumothorax -- therapy
KW - Humans
KW - Pneumothorax -- blood
KW - Pneumothorax -- etiology
KW - Aged
KW - Lymphocyte Count
KW - Adult
KW - Treatment Outcome
KW - Mediastinal Emphysema -- etiology
KW - Biomarkers, Tumor -- blood
KW - Male
KW - Keratin-18 -- blood
KW - Survival Analysis
KW - Infusions, Intravenous
KW - Antigens, Neoplasm -- blood
KW - Lectins, C-Type -- blood
KW - Elafin -- blood
KW - Mediastinal Emphysema -- blood
KW - Transplantation, Homologous
KW - CD8-Positive T-Lymphocytes -- cytology
KW - Middle Aged
KW - Mediastinal Emphysema -- therapy
KW - Female
KW - Graft vs Host Disease -- therapy
KW - Mesenchymal Stem Cell Transplantation -- methods
KW - Graft vs Host Disease -- blood
KW - Bone Marrow Cells -- cytology
KW - Graft vs Host Disease -- etiology
KW - Hematopoietic Stem Cell Transplantation -- methods
KW - Hematopoietic Stem Cell Transplantation -- adverse effects
KW - Mesenchymal Stromal Cells -- cytology
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1517880573?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Stem+cells+%28Dayton%2C+Ohio%29&rft.atitle=Bone+marrow+mesenchymal+stromal+cells+to+treat+tissue+damage+in+allogeneic+stem+cell+transplant+recipients%3A+correlation+of+biological+markers+with+clinical+responses.&rft.au=Yin%2C+Fang%3BBattiwalla%2C+Minoo%3BIto%2C+Sawa%3BFeng%2C+Xingmin%3BChinian%2C+Fariba%3BMelenhorst%2C+Jan+Joseph%3BKoklanaris%2C+Eleftheria%3BSabatino%2C+Marianna%3BStroncek%2C+David%3BSamsel%2C+Leigh%3BKlotz%2C+Jeffrey%3BHensel%2C+Nancy+F%3BRobey%2C+Pamela+G%3BBarrett%2C+A+John&rft.aulast=Yin&rft.aufirst=Fang&rft.date=2014-05-01&rft.volume=32&rft.issue=5&rft.spage=1278&rft.isbn=&rft.btitle=&rft.title=Stem+cells+%28Dayton%2C+Ohio%29&rft.issn=1549-4918&rft_id=info:doi/10.1002%2Fstem.1638
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-12-15
N1 - Date created - 2014-04-17
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
J Immunother. 2009 Sep;32(7):755-64 [19561533]
Bone Marrow Transplant. 2009 Mar;43(6):447-54 [18955980]
Biol Blood Marrow Transplant. 2011 Apr;17(4):534-41 [20457269]
Cytotherapy. 2011 Jul;13(6):661-74 [21250865]
Blood. 2012 Mar 22;119(12):2960-3 [22286196]
J Transl Med. 2012;10:23 [22309358]
Biol Blood Marrow Transplant. 2012 Apr;18(4):557-64 [21820393]
Blood. 2012 Apr 19;119(16):3854-60 [22383800]
Blood. 2013 Jan 24;121(4):585-94 [23165480]
Stem Cells. 2013 Aug;31(8):1715-25 [23554294]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1002/stem.1638
ER -
TY - JOUR
T1 - Phase 2 randomized, flexible crossover, double-blinded, placebo-controlled trial of the farnesyltransferase inhibitor tipifarnib in children and young adults with neurofibromatosis type 1 and progressive plexiform neurofibromas.
AN - 1516722580; 24500418
AB - RAS is dysregulated in neurofibromatosis type 1 (NF1) related plexiform neurofibromas (PNs). The activity of tipifarnib, which blocks RAS signaling by inhibiting its farnesylation, was tested in children and young adults with NF1 and progressive PNs.
Patients aged 3-25 years with NF1-related PNs and imaging evidence of tumor progression were randomized in a double-blinded fashion to receive tipifarnib (200 mg/m(2) orally every 12 h) or placebo (phase A) and crossed over to the opposite treatment arm at the time of tumor progression (phase B). PN volumes were measured with MRI, and progression was defined as ≥20% volume increase. Time to progression (TTP) in phase A was the primary endpoint, and the trial was powered to detect whether tipifarnib doubled TTP compared with placebo. Toxicity, response, and quality of life were also monitored. Sixty-two patients were enrolled. Tipifarnib and placebo were well tolerated. On phase A, the median TTP was 10.6 months on the placebo arm and 19.2 months on the tipifarnib arm (P = .12; 1-sided). Quality of life improved significantly compared with baseline on the tipifarnib arm but not on the placebo arm. Volumetric tumor measurement detected tumor progression earlier than conventional 2-dimensional (WHO) and 1-dimensional (RECIST) methods.
Tipifarnib was well tolerated but did not significantly prolong TTP of PNs compared with placebo. The randomized, flexible crossover design and volumetric PN assessment provided a feasible and efficient means of assessing the efficacy of tipifarnib. The placebo arm serves as an historical control group for phase 2 single-arm trials directed at progressive PNs.
JF - Neuro-oncology
AU - Widemann, Brigitte C
AU - Dombi, Eva
AU - Gillespie, Andrea
AU - Wolters, Pamela L
AU - Belasco, Jean
AU - Goldman, Stewart
AU - Korf, Bruce R
AU - Solomon, Jeffrey
AU - Martin, Staci
AU - Salzer, Wanda
AU - Fox, Elizabeth
AU - Patronas, Nicholas
AU - Kieran, Mark W
AU - Perentesis, John P
AU - Reddy, Alyssa
AU - Wright, John J
AU - Kim, AeRang
AU - Steinberg, Seth M
AU - Balis, Frank M
AD - Pediatric Oncology Branch, National Cancer Institute, Bethesda, Maryland (B.W., E.D., A.G., P.W., S.M., E.F., F.B.); Cancer Therapy Evaluation Program, Investigational Drug Branch, National Cancer Institute, Bethesda, Maryland (J.W.); Biostatistics and Data Management Section, National Cancer Institute, Bethesda, Maryland (S.S.); Diagnostic Radiology Department, National Institutes of Health, Bethesda, Maryland (N.P.); The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania (J.B., E.F., F.B.); Ann and Robert H. Lurie Children's Hospital, Chicago, Illinois (S.G.); Department of Genetics, University of Alabama at Birmingham, South Birmingham, Alabama (B.K.); Expert Image Analysis LC, Potomac, Maryland (J.S.); Dana-Farber/Children's Hospital Cancer Center, Boston, Massachusetts (M.K.); Cincinnati Children's Hospital, Cincinnati, Ohio (J.P.); Children's National Medical Center, Washington, DC (A.K.); US Army Medical Research and Material Command, Fort Detrick, Maryland (W.S.); Children's Hospital of Alabama, Birmingham, Alabama (A.R.).
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 707
EP - 718
VL - 16
IS - 5
KW - Antineoplastic Agents
KW - 0
KW - Enzyme Inhibitors
KW - Quinolones
KW - Farnesyltranstransferase
KW - EC 2.5.1.29
KW - tipifarnib
KW - MAT637500A
KW - Index Medicus
KW - neurofibromatosis type 1
KW - RAS signaling
KW - trial design
KW - phase 2 trial
KW - plexiform neurofibroma
KW - Young Adult
KW - Double-Blind Method
KW - Humans
KW - Adult
KW - Treatment Outcome
KW - Disease Progression
KW - Cross-Over Studies
KW - Child
KW - Adolescent
KW - Male
KW - Female
KW - Child, Preschool
KW - Neurofibromatosis 1 -- drug therapy
KW - Enzyme Inhibitors -- therapeutic use
KW - Quinolones -- therapeutic use
KW - Neurofibroma, Plexiform -- drug therapy
KW - Farnesyltranstransferase -- antagonists & inhibitors
KW - Antineoplastic Agents -- therapeutic use
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1516722580?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuro-oncology&rft.atitle=Phase+2+randomized%2C+flexible+crossover%2C+double-blinded%2C+placebo-controlled+trial+of+the+farnesyltransferase+inhibitor+tipifarnib+in+children+and+young+adults+with+neurofibromatosis+type+1+and+progressive+plexiform+neurofibromas.&rft.au=Widemann%2C+Brigitte+C%3BDombi%2C+Eva%3BGillespie%2C+Andrea%3BWolters%2C+Pamela+L%3BBelasco%2C+Jean%3BGoldman%2C+Stewart%3BKorf%2C+Bruce+R%3BSolomon%2C+Jeffrey%3BMartin%2C+Staci%3BSalzer%2C+Wanda%3BFox%2C+Elizabeth%3BPatronas%2C+Nicholas%3BKieran%2C+Mark+W%3BPerentesis%2C+John+P%3BReddy%2C+Alyssa%3BWright%2C+John+J%3BKim%2C+AeRang%3BSteinberg%2C+Seth+M%3BBalis%2C+Frank+M&rft.aulast=Widemann&rft.aufirst=Brigitte&rft.date=2014-05-01&rft.volume=16&rft.issue=5&rft.spage=707&rft.isbn=&rft.btitle=&rft.title=Neuro-oncology&rft.issn=1523-5866&rft_id=info:doi/10.1093%2Fneuonc%2Fnou004
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-03-31
N1 - Date created - 2014-04-15
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Anticancer Drugs. 2001 Mar;12(3):193-7 [11290865]
Nature. 2002 Jan 31;415(6871):526-30 [11793011]
Cancer Res. 2002 Mar 1;62(5):1573-7 [11894862]
J Med Genet. 2002 May;39(5):311-4 [12011145]
Expert Rev Anticancer Ther. 2003 Oct;3(5):595-614 [14599084]
Value Health. 2003 Sep-Oct;6(5):522-31 [14627058]
Comput Med Imaging Graph. 2004 Jul;28(5):257-65 [15249071]
Curr Opin Drug Discov Devel. 2004 Jul;7(4):478-86 [15338957]
Cancer. 1981 Jan 1;47(1):207-14 [7459811]
Neurofibromatosis. 1988;1(3):172-8 [3152465]
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J Pediatr. 1997 Nov;131(5):678-82 [9403645]
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Cancer Res. 2005 Apr 1;65(7):2755-60 [15805275]
Cancer Cell. 2005 Apr;7(4):297-300 [15837619]
J Clin Oncol. 2006 Jan 20;24(3):507-16 [16421428]
Future Oncol. 2005 Dec;1(6):719-31 [16556050]
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Neurology. 2007 Feb 27;68(9):643-7 [17215493]
Pediatr Neurol. 2007 May;36(5):293-300 [17509460]
BMB Rep. 2009 May 31;42(5):239-44 [19470236]
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Neurology. 2009 Oct 20;73(16):1273-9 [19841379]
Transplant Proc. 2009 Dec;41(10):4285-8 [20005385]
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J Pediatr. 2012 Mar;160(3):461-7 [21996156]
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Neuroscience. 2012 Oct 25;223:102-13 [22750207]
Pediatr Blood Cancer. 2013 Jan;60(1):59-64 [22645095]
Lancet Oncol. 2012 Dec;13(12):1218-24 [23099009]
Pediatr Blood Cancer. 2013 Mar;60(3):396-401 [22961690]
J Clin Oncol. 1999 Nov;17(11):3631-52 [10550163]
J Natl Cancer Inst. 2000 Feb 2;92(3):205-16 [10655437]
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Comment In:
Neuro Oncol. 2014 May;16(5):617-8 [24714524]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/neuonc/nou004
ER -
TY - JOUR
T1 - High frequency of PTEN mutations in nevi and melanomas from xeroderma pigmentosum patients.
AN - 1516401248; 24483290
AB - We examined nevi and melanomas in 10 xeroderma pigmentosum (XP) patients with defective DNA repair. The lesions had a lentiginous appearance with markedly increased numbers of melanocytes. Using laser capture microdissection, we performed DNA sequencing of 18 benign and atypical nevi and 75 melanomas (melanoma in situ and invasive melanomas). The nevi had a similar high frequency of PTEN mutations as melanomas [61% (11/18) versus 53% (39/73)]. Both had a very high proportion of UV-type mutations (occurring at adjacent pyrimidines) [91% (10/11) versus 92% (36/39)]. In contrast to melanomas in the general population, the frequency of BRAF mutations (11%, 7/61), NRAS mutations (21%, 13/62), and KIT mutations (21%, 6/28) in XP melanomas was lower than for PTEN. Phospho-S6 immunostaining indicated activation of the mTOR pathway in the atypical nevi and melanomas. Thus, the clinical and histological appearances and the molecular pathology of these UV-related XP nevi and melanomas were different from nevi and melanomas in the general population.
© 2014 Published 2014. This article is a U.S. Government work and is in the public domain in the USA.
JF - Pigment cell & melanoma research
AU - Masaki, Taro
AU - Wang, Yun
AU - DiGiovanna, John J
AU - Khan, Sikandar G
AU - Raffeld, Mark
AU - Beltaifa, Senda
AU - Hornyak, Thomas J
AU - Darling, Thomas N
AU - Lee, Chyi-Chia R
AU - Kraemer, Kenneth H
AD - Dermatology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA; Division of Dermatology, Graduate School of Medicine, Kobe University, Kobe, Japan.
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 454
EP - 464
VL - 27
IS - 3
KW - DNA, Neoplasm
KW - 0
KW - Membrane Proteins
KW - Neoplasm Proteins
KW - MTOR protein, human
KW - EC 2.7.1.1
KW - TOR Serine-Threonine Kinases
KW - Proto-Oncogene Proteins c-kit
KW - EC 2.7.10.1
KW - BRAF protein, human
KW - EC 2.7.11.1
KW - Proto-Oncogene Proteins B-raf
KW - PTEN Phosphohydrolase
KW - EC 3.1.3.67
KW - PTEN protein, human
KW - GTP Phosphohydrolases
KW - EC 3.6.1.-
KW - NRAS protein, human
KW - Index Medicus
KW - xeroderma pigmentosum
KW - UV carcinogenesis
KW - mTOR
KW - nevi
KW - melanoma
KW - DNA repair
KW - PTEN
KW - Young Adult
KW - Sunlight -- adverse effects
KW - DNA Mutational Analysis
KW - Humans
KW - Neoplasms, Radiation-Induced -- genetics
KW - Membrane Proteins -- genetics
KW - Precancerous Conditions -- pathology
KW - Proto-Oncogene Proteins B-raf -- genetics
KW - Precancerous Conditions -- genetics
KW - Oncogenes
KW - Loss of Heterozygosity
KW - GTP Phosphohydrolases -- genetics
KW - Neoplasms, Radiation-Induced -- pathology
KW - TOR Serine-Threonine Kinases -- physiology
KW - Precancerous Conditions -- etiology
KW - Adult
KW - Neoplasm Proteins -- genetics
KW - Ultraviolet Rays -- adverse effects
KW - DNA, Neoplasm -- genetics
KW - Middle Aged
KW - Dermoscopy
KW - Proto-Oncogene Proteins c-kit -- genetics
KW - Female
KW - Male
KW - Nevus, Pigmented -- genetics
KW - Nevus, Pigmented -- pathology
KW - Melanoma -- etiology
KW - Skin Neoplasms -- etiology
KW - Nevus, Pigmented -- etiology
KW - Xeroderma Pigmentosum -- genetics
KW - Skin Neoplasms -- pathology
KW - Xeroderma Pigmentosum -- complications
KW - PTEN Phosphohydrolase -- genetics
KW - Skin Neoplasms -- genetics
KW - Melanoma -- pathology
KW - Melanoma -- genetics
KW - Mutation
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1516401248?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pigment+cell+%26+melanoma+research&rft.atitle=High+frequency+of+PTEN+mutations+in+nevi+and+melanomas+from+xeroderma+pigmentosum+patients.&rft.au=Masaki%2C+Taro%3BWang%2C+Yun%3BDiGiovanna%2C+John+J%3BKhan%2C+Sikandar+G%3BRaffeld%2C+Mark%3BBeltaifa%2C+Senda%3BHornyak%2C+Thomas+J%3BDarling%2C+Thomas+N%3BLee%2C+Chyi-Chia+R%3BKraemer%2C+Kenneth+H&rft.aulast=Masaki&rft.aufirst=Taro&rft.date=2014-05-01&rft.volume=27&rft.issue=3&rft.spage=454&rft.isbn=&rft.btitle=&rft.title=Pigment+cell+%26+melanoma+research&rft.issn=1755-148X&rft_id=info:doi/10.1111%2Fpcmr.12226
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-12-18
N1 - Date created - 2014-04-14
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1111/pcmr.12226
ER -
TY - JOUR
T1 - Renal cell carcinoma: molecular biology and targeted therapy.
AN - 1515647413; 24675233
AB - Renal cell carcinoma (RCC) continues to be the subject of vigorous clinical and translational investigation. Advances in systemic targeted therapies, new molecular pathways and immunotherapy approaches will be discussed.
Agents targeting the vascular endothelial growth factor (VEGF) and/or the mammalian target of rapamycin (mTOR) pathways continue to be the mainstay for treating metastatic RCC (mRCC). Although enhanced target specificity has improved the toxicity profile associated with newer VEGF-pathway antagonists, durable complete responses remain the exception. Identification of novel pathways/agents, as well as the optimal sequencing and combination of existing targeted agents, remain areas of active study. In addition, emerging data from early clinical trials have reinvigorated interest in immunomodulatory agents. The therapeutic armamentarium available to genitourinary oncologists continues to grow, but much work remains to be done to fully realize the potential of pathway-specific targeted strategies and immune-based approaches for mRCC.
JF - Current opinion in oncology
AU - Su, Daniel
AU - Stamatakis, Lambros
AU - Singer, Eric A
AU - Srinivasan, Ramaprasad
AD - aUrologic Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland bSection of Urologic Oncology, Rutgers Cancer Institute of New Jersey and Robert Wood Johnson Medical School, New Brunswick, New Jersey, USA.
Y1 - 2014/05//
PY - 2014
DA - May 2014
SP - 321
EP - 327
VL - 26
IS - 3
KW - Antineoplastic Agents
KW - 0
KW - Index Medicus
KW - Molecular Biology
KW - Humans
KW - Immunotherapy -- methods
KW - Kidney Neoplasms -- genetics
KW - Kidney Neoplasms -- drug therapy
KW - Carcinoma, Renal Cell -- therapy
KW - Molecular Targeted Therapy -- methods
KW - Antineoplastic Agents -- therapeutic use
KW - Carcinoma, Renal Cell -- genetics
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Current+opinion+in+oncology&rft.atitle=Renal+cell+carcinoma%3A+molecular+biology+and+targeted+therapy.&rft.au=Su%2C+Daniel%3BStamatakis%2C+Lambros%3BSinger%2C+Eric+A%3BSrinivasan%2C+Ramaprasad&rft.aulast=Su&rft.aufirst=Daniel&rft.date=2014-05-01&rft.volume=26&rft.issue=3&rft.spage=321&rft.isbn=&rft.btitle=&rft.title=Current+opinion+in+oncology&rft.issn=1531-703X&rft_id=info:doi/10.1097%2FCCO.0000000000000069
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-11-18
N1 - Date created - 2014-04-11
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Mol Cell Biol. 2004 Aug;24(16):7130-9 [15282312]
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J Clin Oncol. 2010 May 1;28(13):2137-43 [20368558]
Nat Rev Urol. 2010 May;7(5):277-85 [20448661]
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Cancer. 2010 Sep 15;116(18):4256-65 [20549832]
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Oncogene. 2011 Mar 10;30(10):1183-93 [21057538]
Curr Opin Oncol. 2011 May;23(3):283-9 [21330923]
Lancet. 2011 Dec 3;378(9807):1931-9 [22056247]
Nat Genet. 2012 Jan;44(1):17-9 [22138691]
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J Clin Oncol. 2012 May 10;30(14):1678-85 [22493422]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1097/CCO.0000000000000069
ER -
TY - JOUR
T1 - Integrating pharmacogenetic information and clinical decision support into the electronic health record.
AN - 1515643011; 24302286
AB - Pharmacogenetics (PG) examines gene variations for drug disposition, response, or toxicity. At the National Institutes of Health Clinical Center (NIH CC), a multidepartment Pharmacogenetics Testing Implementation Committee (PGTIC) was established to develop clinical decision support (CDS) algorithms for abacavir, carbamazepine, and allopurinol, medications for which human leukocyte antigen (HLA) variants predict severe hypersensitivity reactions. Providing PG CDS in the electronic health record (EHR) during order entry could prevent adverse drug events. Medical Logic Module (MLM) programming was used to implement PG CDS in our EHR. The MLM checks to see if an HLA sequence-based gene test is ordered. A message regarding test status (result present, absent, pending, or test not ordered) is displayed on the order form, and the MLM determines if the prescriber can place the order, place it but require an over-ride reason, or be blocked from placing the order. Since implementation, more than 725 medication orders have been placed for over 230 patients by 154 different prescribers for the three drugs included in our PG program. Prescribers commonly used an over-ride reason when placing the order mainly because patients had been receiving the drug without reaction before implementation of the CDS program. Successful incorporation of PG CDS into the NIH CC EHR required a coordinated, interdisciplinary effort to ensure smooth activation and a positive effect on patient care. Prescribers have adapted to using the CDS and have ordered PG testing as a direct result of the implementation.
JF - Journal of the American Medical Informatics Association : JAMIA
AU - Goldspiel, Barry R
AU - Flegel, Willy A
AU - DiPatrizio, Gary
AU - Sissung, Tristan
AU - Adams, Sharon D
AU - Penzak, Scott R
AU - Biesecker, Leslie G
AU - Fleisher, Thomas A
AU - Patel, Jharana J
AU - Herion, David
AU - Figg, William D
AU - Lertora, Juan J L
AU - McKeeby, Jon W
AD - Pharmacy Department, National Institutes of Health Clinical Center, Bethesda, Maryland, USA.
PY - 2014
SP - 522
EP - 528
VL - 21
IS - 3
KW - HLA Antigens
KW - 0
KW - Index Medicus
KW - Patient Safety
KW - Computerized Prescriber Order Entry
KW - Informatics
KW - Clinical Decision Support
KW - Pharmacogenetics
KW - Genotype
KW - HLA Antigens -- genetics
KW - Systems Integration
KW - Medical Order Entry Systems
KW - Humans
KW - Precision Medicine -- methods
KW - Decision Support Systems, Clinical
KW - Algorithms
KW - User-Computer Interface
KW - Electronic Health Records
KW - Drug Therapy, Computer-Assisted
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+American+Medical+Informatics+Association+%3A+JAMIA&rft.atitle=Integrating+pharmacogenetic+information+and+clinical+decision+support+into+the+electronic+health+record.&rft.au=Goldspiel%2C+Barry+R%3BFlegel%2C+Willy+A%3BDiPatrizio%2C+Gary%3BSissung%2C+Tristan%3BAdams%2C+Sharon+D%3BPenzak%2C+Scott+R%3BBiesecker%2C+Leslie+G%3BFleisher%2C+Thomas+A%3BPatel%2C+Jharana+J%3BHerion%2C+David%3BFigg%2C+William+D%3BLertora%2C+Juan+J+L%3BMcKeeby%2C+Jon+W&rft.aulast=Goldspiel&rft.aufirst=Barry&rft.date=2014-05-01&rft.volume=21&rft.issue=3&rft.spage=522&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+American+Medical+Informatics+Association+%3A+JAMIA&rft.issn=1527-974X&rft_id=info:doi/10.1136%2Famiajnl-2013-001873
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-06-05
N1 - Date created - 2014-04-10
N1 - Date revised - 2017-01-13
N1 - SuppNotes - Cited By:
Ann Intern Med. 2006 Nov 21;145(10):749-57 [17116919]
J Am Med Inform Assoc. 2014 Feb;21(e1):e93-9 [23978487]
N Engl J Med. 2008 Feb 7;358(6):568-79 [18256392]
Ann Pharmacother. 2008 Mar;42(3):387-96 [18303141]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1136/amiajnl-2013-001873
ER -
TY - JOUR
T1 - Cigarette smoking and postmenopausal breast cancer risk in a prospective cohort
AN - 1529922224; 19814340
AB - Background: The relationship between cigarette smoking and breast cancer risk has been inconsistent, potentially due to modification by other factors or confounding. Methods: We examined smoking and breast cancer risk in a prospective cohort of 186 150 female AARP (formerly American Association of Retired Persons) members, ages 50-71 years, who joined the study in 1995-96 by responding to a questionnaire. Through 2006, 7481 breast cancers were diagnosed. Multivariable-adjusted hazard ratios (HRs) were estimated, overall and stratified by breast cancer risk factors, using Cox proportional hazards regression. Multiplicative interactions were evaluated using the likelihood ratio test. Results: Increased breast cancer risk was associated with current (HR 1.19, 95% confidence interval (CI) 1.10-1.28) and former (HR 1.07, CI 1.01-1.13) smoking. The current smoking association was stronger among women without (HR 1.24, CI 1.15-1.35) as compared to those with a family history of breast cancer (HR 0.94, CI 0.78-1.13) (P-interaction=0.03). The current smoking association was also stronger among those with later ([egs]15 years: HR 1.52, CI 1.20-1.94) as compared with earlier ([els]12 years: HR 1.14, CI 1.03-1.27; 13-14 years: HR 1.18, CI 1.05-1.32) ages at menarche (P-interaction=0.03). Conclusions: Risk was elevated in smokers, particularly in those without a family history or late menarche. Research into smoking's effects on the genome and breast development may clarify these relationships.
JF - British Journal of Cancer
AU - Nyante, S J
AU - Gierach, G L
AU - Dallal, C M
AU - Freedman, N D
AU - Park, Y
AU - Danforth, K N
AU - Hollenbeck, A R
AU - Brinton, L A
AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, 9609 Medical Center Drive, Bethesda, MD 20892, USA
Y1 - 2014/04/29/
PY - 2014
DA - 2014 Apr 29
SP - 2339
EP - 2347
PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL - 110
IS - 9
SN - 0007-0920, 0007-0920
KW - Risk Abstracts; Health & Safety Science Abstracts
KW - Health risks
KW - Genetics
KW - Age
KW - Cigarettes
KW - Post-menopause
KW - Risk factors
KW - Breast cancer
KW - H 11000:Diseases/Injuries/Trauma
KW - R2 23060:Medical and environmental health
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+Journal+of+Cancer&rft.atitle=Cigarette+smoking+and+postmenopausal+breast+cancer+risk+in+a+prospective+cohort&rft.au=Nyante%2C+S+J%3BGierach%2C+G+L%3BDallal%2C+C+M%3BFreedman%2C+N+D%3BPark%2C+Y%3BDanforth%2C+K+N%3BHollenbeck%2C+A+R%3BBrinton%2C+L+A&rft.aulast=Nyante&rft.aufirst=S&rft.date=2014-04-29&rft.volume=110&rft.issue=9&rft.spage=2339&rft.isbn=&rft.btitle=&rft.title=British+Journal+of+Cancer&rft.issn=00070920&rft_id=info:doi/10.1038%2Fbjc.2014.132
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-05-01
N1 - Last updated - 2014-06-26
N1 - SubjectsTermNotLitGenreText - Genetics; Health risks; Age; Cigarettes; Post-menopause; Risk factors; Breast cancer
DO - http://dx.doi.org/10.1038/bjc.2014.132
ER -
TY - JOUR
T1 - Tumor microenvironment-based feed-forward regulation of NOS2 in breast cancer progression.
AN - 1520340741; 24733928
AB - Inflammation is widely recognized as an inducer of cancer progression. The inflammation-associated enzyme, inducible nitric oxide synthase (NOS2), has emerged as a candidate oncogene in estrogen receptor (ER)-negative breast cancer, and its increased expression is associated with disease aggressiveness and poor survival. Although these observations implicate NOS2 as an attractive therapeutic target, the mechanisms of both NOS2 induction in tumors and nitric oxide (NO)-driven cancer progression are not fully understood. To enhance our mechanistic understanding of NOS2 induction in tumors and its role in tumor biology, we used stimulants of NOS2 expression in ER(-) and ER(+) breast cancer cells and examined downstream NO-dependent effects. Herein, we show that up-regulation of NOS2 occurs in response to hypoxia, serum withdrawal, IFN-γ, and exogenous NO, consistent with a feed-forward regulation of NO production by the tumor microenvironment in breast cancer biology. Moreover, we found that key indicators of an aggressive cancer phenotype including increased S100 calcium binding protein A8, IL-6, IL-8, and tissue inhibitor matrix metalloproteinase-1 are up-regulated by these NOS2 stimulants, whereas inhibition of NOS2 in MDA-MB-231 breast cancer cells suppressed these markers. Moreover, NO altered cellular migration and chemoresistance of MDA-MB-231 cells to Taxol. Most notably, MDA-MB-231 tumor xenographs and cell metastases from the fat pad to the brain were significantly suppressed by NOS2 inhibition in nude mice. In summary, these results link elevated NOS2 to signals from the tumor microenvironment that arise with cancer progression and show that NO production regulates chemoresistance and metastasis of breast cancer cells.
JF - Proceedings of the National Academy of Sciences of the United States of America
AU - Heinecke, Julie L
AU - Ridnour, Lisa A
AU - Cheng, Robert Y S
AU - Switzer, Christopher H
AU - Lizardo, Michael M
AU - Khanna, Chand
AU - Glynn, Sharon A
AU - Hussain, S Perwez
AU - Young, Howard A
AU - Ambs, Stefan
AU - Wink, David A
AD - Radiation Biology Branch, Tumor and Metastasis Biology Section, Pediatric Oncology Branch, and Laboratory of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
Y1 - 2014/04/29/
PY - 2014
DA - 2014 Apr 29
SP - 6323
EP - 6328
VL - 111
IS - 17
KW - Biomarkers, Tumor
KW - 0
KW - Culture Media, Serum-Free
KW - Guanidines
KW - Nitric Oxide
KW - 31C4KY9ESH
KW - Interferon-gamma
KW - 82115-62-6
KW - NOS2 protein, human
KW - EC 1.14.13.39
KW - Nitric Oxide Synthase Type II
KW - pimagedine
KW - SCQ4EZQ113
KW - Index Medicus
KW - Cell Proliferation -- drug effects
KW - Animals
KW - Humans
KW - Cell Hypoxia -- drug effects
KW - Interferon-gamma -- pharmacology
KW - Mice
KW - Cell Line, Tumor
KW - Models, Biological
KW - Biomarkers, Tumor -- metabolism
KW - Signal Transduction -- drug effects
KW - Neoplasm Metastasis
KW - Cell Movement -- drug effects
KW - Nitric Oxide -- pharmacology
KW - Female
KW - Drug Resistance, Neoplasm -- drug effects
KW - Feedback, Physiological -- drug effects
KW - Breast Neoplasms -- pathology
KW - Disease Progression
KW - Nitric Oxide Synthase Type II -- metabolism
KW - Breast Neoplasms -- enzymology
KW - Tumor Microenvironment -- drug effects
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-06-24
N1 - Date created - 2014-04-30
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1073/pnas.1401799111
ER -
TY - CPAPER
T1 - Role of G Proteins in regulation of energy and glucose metabolism
T2 - 2014 American Society for Pharmacology and Experimental Therapeutics Annual Meeting with the Chinese Pharmacological Society
AN - 1541353123; 6286982
JF - 2014 American Society for Pharmacology and Experimental Therapeutics Annual Meeting with the Chinese Pharmacological Society
AU - Weinstein, Lee
Y1 - 2014/04/26/
PY - 2014
DA - 2014 Apr 26
KW - Energy
KW - Guanine nucleotide-binding protein
KW - Glucose metabolism
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541353123?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Pharmacology+and+Experimental+Therapeutics+Annual+Meeting+with+the+Chinese+Pharmacological+Society&rft.atitle=Role+of+G+Proteins+in+regulation+of+energy+and+glucose+metabolism&rft.au=Weinstein%2C+Lee&rft.aulast=Weinstein&rft.aufirst=Lee&rft.date=2014-04-26&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Pharmacology+and+Experimental+Therapeutics+Annual+Meeting+with+the+Chinese+Pharmacological+Society&rft.issn=&rft_id=info:doi/
L2 - http://www.aspet.org/EB2014/program/
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-27
N1 - Last updated - 2014-06-30
ER -
TY - CPAPER
T1 - Identification of a novel, highly potent D3 dopamine receptor-selective agonist
T2 - 2014 American Society for Pharmacology and Experimental Therapeutics Annual Meeting with the Chinese Pharmacological Society
AN - 1541353104; 6287045
JF - 2014 American Society for Pharmacology and Experimental Therapeutics Annual Meeting with the Chinese Pharmacological Society
AU - Moritz, Amy
Y1 - 2014/04/26/
PY - 2014
DA - 2014 Apr 26
KW - Dopamine D3 receptors
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541353104?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Pharmacology+and+Experimental+Therapeutics+Annual+Meeting+with+the+Chinese+Pharmacological+Society&rft.atitle=Identification+of+a+novel%2C+highly+potent+D3+dopamine+receptor-selective+agonist&rft.au=Moritz%2C+Amy&rft.aulast=Moritz&rft.aufirst=Amy&rft.date=2014-04-26&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Pharmacology+and+Experimental+Therapeutics+Annual+Meeting+with+the+Chinese+Pharmacological+Society&rft.issn=&rft_id=info:doi/
L2 - http://www.aspet.org/EB2014/program/
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-27
N1 - Last updated - 2014-06-30
ER -
TY - CPAPER
T1 - Peripheral CB1 receptors as emerging therapeutic targets in diabetes and obesity
T2 - 2014 American Society for Pharmacology and Experimental Therapeutics Annual Meeting with the Chinese Pharmacological Society
AN - 1541352996; 6287088
JF - 2014 American Society for Pharmacology and Experimental Therapeutics Annual Meeting with the Chinese Pharmacological Society
AU - Kunos, George
Y1 - 2014/04/26/
PY - 2014
DA - 2014 Apr 26
KW - Diabetes mellitus
KW - Obesity
KW - Cannabinoid CB1 receptors
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541352996?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Pharmacology+and+Experimental+Therapeutics+Annual+Meeting+with+the+Chinese+Pharmacological+Society&rft.atitle=Peripheral+CB1+receptors+as+emerging+therapeutic+targets+in+diabetes+and+obesity&rft.au=Kunos%2C+George&rft.aulast=Kunos&rft.aufirst=George&rft.date=2014-04-26&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Pharmacology+and+Experimental+Therapeutics+Annual+Meeting+with+the+Chinese+Pharmacological+Society&rft.issn=&rft_id=info:doi/
L2 - http://www.aspet.org/EB2014/program/
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-27
N1 - Last updated - 2014-06-30
ER -
TY - CPAPER
T1 - Macrophages are required to maintain type 2-dependent inflammation, immunity, and fibrosis
T2 - 2014 American Society for Pharmacology and Experimental Therapeutics Annual Meeting with the Chinese Pharmacological Society
AN - 1541352940; 6287100
JF - 2014 American Society for Pharmacology and Experimental Therapeutics Annual Meeting with the Chinese Pharmacological Society
AU - Barron, Luke
Y1 - 2014/04/26/
PY - 2014
DA - 2014 Apr 26
KW - Macrophages
KW - Fibrosis
KW - Immunity
KW - Inflammation
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541352940?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Pharmacology+and+Experimental+Therapeutics+Annual+Meeting+with+the+Chinese+Pharmacological+Society&rft.atitle=Macrophages+are+required+to+maintain+type+2-dependent+inflammation%2C+immunity%2C+and+fibrosis&rft.au=Barron%2C+Luke&rft.aulast=Barron&rft.aufirst=Luke&rft.date=2014-04-26&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Pharmacology+and+Experimental+Therapeutics+Annual+Meeting+with+the+Chinese+Pharmacological+Society&rft.issn=&rft_id=info:doi/
L2 - http://www.aspet.org/EB2014/program/
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-27
N1 - Last updated - 2014-06-30
ER -
TY - JOUR
T1 - Relationship of immunologic response to antiretroviral therapy with non-AIDS defining cancer incidence
AN - 1765982706; PQ0002610762
AB - The objective of this paper is to estimate the association between immunologic response to anti-retroviral therapy (ART) and non-AIDS defining cancer (NADC) incidence in HIV-infected patients. A prospective cohort including patients with at least 1 cell/[mu[l CD4[sup +] cell count and HIV-1 RNA measure after ART initiation between 1996 and 2011 in the Centers for AIDS Research Network of Integrated Clinical Systems, a collaboration of eight HIV clinics at major academic medical centres in the United States. Cox regression with inverse probability-of-exposure weights was used to calculate adjusted hazard ratios of virus-related and virus-unrelated NADC incidence. Poor CD4[sup +] cell count response was strongly associated with virus-related NADC incidence, suggesting an important role for T-cell mediated immunity in pathogenesis. Lower CD4[sup +] cell count proximal to cancer diagnosis may be a result of sub-clinical cancer. Intensified cancer screening should be considered for patients on ART with low CD4[sup +] cell counts.
JF - AIDS
AU - Yanik, Elizabeth L
AU - Napravnik, Sonia
AU - Cole, Stephen R
AU - Achenbach, Chad J
AU - Gopal, Satish
AU - Dittmer, Dirk P
AU - Olshan, Andrew F
AU - Kitahata, Mari M
AU - Mugavero, Michael J
AU - Saag, Michael
AU - Moore, Richard D
AU - Mathews, W Christopher
AU - Hunt, Peter
AU - Eron, Joseph J
AD - University of North Carolina, Chapel Hill, North Carolina, elizabeth.yanik@nih.gov
Y1 - 2014/04/24/
PY - 2014
DA - 2014 Apr 24
SP - 979
EP - 987
PB - Lippincott Williams & Wilkins, Inc, 530 Walnut Street Philadelphia PA 19106-3621 United States
VL - 28
IS - 7
SN - 0269-9370, 0269-9370
KW - Health & Safety Science Abstracts; Immunology Abstracts; Virology & AIDS Abstracts
KW - antiretroviral therapy
KW - cancers
KW - CD4+ cell count
KW - HIV infections
KW - immune reconstitution
KW - tumour virus infections
KW - Acquired immune deficiency syndrome
KW - Immunity
KW - Antiretroviral agents
KW - Cancer
KW - USA
KW - RNA
KW - Human immunodeficiency virus
KW - Human immunodeficiency virus 1
KW - Lymphocytes T
KW - V 22360:AIDS and HIV
KW - H 11000:Diseases/Injuries/Trauma
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1765982706?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS&rft.atitle=Relationship+of+immunologic+response+to+antiretroviral+therapy+with+non-AIDS+defining+cancer+incidence&rft.au=Yanik%2C+Elizabeth+L%3BNapravnik%2C+Sonia%3BCole%2C+Stephen+R%3BAchenbach%2C+Chad+J%3BGopal%2C+Satish%3BDittmer%2C+Dirk+P%3BOlshan%2C+Andrew+F%3BKitahata%2C+Mari+M%3BMugavero%2C+Michael+J%3BSaag%2C+Michael%3BMoore%2C+Richard+D%3BMathews%2C+W+Christopher%3BHunt%2C+Peter%3BEron%2C+Joseph+J&rft.aulast=Yanik&rft.aufirst=Elizabeth&rft.date=2014-04-24&rft.volume=28&rft.issue=7&rft.spage=979&rft.isbn=&rft.btitle=&rft.title=AIDS&rft.issn=02699370&rft_id=info:doi/10.1097%2FQAD.0000000000000167
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2016-02-01
N1 - Last updated - 2016-03-17
N1 - SubjectsTermNotLitGenreText - Acquired immune deficiency syndrome; RNA; antiretroviral therapy; Lymphocytes T; Immunity; Cancer; Human immunodeficiency virus; Antiretroviral agents; Human immunodeficiency virus 1; USA
DO - http://dx.doi.org/10.1097/QAD.0000000000000167
ER -
TY - JOUR
T1 - Systematic Review and Evidence Integration for Literature-Based Environmental Health Science Assessments
AN - 1551644857; 20395149
AB - Background: Systematic-review methodologies provide objectivity and transparency to the process of collecting and synthesizing scientific evidence in reaching conclusions on specific research questions. There is increasing interest in applying these procedures to address environmental health questions. Objectives: The goal was to develop a systematic-review framework to address environmental health questions by extending approaches developed for clinical medicine to handle the breadth of data relevant to environmental health sciences (e.g., human, animal, and mechanistic studies). Methods: The Office of Health Assessment and Translation (OHAT) adapted guidance from authorities on systematic-review and sought advice during development of the OHAT Approach through consultation with technical experts in systematic review and human health assessments, as well as scientific advisory groups and the public. The method was refined by considering expert and public comments and through application to case studies. Results and Discussion: Here we present a seven-step framework for systematic review and evidence integration for reaching hazard identification conclusions: 1) problem formulation and protocol development, 2) search for and select studies for inclusion, 3) extract data from studies, 4) assess the quality or risk of bias of individual studies, 5) rate the confidence in the body of evidence, 6) translate the confidence ratings into levels of evidence, and 7) integrate the information from different evidence streams (human, animal, and "other relevant data" including mechanistic or in vitro studies) to develop hazard identification conclusions. Conclusion: The principles of systematic review can be successfully applied to environmental health questions to provide greater objectivity and transparency to the process of developing conclusions. Citation: Rooney AA, Boyles AL, Wolfe MS, Bucher JR, Thayer KA. 2014. Systematic review and evidence integration for literature-based environmental health science assessments. Environ Health Perspect 122:711-718; http://dx.doi.org/10.1289/ehp.1307972
JF - Environmental Health Perspectives
AU - Rooney, Andrew A
AU - Boyles, Abee L
AU - Wolfe, Mary S
AU - Bucher, John R
AU - Thayer, Kristina A
AD - Office of Health Assessment and Translation, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA
Y1 - 2014/04/22/
PY - 2014
DA - 2014 Apr 22
SP - 711
EP - 718
PB - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States
VL - 122
IS - 7
SN - 0091-6765, 0091-6765
KW - Risk Abstracts; Environment Abstracts; Health & Safety Science Abstracts
KW - Transparency
KW - Risk assessment
KW - Case studies
KW - Reviews
KW - Environmental health
KW - H 6000:Natural Disasters/Civil Defense/Emergency Management
KW - R2 23060:Medical and environmental health
KW - ENA 07:General
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Health+Perspectives&rft.atitle=Systematic+Review+and+Evidence+Integration+for+Literature-Based+Environmental+Health+Science+Assessments&rft.au=Rooney%2C+Andrew+A%3BBoyles%2C+Abee+L%3BWolfe%2C+Mary+S%3BBucher%2C+John+R%3BThayer%2C+Kristina+A&rft.aulast=Rooney&rft.aufirst=Andrew&rft.date=2014-04-22&rft.volume=122&rft.issue=7&rft.spage=711&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1307972
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-08-01
N1 - Last updated - 2015-05-13
N1 - SubjectsTermNotLitGenreText - Risk assessment; Transparency; Case studies; Reviews; Environmental health
DO - http://dx.doi.org/10.1289/ehp.1307972
ER -
TY - JOUR
T1 - Integrative framework for identification of key cell identity genes uncovers determinants of ES cell identity and homeostasis.
AN - 1518813283; 24711389
AB - Identification of genes associated with specific biological phenotypes is a fundamental step toward understanding the molecular basis underlying development and pathogenesis. Although RNAi-based high-throughput screens are routinely used for this task, false discovery and sensitivity remain a challenge. Here we describe a computational framework for systematic integration of published gene expression data to identify genes defining a phenotype of interest. We applied our approach to rank-order all genes based on their likelihood of determining ES cell (ESC) identity. RNAi-mediated loss-of-function experiments on top-ranked genes unearthed many novel determinants of ESC identity, thus validating the derived gene ranks to serve as a rich and valuable resource for those working to uncover novel ESC regulators. Underscoring the value of our gene ranks, functional studies of our top-hit Nucleolin (Ncl), abundant in stem and cancer cells, revealed Ncl's essential role in the maintenance of ESC homeostasis by shielding against differentiation-inducing redox imbalance-induced oxidative stress. Notably, we report a conceptually novel mechanism involving a Nucleolin-dependent Nanog-p53 bistable switch regulating the homeostatic balance between self-renewal and differentiation in ESCs. Our findings connect the dots on a previously unknown regulatory circuitry involving genes associated with traits in both ESCs and cancer and might have profound implications for understanding cell fate decisions in cancer stem cells. The proposed computational framework, by helping to prioritize and preselect candidate genes for tests using complex and expensive genetic screens, provides a powerful yet inexpensive means for identification of key cell identity genes.
JF - Proceedings of the National Academy of Sciences of the United States of America
AU - Cinghu, Senthilkumar
AU - Yellaboina, Sailu
AU - Freudenberg, Johannes M
AU - Ghosh, Swati
AU - Zheng, Xiaofeng
AU - Oldfield, Andrew J
AU - Lackford, Brad L
AU - Zaykin, Dmitri V
AU - Hu, Guang
AU - Jothi, Raja
AD - Systems Biology Section and Stem Cell Biology Section, Laboratory of Molecular Carcinogenesis, and Biostatistics Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709.
Y1 - 2014/04/22/
PY - 2014
DA - 2014 Apr 22
SP - E1581
EP - E1590
VL - 111
IS - 16
KW - Homeodomain Proteins
KW - 0
KW - Nanog Homeobox Protein
KW - Nanog protein, mouse
KW - Phosphoproteins
KW - RNA-Binding Proteins
KW - Reactive Oxygen Species
KW - Tumor Suppressor Protein p53
KW - nucleolin
KW - Index Medicus
KW - ROS
KW - RNA-binding protein
KW - pluripotency
KW - computational biology
KW - transcription
KW - Reactive Oxygen Species -- metabolism
KW - Animals
KW - Phosphoproteins -- genetics
KW - Reproducibility of Results
KW - RNA-Binding Proteins -- metabolism
KW - RNA-Binding Proteins -- genetics
KW - Cell Differentiation -- genetics
KW - Transcription, Genetic
KW - Mice
KW - Oxidative Stress -- genetics
KW - Cell Proliferation
KW - Tumor Suppressor Protein p53 -- metabolism
KW - Pluripotent Stem Cells -- cytology
KW - Homeodomain Proteins -- metabolism
KW - Gene Expression Regulation
KW - RNA Interference
KW - Phosphoproteins -- metabolism
KW - Pluripotent Stem Cells -- metabolism
KW - Embryonic Stem Cells -- metabolism
KW - Embryonic Stem Cells -- cytology
KW - Homeostasis -- genetics
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-06-17
N1 - Date created - 2014-04-23
N1 - Date revised - 2017-01-14
N1 - Genetic sequence - GSE47872; GEO
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1073/pnas.1318598111
ER -
TY - JOUR
T1 - Free radical metabolism of methyleugenol and related compounds.
AN - 1518242114; 24564854
AB - Methyleugenol, the methyl ether of eugenol, both of which are flavorant constituents of spices, has been listed by the National Toxicology Program's Report on Carcinogens as reasonably anticipated to be a human carcinogen. This finding is based on the observation of increased incidence of malignant tumors at multiple tissue sites in experimental animals of different species. By contrast, eugenol is not listed. In this study, we show that both methyleugenol and eugenol readily undergo peroxidative metabolism in vitro to form free radicals with large hyperfine interactions of the methylene allylic hydrogen atoms. These large hyperfine splittings indicate large electron densities adjacent to those hydrogen atoms. Methyleugenol undergoes autoxidation such that the commercial product contains 10-30 mg/L hydroperoxide and is capable of activating peroxidases without the presence of added hydrogen peroxide. Additionally, the hydroperoxide is not a good substrate for catalase, which demonstrates that these antioxidant defenses will not be effective in protecting against methyleugenol exposure.
JF - Chemical research in toxicology
AU - Sipe, Herbert J
AU - Lardinois, Olivier M
AU - Mason, Ronald P
AD - Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health , P.O. Box 12233, Research Triangle Park, North Carolina 27709, United States.
Y1 - 2014/04/21/
PY - 2014
DA - 2014 Apr 21
SP - 483
EP - 489
VL - 27
IS - 4
KW - Free Radicals
KW - 0
KW - methyleugenol
KW - 29T9VA6R7M
KW - Eugenol
KW - 3T8H1794QW
KW - Index Medicus
KW - Humans
KW - Electron Spin Resonance Spectroscopy
KW - Spectrophotometry, Ultraviolet
KW - Free Radicals -- metabolism
KW - Eugenol -- analogs & derivatives
KW - Eugenol -- metabolism
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-09-15
N1 - Date created - 2014-04-21
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Anticancer Res. 1998 Jan-Feb;18(1A):425-8 [9568113]
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Toxicol In Vitro. 2011 Feb;25(1):267-85 [20828604]
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Xenobiotica. 2012 May;42(5):429-41 [22188410]
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Toxicol Sci. 2012 Sep;129(1):21-34 [22610610]
Carcinogenesis. 2013 May;34(5):1025-30 [23334163]
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Biochem J. 1990 Jun 1;268(2):475-80 [2163614]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1021/tx400256b
ER -
TY - JOUR
T1 - Accommodating Measurements Below a Limit of Detection: A Novel Application of Cox Regression
AN - 1516746342; 19545030
AB - In environmental epidemiology, measurements of exposure biomarkers often fall below the assay's limit of detection. Existing methods for handling this problem, including deletion, substitution, parametric regression, and multiple imputation, can perform poorly if the proportion of "nondetects" is high or parametric models are misspecified. We propose an approach that treats the measured analyte as the modeled outcome, implying a role reversal when the analyte is a putative cause of a health outcome. Following a scale reversal as well, our approach uses Cox regression to model the analyte, with confounder adjustment. The method makes full use of quantifiable analyte measures, while appropriately treating nondetects as censored. Under the proportional hazards assumption, the hazard ratio for a binary health outcome is interpretable as an adjusted odds ratio: the odds for the outcome at any particular analyte concentration divided by the odds given a lower concentration. Our approach is broadly applicable to cohort studies, case-control studies (frequency matched or not), and cross-sectional studies conducted to identify determinants of exposure. We illustrate the method with cross-sectional survey data to assess sex as a determinant of 2,3,7,8-tetrachlorodibenzo-p-dioxin concentration and with prospective cohort data to assess the association between 2,4,4'-trichlorobiphenyl exposure and psychomotor development.
JF - American Journal of Epidemiology
AU - Dinse, Gregg E
AU - Jusko, Todd A
AU - Ho, Lindsey A
AU - Annam, Kaushik
AU - Graubard, Barry I
AU - Hertz-Picciotto, Irva
AU - Miller, Frederick W
AU - Gillespie, Brenda W
AU - Weinberg, Clarice R
AD - Correspondence to Dr. Clarice R. Weinberg, Mail Drop A3-03, P.O. Box 12233, Research Triangle Park, NC 27709., weinber2@niehs.nih.gov
Y1 - 2014/04/15/
PY - 2014
DA - 2014 Apr 15
SP - 1018
EP - 1024
PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL - 179
IS - 8
SN - 0002-9262, 0002-9262
KW - Health & Safety Science Abstracts
KW - Bioindicators
KW - H 12000:Epidemiology and Public Health
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Epidemiology&rft.atitle=Accommodating+Measurements+Below+a+Limit+of+Detection%3A+A+Novel+Application+of+Cox+Regression&rft.au=Dinse%2C+Gregg+E%3BJusko%2C+Todd+A%3BHo%2C+Lindsey+A%3BAnnam%2C+Kaushik%3BGraubard%2C+Barry+I%3BHertz-Picciotto%2C+Irva%3BMiller%2C+Frederick+W%3BGillespie%2C+Brenda+W%3BWeinberg%2C+Clarice+R&rft.aulast=Dinse&rft.aufirst=Gregg&rft.date=2014-04-15&rft.volume=179&rft.issue=8&rft.spage=1018&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Epidemiology&rft.issn=00029262&rft_id=info:doi/10.1093%2Faje%2Fkwu017
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-01
N1 - Last updated - 2014-06-12
N1 - SubjectsTermNotLitGenreText - Bioindicators
DO - http://dx.doi.org/10.1093/aje/kwu017
ER -
TY - JOUR
T1 - MATILDE chemotherapy regimen for primary CNS lymphoma: results at a median follow-up of 12 years.
AN - 1516722335; 24634458
AB - We report updated results at a median follow-up of 12 years of a phase II trial assessing first-line MATILDE chemotherapy and response-tailored radiotherapy in patients with primary CNS lymphomas (PCNSL).
Forty-one HIV-negative patients (18-70 years; Eastern Cooperative Oncology Group performance status ≤3) with histologically confirmed PCNSL received 3 courses of MATILDE chemotherapy followed by whole-brain radiotherapy (WBRT). Chemotherapy activity was the primary endpoint. Overall response rate was 76% (95% confidence interval [CI] 63%-89%) after chemotherapy and 83% (95% CI 71%-95%) after chemotherapy ± radiotherapy. At a median follow-up of 144 months (range 47-153), 31 patients experienced an event: relapse in 24, progressive disease in 3, and toxic death in 4, with a 5-year progression-free survival of 24% ± 8%. Two patients experienced a late relapse (100 and 101 months). Nine patients are alive and disease-free, 8 of whom are alive at >10 years, with a 5-year overall survival of 30% ± 7%. At 10 years from diagnosis, no patient showed chronic hematologic and nonhematologic toxicities, with a Mini-Mental State Examination score of ≥29 in all cases but one.
At a median follow-up of 12 years, MATILDE regimen followed by WBRT confirmed the previously reported survival plateau, which further proves its long-lasting efficacy with acceptable neurologic deficits. This study provides Class IV evidence that in patients with PCNSL, MATILDE chemotherapy followed by response-tailored radiotherapy increases the probability of disease remission at 12 years.
JF - Neurology
AU - Ferreri, Andrés J M
AU - Ciceri, Fabio
AU - Brandes, Alba A
AU - Montanari, Mauro
AU - Balzarotti, Monica
AU - Spina, Michele
AU - Ilariucci, Fiorella
AU - Zaja, Francesco
AU - Stelitano, Caterina
AU - Bobbio, Flavio
AU - Corazzelli, Gaetano
AU - Baldini, Luca
AU - Reni, Michele
AD - From the Unit of Lymphoid Malignancies (A.J.M.F.), UTMO & Hematology Unit, Department of Onco-Hematology (F.C.), and Medical Oncology Unit, Department of Oncology (M.R.), San Raffaele Scientific Institute, Milan; Department of Medical Oncology (A.A.B.), Bellaria-Maggiore Hospital, Azienda Unità Sanitaria Locale, Bologna; Division of Hematology (M.M.), Ospedale di Ancona; Department of Medical Oncology and Hematology (M.B.), Istituto Clinico Humanitas, Rozzano; Division of Medical Oncology A (M.S.), National Cancer Institute, Aviano; Division of Hematology (F.I.), Ospedale di Reggio Emilia; Division of Hematology (F.Z.), Ospedale di Udine; Division of Hematology (C.S.), Ospedale di Reggio Calabria; Division of Hematology (F.B.), Ospedale Maggiore di Novara; Division of Hematology (G.C.), Istituto Nazionale dei Tumori Pascale di Napoli; and the Division of Hematology (L.B.), Ospedale Maggiore di Milano, Italy.
Y1 - 2014/04/15/
PY - 2014
DA - 2014 Apr 15
SP - 1370
EP - 1373
VL - 82
IS - 15
KW - Cytarabine
KW - 04079A1RDZ
KW - Thiotepa
KW - 905Z5W3GKH
KW - Methotrexate
KW - YL5FZ2Y5U1
KW - Idarubicin
KW - ZRP63D75JW
KW - Abridged Index Medicus
KW - Index Medicus
KW - Disease-Free Survival
KW - Combined Modality Therapy
KW - Humans
KW - Cytarabine -- administration & dosage
KW - Idarubicin -- administration & dosage
KW - Idarubicin -- therapeutic use
KW - Cytarabine -- therapeutic use
KW - Thiotepa -- therapeutic use
KW - Treatment Outcome
KW - Methotrexate -- therapeutic use
KW - Thiotepa -- administration & dosage
KW - Follow-Up Studies
KW - Methotrexate -- administration & dosage
KW - Female
KW - Male
KW - Remission Induction
KW - Central Nervous System Neoplasms -- radiotherapy
KW - Central Nervous System Neoplasms -- drug therapy
KW - Lymphoma -- drug therapy
KW - Antineoplastic Combined Chemotherapy Protocols -- administration & dosage
KW - Lymphoma -- radiotherapy
KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-06-09
N1 - Date created - 2014-04-15
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Comment In:
Neurology. 2014 Apr 15;82(15):1373 [24634452]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1212/WNL.0000000000000314
ER -
TY - CPAPER
T1 - How to approach networking
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541355152; 6287661
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Wiest, Jonathan
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Networking
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T1 - Funding opportunities and resources from the NCI's Physical Sciences in Oncology Initiative
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541355125; 6287739
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Hanlon, Sean
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Financing
KW - Oncology
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T1 - NCI-supported tobacco research priorities
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541355117; 6287672
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Croyle, Robert
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Tobacco
KW - Priorities
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T1 - How to Write a CV
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541355107; 6287604
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Wiest, Jonathan
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Oncology
KW - Cancer
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T1 - T cell biology: From the bench to the bedside
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541355033; 6287179
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Mackall, Crystal
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Lymphocytes T
KW - Cytology
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T1 - NCI Genomics Data Commons
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541354959; 6287477
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Zenklusen, Jean
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Data processing
KW - genomics
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T1 - CPTAC: Proteomic resources for cancer research
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541354890; 6287741
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Kinsinger, Christopher
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - proteomics
KW - Cancer
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T1 - Cell-based therapies, cytokines
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541354848; 6287206
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Mackall, Crystal
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Therapy
KW - Cytokines
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T1 - The NCI Cancer Genomics Cloud Pilots
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541354815; 6287478
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Davidsen, Tanja
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Clouds
KW - Pilots
KW - genomics
KW - Cancer
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T1 - Developing novel therapies for rare tumors
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541354805; 6287574
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Kummar, Shivaani
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Therapy
KW - Tumors
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T1 - Why Cancer Research Needs You
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541354800; 6287895
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Springfield, Sanya
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Cancer
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T1 - The role of the tumor microenvironment in mantle cell lymphoma
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541354743; 6287626
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Wiestner, Adrian
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - mantle cell lymphoma
KW - Microenvironments
KW - Tumors
KW - Lymphoma
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T1 - Systemic influence of the gut microbiota on inflammation and immunity: Modulation of the response to antitumor therapy
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541354681; 6287236
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Trinchieri, Giorgio
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Digestive tract
KW - Therapy
KW - Immunity
KW - Inflammation
KW - Antitumor activity
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T1 - Targeting the Genetic and Metabolic Basis of Cancer
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541354665; 6287588
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Linehan, W
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Cancer
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T1 - Ongoing and planned genomicbased trials
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541354540; 6287326
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Doroshow, James
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Oncology
KW - Cancer
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T1 - NCI's Alliance for Nanotechnology in Cancer Program and resources for cancer nanotechnology research
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541354526; 6287740
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Morris, Stephanie
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Cancer
KW - nanotechnology
KW - Nanotechnology
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T1 - Research Funding for New Investigators and Fellowship Opportunities: Postdoctoral Level
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541354458; 6287867
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Marino, Pamela
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Financing
KW - Fellowships
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T1 - Development of effective therapies for neurofibromatosis type 1-related tumors
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541354439; 6287575
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Widemann, Brigitte
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Therapy
KW - Tumors
KW - Neurofibromatosis
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T1 - Integrating model systems into rare tumor research
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541354434; 6287576
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Reilly, Karlyne
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Tumors
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T1 - Value of collecting normal tissue
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541354395; 6287333
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Figueroa, Jonine
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Oncology
KW - Cancer
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T1 - Overview of the Innovation Molecular Analysis Technologies (IMAT) Program
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541354372; 6287737
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Dickherber, Anthony
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Reviews
KW - Technology
KW - Innovations
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T1 - The Cancer Genome Atlas (TCGA): A primer on accessing the data
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541354338; 6287392
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Zenklusen, Jean
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Genomes
KW - Data processing
KW - Atlases
KW - Primers
KW - Cancer
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T1 - Recombinant Immunotoxins: From Conception to Clinical Reality in Mesothelioma and Leukemia
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541354297; 6287585
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Pastan, Ira
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Recombinants
KW - Leukemia
KW - mesothelioma
KW - Mesothelioma
KW - Immunotoxins
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T1 - Grantsmanship: Junior Faculty
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541354274; 6287860
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Ogunbiyi, Peter
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Oncology
KW - Cancer
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T1 - The curative potential of T cell transfer therapy for patients with cancer
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541354244; 6287593
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Rosenberg, Steven
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Lymphocytes T
KW - Therapy
KW - Cancer
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T1 - What's happening in the NCI Office of Cancer Genomics
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541354238; 6287738
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Guidry Auvil, Jaime
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - genomics
KW - Cancer
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T1 - NCI's Provocative Questions Initiative: Program review and evaluation
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541354225; 6287834
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Greenspan, Emily
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Reviews
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T1 - Mechanisms that maintain genome stability
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541354191; 6287434
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Nussenzweig, Andre
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Genomes
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T1 - New lymphoma therapies based on functional and structural genomics
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541354153; 6287420
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Staudt, Louis
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Structure-function relationships
KW - Therapy
KW - genomics
KW - Lymphoma
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T1 - TCGA initiative data overview
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541353997; 6287951
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Zenklusen, Jean
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Data processing
KW - Reviews
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T1 - Translating genomics into theranostics for patients with pediatric cancers
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541353880; 6287961
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Khan, Javed
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Pediatrics
KW - genomics
KW - Cancer
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L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-27
N1 - Last updated - 2014-06-30
ER -
TY - CPAPER
T1 - Future directions for the discovery and characterization of the spectrum of cancer susceptibility variants
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541353853; 6287969
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Chanock, Stephen
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Cancer
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L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-27
N1 - Last updated - 2014-06-30
ER -
TY - CPAPER
T1 - Accessing TARGET genomics data
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541353737; 6287950
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Davidsen, Tanja
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Data processing
KW - genomics
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L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-27
N1 - Last updated - 2014-06-30
ER -
TY - CPAPER
T1 - Cell therapy targeting unique cancer mutations
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541353637; 6288054
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Rosenberg, Steven
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Therapy
KW - Mutation
KW - Cancer
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L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-27
N1 - Last updated - 2014-06-30
ER -
TY - CPAPER
T1 - Development of novel combination targeted therapies for pediatric sarcomas
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541353512; 6288165
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Helman, Lee
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Pediatrics
KW - Therapy
KW - Sarcoma
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L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-27
N1 - Last updated - 2014-06-30
ER -
TY - CPAPER
T1 - Integration of Cancer Epidemiology and Biomarkers in Precision Cancer Medicine
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541353314; 6288035
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Harris, Curtis
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Bioindicators
KW - Integration
KW - Epidemiology
KW - Biomarkers
KW - biomarkers
KW - Cancer
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L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-27
N1 - Last updated - 2014-06-30
ER -
TY - CPAPER
T1 - Translational control and tumor stem cell radio response
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541353309; 6288184
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Tofilon, Philip
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Translation
KW - Stem cells
KW - Radio
KW - Tumors
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=Translational+control+and+tumor+stem+cell+radio+response&rft.au=Tofilon%2C+Philip&rft.aulast=Tofilon&rft.aufirst=Philip&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/
L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-27
N1 - Last updated - 2014-06-30
ER -
TY - CPAPER
T1 - Building highly effective antitumor T cells
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541353253; 6288001
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Restifo, Nicholas
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Lymphocytes T
KW - Antitumor activity
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L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-27
N1 - Last updated - 2014-06-30
ER -
TY - CPAPER
T1 - Chimeric Antigen Receptor-Based Immunotherapy for Pediatric Cancer: Progress and Challenges
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541353228; 6288137
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Mackall, Crystal
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Antigens
KW - Pediatrics
KW - Immunotherapy
KW - Cancer
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L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-27
N1 - Last updated - 2014-06-30
ER -
TY - CPAPER
T1 - Racial disparities and genetics of prostate cancer
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541353225; 6288155
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Cook, Michael
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Genetics
KW - Prostate cancer
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L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-27
N1 - Last updated - 2014-06-30
ER -
TY - CPAPER
T1 - Establishing standards such that cross-platform comparisons and validations can be undertaken to validate variants
T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AN - 1541353196; 6288030
JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014)
AU - Williams, Mickey
Y1 - 2014/04/05/
PY - 2014
DA - 2014 Apr 05
KW - Oncology
KW - Cancer
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L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-27
N1 - Last updated - 2014-06-30
ER -
TY - JOUR
T1 - Cooking Methods and Esophageal Squamous Cell Carcinoma in High-Risk Areas of Iran
AN - 1524403555; 19629836
AB - Cooking methods have been implicated in the etiology of gastrointestinal cancers, reflecting exposure to potential carcinogens as results of cooking. We used a validated food frequency questionnaire and a pretested cooking method questionnaire in 3 groups: 40 esophageal squamous cell carcinoma (ESCC) cases from a high-risk area in northeast of Iran, 40 healthy subjects from the same high-risk area, and 40 healthy subjects from a low-risk area in Southern Iran. We compared the frequency of boiling, grilling, and frying, and the frying score among these 3 groups. We also calculated "frying index" by multiplying the frequency of each fried food item by its frying score. Mean frying to boiling ratios were 18.2:1, 12.8:1, and 2.6:1 for cases, high-risk controls, and low-risk controls, respectively (P < 0.01). Reuse of cooking oil for frying was reported in 37.5% of the ESCC cases, 25% of high-risk controls, and 7.5% of low-risk controls (P < 0.001). Frying index was higher in the high-risk than in the low-risk controls (P < 0.001) and in cases than in the high-risk controls (P < 0.05) after adjusting for smoking, opium use, rural residence, education, and ethnicity. High-temperature cooking and frying may be associated with increased risk of ESCC in high-risk areas.
JF - Nutrition and Cancer
AU - Hakami, Roya
AU - Etemadi, Arash
AU - Kamangar, Farin
AU - Pourshams, Akram
AU - Mohtadinia, Javad
AU - Firoozi, Mehdi Saberi
AU - Birkett, Nicholas
AU - Boffetta, Paolo
AU - Dawsey, Sanford M
AU - Malekzadeh, Reza
AD - Digestive Disease Research Center, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran, arash.etemadi@nih.gov
Y1 - 2014/04/03/
PY - 2014
DA - 2014 Apr 03
SP - 500
EP - 505
PB - Taylor & Francis Group Ltd., 2 Park Square Oxford OX14 4RN United Kingdom
VL - 66
IS - 3
SN - 0163-5581, 0163-5581
KW - Risk Abstracts; Health & Safety Science Abstracts
KW - Iran
KW - Health risks
KW - Smoking
KW - Education
KW - Etiology
KW - Cooking
KW - Carcinogens
KW - Cancer
KW - Ethnic groups
KW - Rural areas
KW - H 11000:Diseases/Injuries/Trauma
KW - R2 23060:Medical and environmental health
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nutrition+and+Cancer&rft.atitle=Cooking+Methods+and+Esophageal+Squamous+Cell+Carcinoma+in+High-Risk+Areas+of+Iran&rft.au=Hakami%2C+Roya%3BEtemadi%2C+Arash%3BKamangar%2C+Farin%3BPourshams%2C+Akram%3BMohtadinia%2C+Javad%3BFiroozi%2C+Mehdi+Saberi%3BBirkett%2C+Nicholas%3BBoffetta%2C+Paolo%3BDawsey%2C+Sanford+M%3BMalekzadeh%2C+Reza&rft.aulast=Hakami&rft.aufirst=Roya&rft.date=2014-04-03&rft.volume=66&rft.issue=3&rft.spage=500&rft.isbn=&rft.btitle=&rft.title=Nutrition+and+Cancer&rft.issn=01635581&rft_id=info:doi/10.1080%2F01635581.2013.779384
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-05-01
N1 - Last updated - 2014-06-26
N1 - SubjectsTermNotLitGenreText - Smoking; Health risks; Etiology; Education; Cooking; Carcinogens; Ethnic groups; Cancer; Rural areas; Iran
DO - http://dx.doi.org/10.1080/01635581.2013.779384
ER -
TY - JOUR
T1 - Human metabolic correlates of body mass index
AN - 1709172176; 19348156
AB - A high body mass index (BMI) is a major risk factor for several chronic diseases, but the biology underlying these associations is not well-understood. Dyslipidemia, inflammation, and elevated levels of growth factors and sex steroid hormones explain some of the increased disease risk, but other metabolic factors not yet identified may also play a role. In order to discover novel metabolic biomarkers of BMI, we used non-targeted metabolomics to assay 317 metabolites in blood samples from 947 participants and examined the cross-sectional associations between metabolite levels and BMI. Participants were from three studies in the United States and China. Height, weight, and potential confounders were ascertained by questionnaire (US studies) or direct measurement (Chinese study). Metabolite levels were measured using liquid-phase chromatography and gas chromatography coupled with mass spectrometry. We evaluated study-specific associations using linear regression, adjusted for age, gender, and smoking, and we estimated combined associations using random effects meta-analysis. The meta-analysis revealed 37 metabolites significantly associated with BMI, including 19 lipids, 12 amino acids, and 6 others, at the Bonferroni significance threshold (P 0.05). In total, 110 metabolites were associated with BMI at the P < 0.05 level. These findings establish a baseline for the BMI metabolome, and suggest new targets for researchers attempting to clarify mechanistic links between BMI and disease risk.
JF - Metabolomics
AU - Moore, Steven C
AU - Matthews, Charles E
AU - Sampson, Joshua N
AU - Stolzenberg-Solomon, Rachael Z
AU - Zheng, Wei
AU - Cai, Qiuyin
AU - Tan, Yu Ting
AU - Chow, Wong-Ho
AU - Ji, Bu-Tian
AU - Liu, Da Ke
AU - Xiao, Qian
AU - Boca, Simina M
AU - Leitzmann, Michael F
AU - Yang, Gong
AU - Xiang, Yong Bing
AU - Sinha, Rashmi
AU - Shu, Xiao Ou
AU - Cross, Amanda J
AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, 9609 Medical Center Drive, Rockville, MD, 20850, USA, moorest@mail.nih.gov
Y1 - 2014/04//
PY - 2014
DA - Apr 2014
SP - 259
EP - 269
PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL - 10
IS - 2
SN - 1573-3882, 1573-3882
KW - Biotechnology and Bioengineering Abstracts
KW - Inventories
KW - Amino acids
KW - Lipids
KW - Metabolites
KW - Steroid hormones
KW - biomarkers
KW - Mass spectroscopy
KW - Inflammation
KW - Smoking
KW - Histidine
KW - Reviews
KW - Risk factors
KW - Oxidation
KW - Dyslipidemia
KW - Fatty acids
KW - Neurotransmitters
KW - Body mass index
KW - metabolomics
KW - Sex
KW - W 30960:Bioinformatics & Computer Applications
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Metabolomics&rft.atitle=Human+metabolic+correlates+of+body+mass+index&rft.au=Moore%2C+Steven+C%3BMatthews%2C+Charles+E%3BSampson%2C+Joshua+N%3BStolzenberg-Solomon%2C+Rachael+Z%3BZheng%2C+Wei%3BCai%2C+Qiuyin%3BTan%2C+Yu+Ting%3BChow%2C+Wong-Ho%3BJi%2C+Bu-Tian%3BLiu%2C+Da+Ke%3BXiao%2C+Qian%3BBoca%2C+Simina+M%3BLeitzmann%2C+Michael+F%3BYang%2C+Gong%3BXiang%2C+Yong+Bing%3BSinha%2C+Rashmi%3BShu%2C+Xiao+Ou%3BCross%2C+Amanda+J&rft.aulast=Moore&rft.aufirst=Steven&rft.date=2014-04-01&rft.volume=10&rft.issue=2&rft.spage=259&rft.isbn=&rft.btitle=&rft.title=Metabolomics&rft.issn=15733882&rft_id=info:doi/10.1007%2Fs11306-013-0574-1
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-09-01
N1 - Number of references - 41
N1 - Last updated - 2015-09-03
N1 - SubjectsTermNotLitGenreText - Inventories; Amino acids; Lipids; Metabolites; Steroid hormones; biomarkers; Mass spectroscopy; Inflammation; Smoking; Risk factors; Reviews; Histidine; Dyslipidemia; Oxidation; Fatty acids; Neurotransmitters; Body mass index; metabolomics; Sex
DO - http://dx.doi.org/10.1007/s11306-013-0574-1
ER -
TY - JOUR
T1 - Targeting the Splicing of mRNA in Autoimmune Diseases: BAFF Inhibition in Sjogren's Syndrome as a Proof of Concept
AN - 1673390604; PQ0001372852
AB - BAFF (B-cell-activating factor of the tumor necrosis factor family), a pivotal cytokine for B-cell activation, is overexpressed by salivary gland (SG) epithelial cells in primary Sjogren's syndrome (pSS). Delta BAFF, a physiological inhibitor of BAFF, is a minor alternative splice variant of BAFF. A U7 RNA was reengineered to deliver antisense sequences targeting BAFF splice regions. A major decrease of BAFF messenger RNA (mRNA) and protein secretion, concomitantly with the increase of Delta BAFF mRNA, was observed in vitro. In vivo, SG retrograd instillation of nonobese diabetic mice by the modified U7 cloned into an adeno-associated virus vector significantly decreased BAFF protein expression and lymphocytic infiltrates and improved salivary flow. This study offers a rationale for localized therapeutic BAFF inhibition in pSS and represents a proof of concept of the interest of exon skipping in autoimmune diseases.
JF - Molecular Therapy
AU - Roescher, N
AU - Vosters, J L
AU - Alsaleh, G
AU - Dreyfus, P
AU - Jacques, S
AU - Chiocchia, G
AU - Sibilia, J
AU - Tak, P P
AU - Chiorini, J A
AU - Mariette, X
AU - Gottenberg, Jacques-Eric
AD - Division of Clinical Immunology and Rheumatology, Academic Medical Center, Amsterdam, The Netherlands; Molecular Physiology and Therapeutics Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland, USA, jacques-eric.gottenberg@chru-strasbourg.fr
Y1 - 2014/04//
PY - 2014
DA - Apr 2014
SP - 821
EP - 827
PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom
VL - 22
IS - 4
SN - 1525-0016, 1525-0016
KW - Immunology Abstracts; Biochemistry Abstracts 2: Nucleic Acids; Biotechnology and Bioengineering Abstracts
KW - Epithelial cells
KW - Lymphocytes B
KW - Tumor necrosis factor
KW - Autoimmune diseases
KW - Salivary gland
KW - Exon skipping
KW - Adeno-associated virus
KW - Alternative splicing
KW - mRNA
KW - Diabetes mellitus
KW - Expression vectors
KW - Sjogren's syndrome
KW - Antisense
KW - Cytokines
KW - BLyS protein
KW - W 30905:Medical Applications
KW - F 06960:Molecular Immunology
KW - N 14830:RNA
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-04-01
N1 - Last updated - 2015-11-16
N1 - SubjectsTermNotLitGenreText - Epithelial cells; Lymphocytes B; Tumor necrosis factor; Autoimmune diseases; Salivary gland; Exon skipping; mRNA; Alternative splicing; Sjogren's syndrome; Expression vectors; Diabetes mellitus; Antisense; Cytokines; BLyS protein; Adeno-associated virus
DO - http://dx.doi.org/10.1038/mt.2013.275
ER -
TY - JOUR
T1 - Rational development of radiopharmaceuticals for HIV-1
AN - 1668264864; 20136170
AB - The global battle against HIV-1 would benefit from a sensitive and specific radiopharmaceutical to localize HIV-infected cells. Ideally, this probe would be able to identify latently infected host cells containing replication competent HIV sequences. Clinical and research applications would include assessment of reservoirs, informing clinical management by facilitating assessment of burden of infection in different compartments, monitoring disease progression and monitoring response to therapy. A "rational" development approach could facilitate efficient identification of an appropriate targeted radiopharmaceutical. Rational development starts with understanding characteristics of the disease that can be effectively targeted and then engineering radiopharmaceuticals to hone in on an appropriate target, which in the case of HIV-1 (HIV) might be an HIV-specific product on or in the host cell, a differentially expressed gene product, an integrated DNA sequence specific enzymatic activity, part of the inflammatory response, or a combination of these. This is different from the current approach that starts with a radiopharmaceutical for a target associated with a disease, mostly from autopsy studies, without a strong rationale for the potential to impact patient care. At present, no targeted therapies are available for HIV latency, although a number of approaches are under study. Here we discuss requirements for a radiopharmaceutical useful in strategies targeting persistently infected cells. The radiopharmaceutical for HIV should be developed based on HIV biology, studied in an animal model and then in humans, and ultimately used in clinical and research settings.
JF - Nuclear Medicine and Biology
AU - Lau, Chuen-Yen
AU - Maldarelli, Frank
AU - Eckelman, William C
AU - Neumann, Ronald D
AD - National Institutes of Health, lauc@mail.nih.gov
Y1 - 2014/04//
PY - 2014
DA - Apr 2014
SP - 299
EP - 308
PB - Elsevier B.V., Box 882 New York NY 10159 United States
VL - 41
IS - 4
SN - 0969-8051, 0969-8051
KW - Biotechnology and Bioengineering Abstracts
KW - Human Immunodeficiency Virus
KW - Radiopharmaceutical
KW - Infectious disease imaging
KW - Autopsy
KW - Latent infection
KW - Replication
KW - Nucleotide sequence
KW - Animal models
KW - Probes
KW - Infection
KW - Inflammation
KW - Human immunodeficiency virus
KW - Human immunodeficiency virus 1
KW - Radioisotopes
KW - Pharmaceuticals
KW - Nuclear medicine
KW - Enzymatic activity
KW - W 30940:Products
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1668264864?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nuclear+Medicine+and+Biology&rft.atitle=Rational+development+of+radiopharmaceuticals+for+HIV-1&rft.au=Lau%2C+Chuen-Yen%3BMaldarelli%2C+Frank%3BEckelman%2C+William+C%3BNeumann%2C+Ronald+D&rft.aulast=Lau&rft.aufirst=Chuen-Yen&rft.date=2014-04-01&rft.volume=41&rft.issue=4&rft.spage=299&rft.isbn=&rft.btitle=&rft.title=Nuclear+Medicine+and+Biology&rft.issn=09698051&rft_id=info:doi/10.1016%2Fj.nucmedbio.2014.01.005
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-03-01
N1 - Last updated - 2015-04-02
N1 - SubjectsTermNotLitGenreText - Latent infection; Autopsy; Replication; Nucleotide sequence; Probes; Animal models; Radioisotopes; Nuclear medicine; Pharmaceuticals; Enzymatic activity; Infection; Inflammation; Human immunodeficiency virus; Human immunodeficiency virus 1
DO - http://dx.doi.org/10.1016/j.nucmedbio.2014.01.005
ER -
TY - JOUR
T1 - Ebola virus vaccines: an overview of current approaches
AN - 1668264148; PQ0001123777
AB - Ebola hemorrhagic fever is one of the most fatal viral diseases worldwide affecting humans and nonhuman primates. Although infections only occur frequently in Central Africa, the virus has the potential to spread globally and is classified as a category A pathogen that could be misused as a bioterrorism agent. As of today there is no vaccine or treatment licensed to counteract Ebola virus infections. DNA, subunit and several viral vector approaches, replicating and non-replicating, have been tested as potential vaccine platforms and their protective efficacy has been evaluated in nonhuman primate models for Ebola virus infections, which closely resemble disease progression in humans. Though these vaccine platforms seem to confer protection through different mechanisms, several of them are efficacious against lethal disease in nonhuman primates attesting that vaccination against Ebola virus infections is feasible.
JF - Expert Review of Vaccines
AU - Marzi, Andrea
AU - Feldmann, Heinz
AD - Laboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rocky Mountain Laboratories, Hamilton, Montana 59840, MT, USA
Y1 - 2014/04//
PY - 2014
DA - Apr 2014
SP - 521
EP - 531
PB - Future Science Group (FSG), Unitec House, 2 Albert Place London N3 1QB United Kingdom
VL - 13
IS - 4
SN - 1476-0584, 1476-0584
KW - Health & Safety Science Abstracts; Virology & AIDS Abstracts
KW - animal model
KW - Ebola virus
KW - filovirus
KW - prophylaxis
KW - vaccine
KW - bioterrorism
KW - Disasters
KW - Animal models
KW - Pathogens
KW - Bioterrorism
KW - Infection
KW - Primates
KW - Viral diseases
KW - Reviews
KW - DNA
KW - Africa
KW - Hemorrhagic fever
KW - Vaccines
KW - H 4000:Food and Drugs
KW - V 22400:Human Diseases
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-03-01
N1 - Number of references - 77
N1 - Last updated - 2015-08-05
N1 - SubjectsTermNotLitGenreText - bioterrorism; Reviews; Animal models; Hemorrhagic fever; Pathogens; Vaccines; Infection; Viral diseases; DNA; Disasters; Bioterrorism; Primates; Ebola virus; Africa
ER -
TY - JOUR
T1 - Transient Increase of Interferon-Stimulated Genes and No Clinical Benefit by Chloroquine Treatment During Acute Simian Immunodeficiency Virus Infection of Macaques
AN - 1635021473; 21057628
AB - Simian immunodeficiency virus (SIV) infection leads to AIDS in experimentally infected Rhesus macaques similarly to HIV-infected humans. In contrast, SIV infection of natural hosts is characterized by a down-regulation of innate acute responses to the vims within a few weeks of infection and results in limited pathology. Chloroquine (CQ) has been used in the treatment or prevention of malaria AIDS has recently been shown to cause a decrease of immune activation and CD4 cell loss in HIV-induced individuals treated with antiretroviral therapy. Here, we treated Rhesus macaques with CQ during the acute phase of SIV sub(mac251) infection with the intent to decrease viral-induced immune activation and possibly limit disease progression. Contrary to what was expected, CQ treatment resulted in a temporary increased expression of interferon (IFN)-stimulating genes and it worsened the recovery of CD4 super(+) T cells in the blood. Our findings confirm recent results observed in asymptomatic HIV-infected patients and suggest that CQ does not provide an obvious benefit in the absence of antiretroviral therapy.
JF - AIDS Research and Human Retroviruses
AU - Vaccari, Monica
AU - Fenizia, Claudio
AU - Ma, Zhong-Min
AU - Hryniewicz, Anna
AU - Boasso, Adriano
AU - Doster, Melvin N
AU - Miller, Christopher J
AU - Lindegardh, Niklas
AU - Tarning, Joel
AU - Landay, Alan L
AU - Shearer, Gene M
AU - Franchini, Genoveffa
AD - Animal Models and Retroviral Vaccines Section, NCI, NIH, Bethesda, Maryland
Y1 - 2014/04//
PY - 2014
DA - April 2014
SP - 355
EP - 362
PB - Mary Ann Liebert, Inc., 140 Huguenot Street New Rochelle NY 10801 United States
VL - 30
IS - 4
SN - 0889-2229, 0889-2229
KW - Genetics Abstracts; ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Immunology Abstracts; Virology & AIDS Abstracts
KW - Acquired immune deficiency syndrome
KW - Human diseases
KW - Pathology
KW - antiretroviral therapy
KW - Disease control
KW - Therapy
KW - Chloroquine
KW - Malaria
KW - Hosts
KW - Infection
KW - Swine influenza virus
KW - Public health
KW - Blood
KW - Interferon
KW - CD4 antigen
KW - Retrovirus
KW - Genes
KW - Human immunodeficiency virus
KW - Lymphocytes T
KW - Macaca mulatta
KW - Immune response
KW - Simian immunodeficiency virus
KW - V 22360:AIDS and HIV
KW - Q1 08484:Species interactions: parasites and diseases
KW - G 07730:Development & Cell Cycle
KW - F 06910:Microorganisms & Parasites
KW - Q5 08524:Public health, medicines, dangerous organisms
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS+Research+and+Human+Retroviruses&rft.atitle=Transient+Increase+of+Interferon-Stimulated+Genes+and+No+Clinical+Benefit+by+Chloroquine+Treatment+During+Acute+Simian+Immunodeficiency+Virus+Infection+of+Macaques&rft.au=Vaccari%2C+Monica%3BFenizia%2C+Claudio%3BMa%2C+Zhong-Min%3BHryniewicz%2C+Anna%3BBoasso%2C+Adriano%3BDoster%2C+Melvin+N%3BMiller%2C+Christopher+J%3BLindegardh%2C+Niklas%3BTarning%2C+Joel%3BLanday%2C+Alan+L%3BShearer%2C+Gene+M%3BFranchini%2C+Genoveffa&rft.aulast=Vaccari&rft.aufirst=Monica&rft.date=2014-04-01&rft.volume=30&rft.issue=4&rft.spage=355&rft.isbn=&rft.btitle=&rft.title=AIDS+Research+and+Human+Retroviruses&rft.issn=08892229&rft_id=info:doi/10.1089%2Faid.2013.0218
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-12-01
N1 - Last updated - 2016-10-12
N1 - SubjectsTermNotLitGenreText - Human diseases; Genes; Pathology; Therapy; Disease control; Malaria; Hosts; Public health; Interferon; Blood; CD4 antigen; Acquired immune deficiency syndrome; antiretroviral therapy; Lymphocytes T; Chloroquine; Immune response; Infection; Retrovirus; Human immunodeficiency virus; Macaca mulatta; Swine influenza virus; Simian immunodeficiency virus
DO - http://dx.doi.org/10.1089/aid.2013.0218
ER -
TY - JOUR
T1 - Impact of Socio-Economic Status in Meeting the Needs of People with Mental Illness; Human Rights Perspective
AN - 1559003765; 201407068
AB - The present descriptive study investigated the impact of socio-economic status in meeting the human rights needs among randomly selected recovered psychiatric patients (n = 100) at a tertiary care center. Data was collected through face to face interview, using structured Needs Assessment Questionnaire. The findings revealed that the participants from below poverty line were deprived of physical needs such as 'electricity facilities' (X 2 = 6.821, p < .009) 'safe drinking water' (X 2 = 13.506, p < .004) and purchasing medications (X 2 = 9.958, p < .019). Conversely, participants from above poverty line were dissatisfied in emotional needs dimension i.e. 'commenting on physical appearance (X 2 = 8.337, p < .040), afraid of family members (X 2 = 17.809, p < .000). Thus, there is an urgent need to implement mental illness awareness campaigns and government should take active steps for providing employment, disability pension, free housing, free treatment and free transportation service for people with mental illness to attend hospital or rehabilitation centres. Adapted from the source document.
JF - Community Mental Health Journal
AU - Vijayalakshmi, Poreddi
AU - Ramachandra, Ramachandra
AU - Reddemma, Konduru
AU - Math, Suresh Bada
AD - Department of Nursing, College of Nursing, National Institute of Mental Health and Neuro Sciences, Deemed University, Bangalore, 560 029, India pvijayalakshmireddy@gmail.com
Y1 - 2014/04//
PY - 2014
DA - April 2014
SP - 245
EP - 250
PB - Springer, Dordrecht The Netherlands
VL - 50
IS - 3
SN - 0010-3853, 0010-3853
KW - Consciousness
KW - Physically Handicapped
KW - Purchasing
KW - Poverty
KW - Socioeconomic Status
KW - Disadvantaged
KW - Water Supply
KW - Mental Illness
KW - Human Rights
KW - article
KW - 6142: mental & emotional health problems
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Asocialservices&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Community+Mental+Health+Journal&rft.atitle=Impact+of+Socio-Economic+Status+in+Meeting+the+Needs+of+People+with+Mental+Illness%3B+Human+Rights+Perspective&rft.au=Vijayalakshmi%2C+Poreddi%3BRamachandra%2C+Ramachandra%3BReddemma%2C+Konduru%3BMath%2C+Suresh+Bada&rft.aulast=Vijayalakshmi&rft.aufirst=Poreddi&rft.date=2014-04-01&rft.volume=50&rft.issue=3&rft.spage=245&rft.isbn=&rft.btitle=&rft.title=Community+Mental+Health+Journal&rft.issn=00103853&rft_id=info:doi/10.1007%2Fs10597-012-9577-z
LA - English
DB - Social Services Abstracts
N1 - Date revised - 2014-09-01
N1 - Number of references - 41
N1 - Last updated - 2016-09-28
N1 - CODEN - CMHJAY
N1 - SubjectsTermNotLitGenreText - Mental Illness; Socioeconomic Status; Human Rights; Poverty; Purchasing; Physically Handicapped; Water Supply; Consciousness; Disadvantaged
DO - http://dx.doi.org/10.1007/s10597-012-9577-z
ER -
TY - JOUR
T1 - Vocal coordination and vocal imitation: A role for mirror neurons?
AN - 1558998570; 201413406
AB - Some birds and mammals have vocal communication systems in which coordination between individuals is important. Examples would include duetting or antiphonal calling in some birds and mammals, rapid exchanges of the same vocalization, and vocal exchanges between paired individuals and other nearby pairs. Mirror neurons may play a role in such systems but become functional only after experience. Adapted from the source document
JF - Behavioral and Brain Sciences
AU - Newman, John D
AD - Laboratory of Comparative Ethology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health (NIH), Poolesville, MD 20837. jn1g@nih.gov
Y1 - 2014/04//
PY - 2014
DA - April 2014
SP - 211
EP - 212
VL - 37
IS - 2
SN - 0140-525X, 0140-525X
KW - Imitation (34600)
KW - Animal Communication (03150)
KW - Mirror Neurons (54280)
KW - Communication (13600)
KW - Birds (08980)
KW - Drama (19750)
KW - article
KW - 6410: language-pathological and normal; language and speech pathology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Allba&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Behavioral+and+Brain+Sciences&rft.atitle=Vocal+coordination+and+vocal+imitation%3A+A+role+for+mirror+neurons%3F&rft.au=Newman%2C+John+D&rft.aulast=Newman&rft.aufirst=John&rft.date=2014-04-01&rft.volume=37&rft.issue=2&rft.spage=211&rft.isbn=&rft.btitle=&rft.title=Behavioral+and+Brain+Sciences&rft.issn=0140525X&rft_id=info:doi/
LA - English
DB - Linguistics and Language Behavior Abstracts (LLBA)
N1 - Date revised - 2014-09-01
N1 - Last updated - 2016-09-27
N1 - CODEN - BBSCDH
N1 - SubjectsTermNotLitGenreText - Mirror Neurons (54280); Birds (08980); Animal Communication (03150); Drama (19750); Imitation (34600); Communication (13600)
ER -
TY - JOUR
T1 - Identification of Volatile Organic Compounds Produced by Bacteria Using HS-SPME-GC-MS
AN - 1551618775; 20177086
AB - The analysis of volatile organic compounds (VOCs) as a tool for bacterial identification is reported. Head space solid-phase microextraction (HSSPME) coupled to gas chromatography-mass spectrometry (GC-MS) was applied to the analysis of bacterial VOCs with the aim of determining the impact of experimental parameters on the generated VOC profiles. The effect of culture medium, SPME fiber type and GC column were fully evaluated with the Gram-negative bacteria Escherichia coli and Klebsiella pneumoniae and the Gram-positive species Staphylococcus aureus. Multivariate analysis, including cluster analysis and principal component analysis, was applied to VOC data to determine whether the parameters under investigation significantly affected bacterial VOC profiles. Culture medium, and to a lesser extent, SPME fiber type, were found to significantly alter detected bacterial VOC profiles. The detected VOCs varied little with the polarity of the GC column. The results indicate that the generated bacterial VOC profiles need careful evaluation if they are to be used for clinical diagnostics. The whole process is limited by the need to grow the bacteria in broth (18 h) before extraction and analysis (63 min).
JF - Journal of Chromatographic Science
AU - Tait, Emma
AU - Perry, John D
AU - Stanforth, Stephen P
AU - Dean, John R
AD - Department of Applied Sciences, Northumbria University, Ellison Building, Newcastle upon Tyne, NEI 8ST, UK, john.dean@unn.ac.uk
Y1 - 2014/04//
PY - 2014
DA - April 2014
SP - 363
EP - 373
PB - Preston Publications, Inc., 6600 W. Touhy Ave. Niles IL 60714 United States
VL - 52
IS - 4
SN - 0021-9665, 0021-9665
KW - Microbiology Abstracts B: Bacteriology
KW - Data processing
KW - Head
KW - Mass spectroscopy
KW - Fibers
KW - Gas chromatography
KW - Multivariate analysis
KW - Principal components analysis
KW - Gram-negative bacteria
KW - Headspace
KW - Escherichia coli
KW - volatile organic compounds
KW - Polarity
KW - Staphylococcus aureus
KW - Solid phase methods
KW - Klebsiella pneumoniae
KW - J 02320:Cell Biology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Chromatographic+Science&rft.atitle=Identification+of+Volatile+Organic+Compounds+Produced+by+Bacteria+Using+HS-SPME-GC-MS&rft.au=Tait%2C+Emma%3BPerry%2C+John+D%3BStanforth%2C+Stephen+P%3BDean%2C+John+R&rft.aulast=Tait&rft.aufirst=Emma&rft.date=2014-04-01&rft.volume=52&rft.issue=4&rft.spage=363&rft.isbn=&rft.btitle=&rft.title=Journal+of+Chromatographic+Science&rft.issn=00219665&rft_id=info:doi/10.1093%2Fchromsci%2Fbmt042
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-08-01
N1 - Last updated - 2016-05-13
N1 - SubjectsTermNotLitGenreText - Fibers; Data processing; Head; Multivariate analysis; Gas chromatography; Gram-negative bacteria; Principal components analysis; Headspace; volatile organic compounds; Polarity; Solid phase methods; Mass spectroscopy; Escherichia coli; Staphylococcus aureus; Klebsiella pneumoniae
DO - http://dx.doi.org/10.1093/chromsci/bmt042
ER -
TY - JOUR
T1 - Genetics and personal responsibility for health
AN - 1550999669; 201430519
AB - Advances in genetic medicine may have implications for how we should think about personal responsibility for health, because they may show how it is possible to exert some control over risk factors that were previously thought as beyond the individual's control. Although we cannot control the genes that we are born with, we can often make decisions concerning genetic testing, disease prevention, and treatment. One might argue, therefore, that individuals should be treated as morally responsible for taking effective action in response to genetic risks factors, since genetically based health risks are similar to other health risks. While this argument makes sense as an abstract, philosophical position, it is not a useful guide to public policy. Given these concerns, there is little society can or should do to encourage individuals to address their genetic risk factors, other than praising those who make prudent choices. Adapted from the source document.
JF - New Genetics and Society
AU - Resnik, David B
AD - National Institute of Environmental Health Sciences, National Institutes of Health, Box 12233, Mail Drop CU 03, Research Triangle Park, NC 27709, USA
Y1 - 2014/04//
PY - 2014
DA - April 2014
SP - 113
EP - 125
PB - Routledge/Taylor & Francis, Abingdon UK
VL - 33
IS - 2
SN - 1463-6778, 1463-6778
KW - Genetic Testing
KW - Risk
KW - Genetics
KW - Prevention
KW - Responsibility
KW - Choices
KW - Health Behavior
KW - Health
KW - Medical Decision Making
KW - article
KW - 1864: demography and human biology; genetic engineering/reproductive biotechnology
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1550999669?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Asocabs&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=New+Genetics+and+Society&rft.atitle=Genetics+and+personal+responsibility+for+health&rft.au=Resnik%2C+David+B&rft.aulast=Resnik&rft.aufirst=David&rft.date=2014-04-01&rft.volume=33&rft.issue=2&rft.spage=113&rft.isbn=&rft.btitle=&rft.title=New+Genetics+and+Society&rft.issn=14636778&rft_id=info:doi/10.1080%2F14636778.2014.905195
LA - English
DB - Sociological Abstracts
N1 - Date revised - 2014-08-01
N1 - Last updated - 2016-09-28
N1 - SubjectsTermNotLitGenreText - Genetics; Health; Risk; Responsibility; Medical Decision Making; Health Behavior; Prevention; Genetic Testing; Choices
DO - http://dx.doi.org/10.1080/14636778.2014.905195
ER -
TY - JOUR
T1 - Cancer stem cells: a systems biology view of their role in prognosis and therapy
AN - 1544017127; 20150164
AB - Evidence has accumulated that characterizes highly tumorigenic cancer cells residing in heterogeneous populations. The accepted term for such a subpopulation is cancer stem cells (CSCs). While many questions still remain about their precise role in the origin, progression, and drug resistance of tumors, it is clear they exist. In this review, a current understanding of the nature of CSC, their potential usefulness in prognosis, and the need to target them will be discussed. In particular, separate studies now suggest that the CSC is plastic in its phenotype, toggling between tumorigenic and nontumorigenic states depending on both intrinsic and extrinsic conditions. Because of this, a static view of gene and protein levels defined by correlations may not be sufficient to either predict disease progression or aid in the discovery and development of drugs to molecular targets leading to cures. Quantitative dynamic modeling, a bottom up systems biology approach whereby signal transduction pathways are described by differential equations, may offer a novel means to overcome the challenges of oncology today. In conclusion, the complexity of CSCs can be captured in mathematical models that may be useful for selecting molecular targets, defining drug action, and predicting sensitivity or resistance pathways for improved patient outcomes.
JF - Anti-Cancer Drugs
AU - Merlins, Susan D
AD - Screening Technologies Branch, Developmental Therapeutics Program, Division of Cancer Diagnosis and Treatment, National Cancer Institute at Frederick, PO Box B, Bldg. 315, Room 6, Frederick, Maryland, USA, smertins@mail.nih.gov
Y1 - 2014/04//
PY - 2014
DA - Apr 2014
SP - 353
EP - 367
PB - Rapid Science Publishers, The Old Malthouse Oxford OX1 1LD United Kingdom
VL - 25
IS - 4
SN - 0959-4973, 0959-4973
KW - Biotechnology and Bioengineering Abstracts; Oncogenes & Growth Factors Abstracts
KW - cancer stem cells
KW - dynamic modeling
KW - plasticity
KW - prognosis
KW - signal transduction pathways
KW - systems biology
KW - therapeutics
KW - Stem cells
KW - Mathematical models
KW - Drug resistance
KW - Prognosis
KW - Drug development
KW - Oncology
KW - Tumors
KW - Plastics
KW - Cancer
KW - Signal transduction
KW - W 30915:Pharmaceuticals & Vaccines
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-07-01
N1 - Last updated - 2015-04-02
N1 - SubjectsTermNotLitGenreText - Stem cells; Mathematical models; Drug resistance; Prognosis; Oncology; Drug development; Plastics; Tumors; Cancer; Signal transduction
DO - http://dx.doi.org/10.1097/CAD.0000000000000075
ER -
TY - JOUR
T1 - Exploiting sensitization windows of opportunity in hyper and hypo-fractionated radiation therapy.
AN - 1540117966; 24688774
AB - In contrast to the conventional radiotherapy/chemoradiotherapy paradigms used in the treatment of majority of cancer types, this review will describe two areas of radiobiology, hyperfractionated and hypofractionated radiation therapy, for cancer treatment focusing on application of novel concepts underlying these treatment modalities. The initial part of the review discusses the phenomenon of hyper-radiation sensitivity (HRS) at lower doses (0.1 to 0.6 Gy), describing the underlying mechanisms and how this could enhance the effects of chemotherapy, particularly, in hyperfractionated settings. The second part examines the radiobiological/physiological mechanisms underlying the effects of high-dose hypofractionated radiation therapy that can be exploited for tumor cure. These include abscopal/bystander effects, activation of immune system, endothelial cell death and effect of hypoxia with re-oxygenation. These biological properties along with targeted dose delivery and distribution to reduce normal tissue toxicity may make high-dose hypofractionation more effective than conventional radiation therapy for treatment of advanced cancers. The novel radiation physics based methods that take into consideration the tumor volume to be irradiated and normal tissue avoidance/tolerance can further improve treatment outcome and post-treatment quality of life. In conclusion, there is enough evidence to further explore novel avenues to exploit biological mechanisms from hyper-fractionation by enhancing the efficacy of chemotherapy and hypo-fractionated radiation therapy that could enhance tumor control and use imaging and technological advances to reduce toxicity.
JF - Journal of thoracic disease
AU - Prasanna, Anish
AU - Ahmed, Mansoor M
AU - Mohiuddin, Mohammed
AU - Coleman, C Norman
AD - 1 Radiation Research Program, Division of Cancer Treatment and Diagnosis, National Cancer Institute, National Institutes of Health, Rockville, MD, USA ; 2 Oncology Centre, King Faisal Specialist Hospital and Research Centre, Riyadh, Kingdom of Saudi Arabia.
Y1 - 2014/04//
PY - 2014
DA - April 2014
SP - 287
EP - 302
VL - 6
IS - 4
SN - 2072-1439, 2072-1439
KW - hyperfractionation
KW - spatially fractionated GRID radiotherapy (SFGRT)
KW - lattice
KW - hyper-radiation sensitivity (HRS)
KW - stereotactic ablative radiotherapy (SABR)
KW - chemopotentiation
KW - stereotactic radiosurgery (SRS)
KW - induced radiation resistance (IRR)
KW - Low Doses Fractionated Radiation Therapy (LDFRT)
KW - stereotactic ablative radiosurgery (SARS)
KW - stereotactic body radiation therapy (SBRT)
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+thoracic+disease&rft.atitle=Exploiting+sensitization+windows+of+opportunity+in+hyper+and+hypo-fractionated+radiation+therapy.&rft.au=Prasanna%2C+Anish%3BAhmed%2C+Mansoor+M%3BMohiuddin%2C+Mohammed%3BColeman%2C+C+Norman&rft.aulast=Prasanna&rft.aufirst=Anish&rft.date=2014-04-01&rft.volume=6&rft.issue=4&rft.spage=287&rft.isbn=&rft.btitle=&rft.title=Journal+of+thoracic+disease&rft.issn=20721439&rft_id=info:doi/10.3978%2Fj.issn.2072-1439.2014.01.14
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-06-24
N1 - Date created - 2014-04-01
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.3978/j.issn.2072-1439.2014.01.14
ER -
TY - JOUR
T1 - Plasmodium genetic loci linked to host cytokine and chemokine responses
AN - 1529957668; 19859602
AB - Both host and parasite factors contribute to disease severity of malaria infection; however, the molecular mechanisms responsible for the disease and the host-parasite interactions involved remain largely unresolved. To investigate the effects of parasite factors on host immune responses and pathogenesis, we measured levels of plasma cytokines/chemokines (CCs) and growth rates in mice infected with two Plasmodium yoelii strains having different virulence phenotypes and in progeny from a genetic cross of the two parasites. Quantitative trait loci (QTL) analysis linked levels of many CCs, particularly IL-1 beta , IP-10, IFN- gamma , MCP-1 and MIG, and early parasite growth rate to loci on multiple parasite chromosomes, including chromosomes 7, 9, 10, 12 and 13. Comparison of the genome sequences spanning the mapped loci revealed various candidate genes. The loci on chromosomes 7 and 13 had significant (P<0.005) additive effects on IL-1 beta , IL-5 and IP-10 responses, and the chromosome 9 and 12 loci had significant (P=0.017) interaction. Infection of knockout mice showed critical roles of MCP-1 and IL-10 in parasitemia control and host mortality. These results provide important information for a better understanding of malaria pathogenesis and can be used to examine the role of these factors in human malaria infection.
JF - Genes and Immunity
AU - Pattaradilokrat, S
AU - Li, J
AU - Wu, J
AU - Qi, Y
AU - Eastman, R T
AU - Zilversmit, M
AU - Nair, S C
AU - Huaman, M C
AU - Quinones, M
AU - Jiang, H
AU - Li, N
AU - Zhu, J
AU - Zhao, K
AU - Kaneko, O
AU - Long, C A
AU - Su, X-z
AD - 1] Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, MD, USA [2] Department of Biology, Faculty of Science, Chulalongkorn University, Bangkok, Thailand
Y1 - 2014/04//
PY - 2014
DA - April 2014
SP - 145
EP - 152
PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL - 15
IS - 3
SN - 1466-4879, 1466-4879
KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Microbiology Abstracts C: Algology, Mycology & Protozoology; Genetics Abstracts; Immunology Abstracts
KW - Genomes
KW - gamma -Interferon
KW - Molecular modelling
KW - Parasites
KW - Chemokines
KW - Human diseases
KW - Interleukin 5
KW - Interleukin 1
KW - Malaria
KW - Hosts
KW - Infection
KW - Phenotypes
KW - Interleukin 10
KW - chromosome 7
KW - Public health
KW - Virulence
KW - chromosome 9
KW - Chromosomes
KW - IP-10 protein
KW - Cytokines
KW - Plasmodium yoelii
KW - Host-parasite interactions
KW - Growth rate
KW - Mortality
KW - Quantitative trait loci
KW - Monocyte chemoattractant protein 1
KW - parasitemia
KW - Immune response
KW - Genetic crosses
KW - Mortality causes
KW - K 03410:Animal Diseases
KW - G 07720:Immunogenetics
KW - Q1 08485:Species interactions: pests and control
KW - Q5 08524:Public health, medicines, dangerous organisms
KW - F 06950:Immunogenetics, MHC, HLA
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Genes+and+Immunity&rft.atitle=Plasmodium+genetic+loci+linked+to+host+cytokine+and+chemokine+responses&rft.au=Pattaradilokrat%2C+S%3BLi%2C+J%3BWu%2C+J%3BQi%2C+Y%3BEastman%2C+R+T%3BZilversmit%2C+M%3BNair%2C+S+C%3BHuaman%2C+M+C%3BQuinones%2C+M%3BJiang%2C+H%3BLi%2C+N%3BZhu%2C+J%3BZhao%2C+K%3BKaneko%2C+O%3BLong%2C+C+A%3BSu%2C+X-z&rft.aulast=Pattaradilokrat&rft.aufirst=S&rft.date=2014-04-01&rft.volume=15&rft.issue=3&rft.spage=145&rft.isbn=&rft.btitle=&rft.title=Genes+and+Immunity&rft.issn=14664879&rft_id=info:doi/10.1038%2Fgene.2013.74
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-05-01
N1 - Last updated - 2016-02-04
N1 - SubjectsTermNotLitGenreText - Growth rate; Parasites; Human diseases; Chromosomes; Malaria; Hosts; Phenotypes; Mortality causes; Public health; Genomes; Molecular modelling; Quantitative trait loci; gamma -Interferon; Mortality; Chemokines; Interleukin 5; Monocyte chemoattractant protein 1; Interleukin 1; Infection; Interleukin 10; chromosome 7; chromosome 9; Virulence; parasitemia; IP-10 protein; Cytokines; Immune response; Genetic crosses; Host-parasite interactions; Plasmodium yoelii
DO - http://dx.doi.org/10.1038/gene.2013.74
ER -
TY - JOUR
T1 - Genetics of low spinal muscular atrophy carrier frequency in sub-Saharan Africa
AN - 1529945116; 19812897
AB - Objective Spinal muscular atrophy (SMA) is one of the most common severe hereditary diseases of infancy and early childhood in North America, Europe, and Asia. SMA is usually caused by deletions of the survival motor neuron 1 (SMN1) gene. A closely related gene, SMN2, modifies the disease severity. SMA carriers have only 1 copy of SMN1 and are relatively common (1 in 30-50) in populations of European and Asian descent. SMN copy numbers and SMA carrier frequencies have not been reliably estimated in Malians and other sub-Saharan Africans. Methods We used a quantitative polymerase chain reaction assay to determine SMN1 and SMN2 copy numbers in 628 Malians, 120 Nigerians, and 120 Kenyans. We also explored possible mechanisms for SMN1 and SMN2 copy number differences in Malians, and investigated their effects on SMN mRNA and protein levels. Results The SMA carrier frequency in Malians is 1 in 209, lower than in Eurasians. Malians and other sub-Saharan Africans are more likely to have greater than or equal to 3 copies of SMN1 than Eurasians, and more likely to lack SMN2 than Europeans. There was no evidence of gene conversion, gene locus duplication, or natural selection from malaria resistance to account for the higher SMN1 copy numbers in Malians. High SMN1 copy numbers were not associated with increased SMN mRNA or protein levels in human cell lines. Interpretation SMA carrier frequencies are much lower in sub-Saharan Africans than in Eurasians. This finding is important to consider in SMA genetic counseling in individuals with black African ancestry. Ann Neurol 2014; 75:525-532
JF - Annals of Neurology
AU - Sangare, Modibo
AU - Hendrickson, Brant
AU - Sango, Hammadoun Ali
AU - Chen, Kelian
AU - Nofziger, Jonathan
AU - Amara, Abdelbasset
AU - Dutra, Amalia
AU - Schindler, Alice B
AU - Guindo, Aldiouma
AU - Traore, Mahamadou
AU - Harmison, George
AU - Pak, Evgenia
AU - Yaro, Fatoumata N'Go
AU - Bricceno, Katherine
AU - Grunseich, Christopher
AU - Chen, Guibin
AU - Boehm, Manfred
AU - Zukosky, Kristen
AU - Bocoum, Nouhoum
AU - Meilleur, Katherine G
AU - Daou, Fatoumata
AU - Bagayogo, Koumba
AU - Coulibaly, Yaya Ibrahim
AU - Diakite, Mahamadou
AU - Fay, Michael P
AU - Lee, Hee-Suk
AU - Saad, Ali
AU - Gribaa, Moez
AU - Singleton, Andrew B
AU - Maiga, Youssoufa
AU - Auh, Sungyoung
AU - Landoure, Guida
AU - Fairhurst, Rick M
AU - Burnett, Barrington G
AU - Scholl, Thomas
AU - Fischbeck, Kenneth H
AD - Neurogenetics Branch, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD.
Y1 - 2014/04//
PY - 2014
DA - April 2014
SP - 525
EP - 532
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 75
IS - 4
SN - 0364-5134, 0364-5134
KW - Genetics Abstracts; ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; CSA Neurosciences Abstracts
KW - Cell survival
KW - Human diseases
KW - Nucleotide sequence
KW - Malaria
KW - Natural selection
KW - Public health
KW - Gene deletion
KW - ANE, Europe
KW - Polymerase chain reaction
KW - spinal muscular atrophy
KW - Asia
KW - North America
KW - SMN protein
KW - Hereditary diseases
KW - Children
KW - Gene conversion
KW - mRNA
KW - copy number
KW - Motor neurons
KW - Neurons
KW - Africa
KW - Q1 08443:Population genetics
KW - G 07730:Development & Cell Cycle
KW - Q5 08524:Public health, medicines, dangerous organisms
KW - N3 11027:Neurology & neuropathology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+Neurology&rft.atitle=Genetics+of+low+spinal+muscular+atrophy+carrier+frequency+in+sub-Saharan+Africa&rft.au=Sangare%2C+Modibo%3BHendrickson%2C+Brant%3BSango%2C+Hammadoun+Ali%3BChen%2C+Kelian%3BNofziger%2C+Jonathan%3BAmara%2C+Abdelbasset%3BDutra%2C+Amalia%3BSchindler%2C+Alice+B%3BGuindo%2C+Aldiouma%3BTraore%2C+Mahamadou%3BHarmison%2C+George%3BPak%2C+Evgenia%3BYaro%2C+Fatoumata+N%27Go%3BBricceno%2C+Katherine%3BGrunseich%2C+Christopher%3BChen%2C+Guibin%3BBoehm%2C+Manfred%3BZukosky%2C+Kristen%3BBocoum%2C+Nouhoum%3BMeilleur%2C+Katherine+G%3BDaou%2C+Fatoumata%3BBagayogo%2C+Koumba%3BCoulibaly%2C+Yaya+Ibrahim%3BDiakite%2C+Mahamadou%3BFay%2C+Michael+P%3BLee%2C+Hee-Suk%3BSaad%2C+Ali%3BGribaa%2C+Moez%3BSingleton%2C+Andrew+B%3BMaiga%2C+Youssoufa%3BAuh%2C+Sungyoung%3BLandoure%2C+Guida%3BFairhurst%2C+Rick+M%3BBurnett%2C+Barrington+G%3BScholl%2C+Thomas%3BFischbeck%2C+Kenneth+H&rft.aulast=Sangare&rft.aufirst=Modibo&rft.date=2014-04-01&rft.volume=75&rft.issue=4&rft.spage=525&rft.isbn=&rft.btitle=&rft.title=Annals+of+Neurology&rft.issn=03645134&rft_id=info:doi/10.1002%2Fana.24114
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-05-01
N1 - Last updated - 2016-02-04
N1 - SubjectsTermNotLitGenreText - Human diseases; Nucleotide sequence; Neurons; Polymerase chain reaction; Malaria; Natural selection; Public health; Cell survival; SMN protein; Hereditary diseases; Children; copy number; mRNA; Gene conversion; Motor neurons; Gene deletion; spinal muscular atrophy; North America; ANE, Europe; Africa; Asia
DO - http://dx.doi.org/10.1002/ana.24114
ER -
TY - JOUR
T1 - Vaccination with tumor cells expressing IL-15 and IL-15R alpha inhibits murine breast and prostate cancer
AN - 1524404496; 19750152
AB - A number of antitumor vaccines have recently shown promise in upregulating immune responses against tumor antigens and improving patient survival. In this study, we examine the effectiveness of vaccination using interleukin (IL)-15-expressing tumor cells and also examine their ability to upregulate immune responses to tumor antigens. We demonstrated that the coexpression of IL-15 with its receptor, IL-15R alpha , increased the cell-surface expression and secretion of IL-15. We show that a gene transfer approach using recombinant adenovirus to express IL-15 and IL-15R alpha in murine TRAMP-C2 prostate or TS/A breast tumors induced antitumor immune responses. From this, we developed a vaccine platform, consisting of TRAMP-C2 prostate cancer cells or TS/A breast cancer cells coexpressing IL-15 and IL-15R alpha that inhibited tumor formation when mice were challenged with tumor. Inhibition of tumor growth led to improved survival when compared with animals receiving cells expressing IL-15 alone or unmodified tumor cells. Animals vaccinated with tumor cells coexpressing IL-15 and IL-15R alpha showed greater tumor infiltration with CD8 super(+) T and natural killer (NK) cells, as well as increased antitumor CD8 super(+) T-cell responses. Vaccination with IL-15/IL-15R alpha -modified TS/A breast cancer cells provided a survival advantage to mice challenged with unrelated murine TUBO breast cancer cells, indicating the potential for allogeneic IL-15/IL-15R alpha -expressing vaccines.
JF - Gene Therapy
AU - Morris, J C
AU - Ramlogan-Steel, C A
AU - Yu, P
AU - Black, B A
AU - Mannan, P
AU - Allison, J P
AU - Waldmann, T A
AU - Steel, J C
AD - 1] Division of Hematology/Oncology, Department of Internal Medicine, University of Cincinnati, Cincinnati, OH, USA [2] Metabolism Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA
Y1 - 2014/04//
PY - 2014
DA - Apr 2014
SP - 393
EP - 401
PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL - 21
IS - 4
SN - 0969-7128, 0969-7128
KW - Genetics Abstracts; Biotechnology and Bioengineering Abstracts
KW - Cell survival
KW - Gene therapy
KW - Adenovirus
KW - Natural killer cells
KW - CD8 antigen
KW - Tumors
KW - Tumor cells
KW - Metastases
KW - Prostate cancer
KW - Interleukin 15
KW - Antigen (tumor-associated)
KW - Lymphocytes T
KW - Breast cancer
KW - Immune response
KW - Vaccines
KW - Antitumor activity
KW - G 07720:Immunogenetics
KW - W 30905:Medical Applications
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-05-01
N1 - Last updated - 2014-05-29
N1 - SubjectsTermNotLitGenreText - Cell survival; Gene therapy; Natural killer cells; Tumors; CD8 antigen; Tumor cells; Metastases; Prostate cancer; Interleukin 15; Antigen (tumor-associated); Lymphocytes T; Breast cancer; Vaccines; Immune response; Antitumor activity; Adenovirus
DO - http://dx.doi.org/10.1038/gt.2014.10
ER -
TY - JOUR
T1 - Personality traits and vulnerability or resilience to substance use disorders.
AN - 1522680053; 24612993
AB - Clear evidence supports a genetic basis for substance use disorders (SUD). Yet, the search to identify individual gene contributions to SUD has been unsuccessful. Here, we argue for the study of endophenotypes within the frame of individual differences, and identify three high-order personality traits that are tied to specific brain systems and genes, and that offer a tractable approach to studying SUD. These personality traits, and the genes that moderate them, interact dynamically with the environment and with the drugs themselves to determine ultimately an individual's vulnerability or resilience to developing SUD.
Published by Elsevier Ltd.
JF - Trends in cognitive sciences
AU - Belcher, Annabelle M
AU - Volkow, Nora D
AU - Moeller, F Gerard
AU - Ferré, Sergi
AD - National Institute on Drug Abuse, Intramural Research Program, National Institutes of Health, Baltimore, MD 21224, USA. ; National Institute on Drug Abuse, National Institutes of Health, Bethesda, MD 20892, USA. ; Departments of Psychiatry and Pharmacology and Toxicology, Virginia Commonwealth University School of Medicine, Richmond, VA 23219, USA. ; National Institute on Drug Abuse, Intramural Research Program, National Institutes of Health, Baltimore, MD 21224, USA. Electronic address: sferre@intra.nida.nih.gov.
Y1 - 2014/04//
PY - 2014
DA - April 2014
SP - 211
EP - 217
VL - 18
IS - 4
KW - Index Medicus
KW - Humans
KW - Endophenotypes
KW - Personality
KW - Substance-Related Disorders -- psychology
KW - Substance-Related Disorders -- genetics
KW - Individuality
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-11-17
N1 - Date created - 2014-04-01
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.tics.2014.01.010
ER -
TY - JOUR
T1 - A systematic review comparing cisplatin and carboplatin plus paclitaxel-based chemotherapy for recurrent or metastatic cervical cancer.
AN - 1521913393; 24486604
AB - The prognosis of advanced/recurrent cervical cancer patients is generally poor with 1-year survival ranging between 15 and 20%. Cisplatin (CDDP) based treatments are considered the most effective regimens; unfortunately toxicity is an issue in a population in which the treatment remains palliative in the finality. Carboplatin (CBDCA), with its more favorable non toxicity profile and the convenience of outpatient administration, may be a suitable alternative to CDDP in combination regimens.
We performed a systematic review of the literature comparing CDDP and CBDCA based chemotherapy for advanced cervical cancer (recurrent, persistent or metastatic disease). Only studies that met the following criteria were considered for the present review: 1) patients treated with CDDP/paclitaxel or CBDCA/paclitaxel combinations as first line chemotherapy for metastatic disease; 2) one or more of the following data available: overall response rate (RR), progression free survival (PFS) or time to progression (TTP), overall survival (OS); 3) single-arm retrospective or prospective study; and 4) at least 20 patients enrolled. 17 eligible studies comprehensive of 1181 patients were included in the final analysis. The objective RR was 48.5% for CBDCA and 49.3% for CDDP-based chemotherapy. Median PFS for CDDP and CBDCA-based treatments was 6.9months and 5months respectively (p=0.03); the corresponding figures for median OS were 12.87 and 10months respectively (p=0.17).
Our study indicates that CBDCA may represent an attractive and valid alternative to the more toxic and equally effective CDDP in the treatment of advanced or recurrent cervical cancer.
Copyright © 2014 Elsevier Inc. All rights reserved.
JF - Gynecologic oncology
AU - Lorusso, Domenica
AU - Petrelli, Fausto
AU - Coinu, Andrea
AU - Raspagliesi, Francesco
AU - Barni, Sandro
AD - Gynecologic Oncology Unit, Fodazione IRCCS National Cancer Institute, Via Venezian 1, 20133 Milan, Italy. ; Medical Oncology Unit, Oncology Department, Azienda Ospedaliera Treviglio, Piazzale Ospedale 1, 24047 Treviglio, BG, Italy. Electronic address: faupe@libero.it. ; Medical Oncology Unit, Oncology Department, Azienda Ospedaliera Treviglio, Piazzale Ospedale 1, 24047 Treviglio, BG, Italy.
Y1 - 2014/04//
PY - 2014
DA - April 2014
SP - 117
EP - 123
VL - 133
IS - 1
KW - Carboplatin
KW - BG3F62OND5
KW - Paclitaxel
KW - P88XT4IS4D
KW - Cisplatin
KW - Q20Q21Q62J
KW - Index Medicus
KW - Chemotherapy
KW - Advanced cervical cancer
KW - Paclitaxel -- administration & dosage
KW - Disease-Free Survival
KW - Humans
KW - Treatment Outcome
KW - Carboplatin -- administration & dosage
KW - Female
KW - Cisplatin -- administration & dosage
KW - Uterine Cervical Neoplasms -- drug therapy
KW - Neoplasm Recurrence, Local -- drug therapy
KW - Neoplasm Metastasis -- drug therapy
KW - Carcinoma -- drug therapy
KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gynecologic+oncology&rft.atitle=A+systematic+review+comparing+cisplatin+and+carboplatin+plus+paclitaxel-based+chemotherapy+for+recurrent+or+metastatic+cervical+cancer.&rft.au=Lorusso%2C+Domenica%3BPetrelli%2C+Fausto%3BCoinu%2C+Andrea%3BRaspagliesi%2C+Francesco%3BBarni%2C+Sandro&rft.aulast=Lorusso&rft.aufirst=Domenica&rft.date=2014-04-01&rft.volume=133&rft.issue=1&rft.spage=117&rft.isbn=&rft.btitle=&rft.title=Gynecologic+oncology&rft.issn=1095-6859&rft_id=info:doi/10.1016%2Fj.ygyno.2014.01.042
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-05-13
N1 - Date created - 2014-03-31
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.ygyno.2014.01.042
ER -
TY - JOUR
T1 - New antituberculosis drugs, regimens, and adjunct therapies: needs, advances, and future prospects.
AN - 1521324288; 24670627
AB - About 1·3 million people died of tuberculosis in 2012, despite availability of effective drug treatment. Barriers to improvements in outcomes include long treatment duration (resulting in poor patient adherence and loss of patients to follow-up), complex regimens that involve expensive and toxic drugs, toxic effects when given with antiretroviral therapy, and multidrug resistance. After 50 years of no antituberculosis drug development, a promising pipeline is emerging through the repurposing of old drugs, re-engineering of existing antibacterial compounds, and discovery of new compounds. A range of novel antituberculosis drugs are in preclinical development, several phase 2 and 3 trials are underway, and use of adjunct therapies is being explored for drug-sensitive and drug-resistant tuberculosis. Historical advances include approval of two new drugs, delamanid and bedaquiline. Combinations of new and existing drugs are being assessed to shorten the duration of therapy and to treat multidrug-resistant tuberculosis. There has also been progress in development of new antituberculosis drugs that are active against dormant or persister populations of Mycobacterium tuberculosis. In this Review, we discuss recent advances in antituberculosis drug discovery and development, clinical trial designs, laboratory methods, and adjunct host-directed therapies, and we provide an update of phase 3 trials of various fluoroquinolones (RIFAQUIN, NIRT, OFLOTUB, and REMoxTB). We also emphasise the need to engage the community in design, implementation, and uptake of research, to increase international cooperation between drug developers and health-care providers adopting new regimens. Copyright © 2014 Elsevier Ltd. All rights reserved.
JF - The Lancet. Infectious diseases
AU - Zumla, Alimuddin I
AU - Gillespie, Stephen H
AU - Hoelscher, Michael
AU - Philips, Patrick P J
AU - Cole, Stewart T
AU - Abubakar, Ibrahim
AU - McHugh, Timothy D
AU - Schito, Marco
AU - Maeurer, Markus
AU - Nunn, Andrew J
AD - Centre for Clinical Microbiology, Division of Infection and Immunity, University College London, London, UK; University College London Hospitals NHS Foundation Trust, London, UK. Electronic address: a.zumla@ucl.ac.uk. ; School of Medicine, University of St Andrews, St Andrews, UK. ; Department for Infectious Diseases and Tropical Medicine, University of Munich, Munich, Germany; German Centre for Infection Research, Munich, Germany. ; Medical Research Council Clinical Trials Unit at University College London, London, UK. ; Global Health Institute, Ecole Polytechnique Fédérale de Lausanne, EPFLSV/GHI/UPCOL, Lausanne, Switzerland. ; Centre for Clinical Microbiology, Division of Infection and Immunity, University College London, London, UK. ; Henry M Jackson Foundation-Division of AIDS, TB Clinical Research Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA. ; Centre for Allogeneic Stem Cell Transplantation, Therapeutic Immunology Division, Department of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden.
Y1 - 2014/04//
PY - 2014
DA - April 2014
SP - 327
EP - 340
VL - 14
IS - 4
KW - Antitubercular Agents
KW - 0
KW - Biomarkers
KW - Index Medicus
KW - Drug Therapy, Combination
KW - Medication Adherence
KW - Immunotherapy
KW - Humans
KW - Research Design
KW - Drug Discovery
KW - Clinical Trials as Topic
KW - Antitubercular Agents -- adverse effects
KW - Tuberculosis, Pulmonary -- therapy
KW - Tuberculosis, Multidrug-Resistant -- drug therapy
KW - Antitubercular Agents -- therapeutic use
KW - Tuberculosis, Pulmonary -- drug therapy
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-06-09
N1 - Date created - 2014-03-27
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Comment In:
Lancet Infect Dis. 2014 Sep;14(9):795-6 [25164192]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/S1473-3099(13)70328-1
ER -
TY - JOUR
T1 - Adiabatic inversion pulses for myocardial T1 mapping
AN - 1520377711; 19634666
AB - Purpose To evaluate the error in T1 estimates using inversion-recovery-based T1 mapping due to imperfect inversion and to perform a systematic study of adiabatic inversion pulse designs in order to maximize inversion efficiency for values of transverse relaxation (T2) in the myocardium subject to a peak power constraint. Methods The inversion factor for hyperbolic secant and tangent/hyperbolic tangent adiabatic full passage waveforms was calculated using Bloch equations. A brute-force search was conducted for design parameters: pulse duration, frequency range, shape parameters, and peak amplitude. A design was selected that maximized the inversion factor over a specified range of amplitude and off-resonance and validated using phantom measurements. Empirical correction for imperfect inversion was performed. Results The tangent/hyperbolic tangent adiabatic pulse was found to outperform hyperbolic secant designs and achieve an inversion factor of 0.96 within plus or minus 150 Hz over 25% amplitude range with 14.7 mu T peak amplitude. T1 mapping errors of the selected design due to imperfect inversion was 4% and could be corrected to <1%. Conclusions Nonideal inversion leads to significant errors in inversion-recovery-based T1 mapping. The inversion efficiency of adiabatic pulses is sensitive to transverse relaxation. The tangent/hyperbolic tangent design achieved the best performance subject to the peak amplitude constraint. Magn Reson Med 71:1428-1434, 2014. copyright 2013 Wiley Periodicals, Inc.
JF - Magnetic Resonance in Medicine
AU - Kellman, Peter
AU - Herzka, Daniel A
AU - Hansen, Michael Schacht
AD - National Institutes of Health, Department of Health and Human Services, National Heart, Lung and Blood Institute, Bethesda, Maryland, USA.
Y1 - 2014/04//
PY - 2014
DA - Apr 2014
SP - 1428
EP - 1434
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 71
IS - 4
SN - 0740-3194, 0740-3194
KW - Biotechnology and Bioengineering Abstracts
KW - Mathematical models
KW - Inversion
KW - Adiabatic
KW - N.M.R.
KW - Mapping
KW - Myocardium
KW - W 30910:Imaging
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Magnetic+Resonance+in+Medicine&rft.atitle=Adiabatic+inversion+pulses+for+myocardial+T1+mapping&rft.au=Kellman%2C+Peter%3BHerzka%2C+Daniel+A%3BHansen%2C+Michael+Schacht&rft.aulast=Kellman&rft.aufirst=Peter&rft.date=2014-04-01&rft.volume=71&rft.issue=4&rft.spage=1428&rft.isbn=&rft.btitle=&rft.title=Magnetic+Resonance+in+Medicine&rft.issn=07403194&rft_id=info:doi/10.1002%2Fmrm.24793
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-01
N1 - Last updated - 2014-05-02
N1 - SubjectsTermNotLitGenreText - Mathematical models; Inversion; Adiabatic; N.M.R.; Mapping; Myocardium
DO - http://dx.doi.org/10.1002/mrm.24793
ER -
TY - JOUR
T1 - Prediction of cartilage compressive modulus using multiexponential analysis of T sub(2) relaxation data and support vector regression
AN - 1520377622; 19634775
AB - Evaluation of mechanical characteristics of cartilage by magnetic resonance imaging would provide a noninvasive measure of tissue quality both for tissue engineering and when monitoring clinical response to therapeutic interventions for cartilage degradation. We use results from multiexponential transverse relaxation analysis to predict equilibrium and dynamic stiffness of control and degraded bovine nasal cartilage, a biochemical model for articular cartilage. Sulfated glycosaminoglycan concentration/wet weight (ww) and equilibrium and dynamic stiffness decreased with degradation from 103.6 plus or minus 37.0 mu g/mg ww, 1.71 plus or minus 1.10 MPa and 15.3 plus or minus 6.7 MPa in controls to 8.25 plus or minus 2.4 mu g/mg ww, 0.015 plus or minus 0.006 MPa and 0.89 plus or minus 0.25MPa, respectively, in severely degraded explants. Magnetic resonance measurements were performed on cartilage explants at 4 degree C in a 9.4 T wide-bore NMR spectrometer using a Carr-Purcell-Meiboom-Gill sequence. Multiexponential T sub(2) analysis revealed four water compartments with T sub(2) values of approximately 0.14, 3, 40 and 150 ms, with corresponding weight fractions of approximately 3, 2, 4 and 91%. Correlations between weight fractions and stiffness based on conventional univariate and multiple linear regressions exhibited a maximum r super(2) of 0.65, while those based on support vector regression (SVR) had a maximum r super(2) value of 0.90. These results indicate that (i) compartment weight fractions derived from multiexponential analysis reflect cartilage stiffness and (ii) SVR-based multivariate regression exhibits greatly improved accuracy in predicting mechanical properties as compared with conventional regression. Published 2014. This article is a U.S. Government work and is in the public domain in the USA. We performed multiexponential transverse relaxation analysis on bovine nasal cartilage, and detected four water compartments with weight fractions of approximately 3, 2, 4 and 91%. Correlations between weight fractions and mechanical stiffness based on conventional univariate and multivariate linear regressions exhibited a maximum r super(2) = 0.65, while those based on support vector regression had a maximum r super(2) = 0.90. This indicates that support vector regression analysis using underlying tissue component fractions as input parameters may be useful for the noninvasive determination of cartilage mechanical quality.
JF - NMR in Biomedicine
AU - Irrechukwu, Onyi N
AU - Thaer, Sarah Von
AU - Frank, Eliot H
AU - Lin, Ping-Chang
AU - Reiter, David A
AU - Grodzinsky, Alan J
AU - Spencer, Richard G
AD - National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Y1 - 2014/04//
PY - 2014
DA - Apr 2014
SP - 468
EP - 477
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 27
IS - 4
SN - 0952-3480, 0952-3480
KW - Calcium & Calcified Tissue Abstracts; Biotechnology and Bioengineering Abstracts
KW - biomechanical stiffness
KW - multiexponential T sub(2) relaxation
KW - cartilage
KW - water compartments
KW - Data processing
KW - Cartilage
KW - Magnetic resonance imaging
KW - Therapeutic applications
KW - Tissue engineering
KW - Models
KW - Glycosaminoglycans
KW - Regression analysis
KW - N.M.R.
KW - Cartilage (articular)
KW - Explants
KW - Mechanical properties
KW - T 2030:Cartilage and Cartilage Diseases
KW - W 30920:Tissue Engineering
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NMR+in+Biomedicine&rft.atitle=Prediction+of+cartilage+compressive+modulus+using+multiexponential+analysis+of+T+sub%282%29+relaxation+data+and+support+vector+regression&rft.au=Irrechukwu%2C+Onyi+N%3BThaer%2C+Sarah+Von%3BFrank%2C+Eliot+H%3BLin%2C+Ping-Chang%3BReiter%2C+David+A%3BGrodzinsky%2C+Alan+J%3BSpencer%2C+Richard+G&rft.aulast=Irrechukwu&rft.aufirst=Onyi&rft.date=2014-04-01&rft.volume=27&rft.issue=4&rft.spage=468&rft.isbn=&rft.btitle=&rft.title=NMR+in+Biomedicine&rft.issn=09523480&rft_id=info:doi/10.1002%2Fnbm.3083
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-01
N1 - Last updated - 2014-10-30
N1 - SubjectsTermNotLitGenreText - Glycosaminoglycans; Data processing; Cartilage; Magnetic resonance imaging; Regression analysis; Therapeutic applications; N.M.R.; Tissue engineering; Cartilage (articular); Explants; Models; Mechanical properties
DO - http://dx.doi.org/10.1002/nbm.3083
ER -
TY - JOUR
T1 - Subsite Awareness in Neuropathology Evaluation of National Toxicology Program (NTP) Studies: A Review of Select Neuroanatomical Structures with Their Functional Significance in Rodents
AN - 1520377510; 19503700
AB - This review article is designed to serve as an introductory guide in neuroanatomy for toxicologic pathologists evaluating general toxicity studies. The article provides an overview of approximately 50 neuroanatomical subsites and their functional significance across 7 transverse sections of the brain. Also reviewed are 3 sections of the spinal cord, cranial and peripheral nerves (trigeminal and sciatic, respectively), and intestinal autonomic ganglia. The review is limited to the evaluation of hematoxylin and eosin-stained tissue sections, as light microscopic evaluation of these sections is an integral part of the first-tier toxicity screening of environmental chemicals, drugs, and other agents. Prominent neuroanatomical sites associated with major neurological disorders are noted. This guide, when used in conjunction with detailed neuroanatomic atlases, may aid in an understanding of the significance of functional neuroanatomy, thereby improving the characterization of neurotoxicity in general toxicity and safety evaluation studies.
JF - Toxicologic Pathology
AU - Rao, Deepa B
AU - Little, Peter B
AU - Sills, Robert C
AD - Integrated Laboratory Systems, Inc., Research Triangle Park, North Carolina, USA, sills@niehs.nih.gov
PY - 2014
SP - 487
EP - 509
PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom
VL - 42
IS - 3
SN - 0192-6233, 0192-6233
KW - CSA Neurosciences Abstracts; Toxicology Abstracts
KW - neuropathology
KW - neuroanatomy
KW - NTP
KW - brain
KW - spinal cord
KW - nerve
KW - functional neuroanatomy.
KW - Neurological diseases
KW - Spinal cord
KW - Brain
KW - Functional anatomy
KW - Anatomy
KW - Skull
KW - Atlases
KW - Reviews
KW - Neurotoxicity
KW - Intestine
KW - Autonomic ganglia
KW - Drugs
KW - Peripheral nerves
KW - Neuropathology
KW - Brain architecture
KW - N3 11027:Neurology & neuropathology
KW - X 24300:Methods
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-01
N1 - Number of references - 144
N1 - Last updated - 2016-01-21
N1 - SubjectsTermNotLitGenreText - Neurological diseases; Spinal cord; Brain; Functional anatomy; Anatomy; Atlases; Skull; Reviews; Neurotoxicity; Intestine; Drugs; Autonomic ganglia; Neuropathology; Peripheral nerves; Brain architecture
DO - http://dx.doi.org/10.1177/0192623313501893
ER -
TY - JOUR
T1 - N,N-Dimethyl-p-toluidine, a Component in Dental Materials, Causes Hematologic Toxic and Carcinogenic Responses in Rodent Model Systems
AN - 1520375681; 19503691
AB - Because of the potential for exposure to N,N-dimethyl-p-toluidine (DMPT) in medical devices and the lack of toxicity and carcinogenicity information available in the literature, the National Toxicology Program conducted toxicity and carcinogenicity studies of DMPT in male and female F344/N rats and B6C3F1/N mice. In these studies, a treatment-related macrocytic regenerative anemia characterized by increased levels of methemoglobin and Heinz body formation developed within a few weeks of DMPT exposure in rats and mice. DMPT induced nasal cavity, splenic, and liver toxicity in rats and mice at 3 months and 2 years. DMPT carcinogenic effects were seen in the liver of male and female rats and mice, the nasal cavity of male and female rats, and the lung and forestomach of female mice. In rodents, DMPT is distributed to many of the sites where toxic and carcinogenic effects occurred. DMPT-induced oxidative damage at these target sites may be one mechanism for the treatment-related lesions. Methemoglobinemia, as seen in these DMPT studies, is caused by oxidation of the heme moiety, and this end point served as an early alert for other target organ toxicities and carcinogenic responses that followed with longer term exposure.
JF - Toxicologic Pathology
AU - Dunnick, June K
AU - Brix, A
AU - Sanders, J M
AU - Travlos, G S
AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA, dunnickj@niehs.nih.gov
Y1 - 2014/04//
PY - 2014
DA - Apr 2014
SP - 603
EP - 615
PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom
VL - 42
IS - 3
SN - 0192-6233, 0192-6233
KW - Toxicology Abstracts
KW - N,N-dimethyl-p-toluidine
KW - carcinogenic effects
KW - hematologic toxicity.
KW - Methemoglobinemia
KW - Heme
KW - Carcinogenicity
KW - Lung
KW - Oxidation
KW - Liver
KW - Anemia
KW - Spleen
KW - Nose
KW - Toxicity
KW - Methemoglobin
KW - X 24300:Methods
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+Pathology&rft.atitle=N%2CN-Dimethyl-p-toluidine%2C+a+Component+in+Dental+Materials%2C+Causes+Hematologic+Toxic+and+Carcinogenic+Responses+in+Rodent+Model+Systems&rft.au=Dunnick%2C+June+K%3BBrix%2C+A%3BSanders%2C+J+M%3BTravlos%2C+G+S&rft.aulast=Dunnick&rft.aufirst=June&rft.date=2014-04-01&rft.volume=42&rft.issue=3&rft.spage=603&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F0192623313489604
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-01
N1 - Number of references - 52
N1 - Last updated - 2014-10-15
N1 - SubjectsTermNotLitGenreText - Methemoglobinemia; Heme; Lung; Carcinogenicity; Oxidation; Anemia; Liver; Spleen; Nose; Toxicity; Methemoglobin
DO - http://dx.doi.org/10.1177/0192623313489604
ER -
TY - JOUR
T1 - Mutation Spectra of Kras and Tp53 in Urethral and Lung Neoplasms in B6C3F1 Mice Treated with 3,3',4,4'-Tetrachloroazobenzene
AN - 1520375580; 19503692
AB - 3,3',4,4'-tetrachloroazobenzene (TCAB) is a contaminant formed during manufacture of various herbicide compounds. A recent National Toxicology Program study showed B6C3F1 mice exposed to TCAB developed a treatment-related increase in lung carcinomas in the high-dose group, and urethral carcinomas, an extremely rare lesion in rodents, in all dose groups. As the potential for environmental exposure to TCAB is widespread, and the mechanisms of urethral carcinogenesis are unknown, TCAB-induced urethral and pulmonary tumors were evaluated for alterations in critical human cancer genes, Kras and Tp53. Uroplakin III, CK20, and CK7 immunohistochemistry was performed to confirm the urothelial origin of urethral tumors. TCAB-induced urethral carcinomas harbored transforming point mutations in K-ras (38%) and Tp53 (63%), and 71% displayed nuclear TP53 expression, consistent with formation of mutant protein. Transition mutations accounted for 88% of Tp53 mutations in urethral carcinomas, suggesting that TCAB or its metabolites target guanine or cytosine bases and that these mutations are involved in urethral carcinogenesis. Pulmonary carcinomas in TCAB-exposed animals harbored similar rates of Tp53 (55%) and Kras (36%) mutations as urethral carcinomas, suggesting that TCAB may induce mutations at multiple sites by a common mechanism. In conclusion, TCAB is carcinogenic at multiple sites in male and female B6C3F1 mice through mechanisms involving Tp53 and Kras mutation.
JF - Toxicologic Pathology
AU - Bhusari, Sachin
AU - Malarkey, David E
AU - Hong, Hue-Hua
AU - Wang, Yu
AU - Masinde, Tiwanda
AU - Nolan, Michael
AU - Hooth, Michelle J
AU - Lea, Isabel A
AU - Vasconcelos, Daphne
AU - Sills, Robert C
AU - Hoenerhoff, Mark J
AD - Cellular and Molecular Pathology Branch, National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA, hoenerhm@niehs.nih.gov
Y1 - 2014/04//
PY - 2014
DA - Apr 2014
SP - 555
EP - 564
PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom
VL - 42
IS - 3
SN - 0192-6233, 0192-6233
KW - Genetics Abstracts; Toxicology Abstracts
KW - environmental toxicology
KW - agricultural products
KW - animal models
KW - carcinogenesis
KW - genotoxins/nongenotoxins
KW - mechanisms of toxicity
KW - molecular pathology.
KW - Lung carcinoma
KW - Point mutation
KW - Herbicides
KW - Metabolites
KW - Tumors
KW - Cancer
KW - Carcinoma
KW - p53 protein
KW - Cytosine
KW - K-Ras protein
KW - Guanine
KW - Carcinogenesis
KW - Contaminants
KW - Immunohistochemistry
KW - G 07720:Immunogenetics
KW - X 24330:Agrochemicals
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-01
N1 - Number of references - 43
N1 - Last updated - 2015-04-02
N1 - SubjectsTermNotLitGenreText - Lung carcinoma; Point mutation; Metabolites; Herbicides; Tumors; Cancer; p53 protein; Carcinoma; K-Ras protein; Cytosine; Guanine; Carcinogenesis; Contaminants; Immunohistochemistry
DO - http://dx.doi.org/10.1177/0192623313491169
ER -
TY - JOUR
T1 - The Problem of Helicobacter pylori Resistance to Antibiotics: A Systematic Review in Latin America
AN - 1520363818; 19633621
AB - OBJECTIVES: Latin America has a high prevalence of Helicobacter pylori infection and associated diseases, including gastric cancer. Antibiotic therapy can eradicate the bacterial infection and decrease associated morbidity and mortality. To tailor recommendations for optimal treatments, we summarized published literature and calculated region- and country-specific prevalences of antibiotic resistance. METHODS: Searches of PubMed and regional databases for observational studies evaluating H. pylori antibiotic resistance yielded a total of 59 independent studies (56 in adults, 2 in children, and 1 in both groups) published up to October 2013 regarding H. pylori isolates collected between 1988 and 2011. Study-specific prevalences of primary resistance to commonly prescribed antibiotics were summarized using random-effects models. Between-study heterogeneity was assessed by meta-regression. As a sensitivity analysis, we extended our research to studies of patients with prior H. pylori-eradication therapy. RESULTS: Summary prevalences of antimicrobial primary resistance among adults varied by antibiotic, including 12% for clarithromycin (n=35 studies), 53% for metronidazole (n=34), 4% for amoxicillin (n=28), 6% for tetracycline (n=20), 3% for furazolidone (n=6), 15% for fluoroquinolones (n=5), and 8% for dual clarithromycin and metronidazole (n=10). Resistance prevalence varied significantly by country, but not by year of sample collection. Analyses including studies of patients with prior therapy yielded similar estimates. Pediatric reports were too few to be summarized by meta-analysis. CONCLUSIONS: Resistance to first-line anti-H. pylori antibiotics is high in Latin American populations. In some countries, the empirical use of clarithromycin without susceptibility testing may not be appropriate. These findings stress the need for appropriate surveillance programs, improved antimicrobial regulations, and increased public awareness.
JF - American Journal of Gastroenterology
AU - Camargo, M Constanza
AU - Garcia, Apolinaria
AU - Riquelme, Arnoldo
AU - Otero, William
AU - Camargo, Claudia A
AU - Hernandez-Garcia, Tomas
AU - Candia, Roberto
AU - Bruce, Michael G
AU - Rabkin, Charles S
AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland, USA
Y1 - 2014/04//
PY - 2014
DA - Apr 2014
SP - 485
EP - 495
PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL - 109
IS - 4
SN - 0002-9270, 0002-9270
KW - Microbiology Abstracts B: Bacteriology
KW - Helicobacter pylori
KW - Mortality
KW - Metronidazole
KW - Amoxicillin
KW - Fluoroquinolones
KW - Pediatrics
KW - Antibiotics
KW - Children
KW - Tetracyclines
KW - Infection
KW - Morbidity
KW - Antimicrobial agents
KW - Models
KW - Clarithromycin
KW - Databases
KW - Furazolidone
KW - Reviews
KW - Gastric cancer
KW - Antibiotic resistance
KW - J 02310:Genetics & Taxonomy
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-01
N1 - Last updated - 2014-06-26
N1 - SubjectsTermNotLitGenreText - Metronidazole; Mortality; Amoxicillin; Fluoroquinolones; Pediatrics; Antibiotics; Infection; Tetracyclines; Children; Morbidity; Models; Antimicrobial agents; Databases; Clarithromycin; Furazolidone; Reviews; Gastric cancer; Antibiotic resistance; Helicobacter pylori
DO - http://dx.doi.org/10.1038/ajg.2014.24
ER -
TY - JOUR
T1 - Targeting the mTOR pathway in hepatocellular carcinoma: current state and future trends.
AN - 1519836056; 24308993
AB - Mechanistic target of rapamycin (mTOR) regulates cell growth, metabolism and aging in response to nutrients, cellular energy stage and growth factors. mTOR is frequently up-regulated in cancer including hepatocellular carcinoma (HCC) and is associated with bad prognosis, poorly differentiated tumors, and earlier recurrence. Blocking mTOR with rapamycin and first generation mTOR inhibitors, called rapalogs, has shown promising reduction of HCC tumor growth in preclinical models. Currently, rapamycin/rapalogs are used in several clinical trials for the treatment of advanced HCC, and as adjuvant therapy in HCC patients after liver transplantation and TACE. A second generation of mTOR pathway inhibitors has been developed recently and is being tested in various clinical trials of solid cancers, and has been used in preclinical HCC models. The results of series of clinical trials using mTOR inhibitors in HCC treatment will emerge in the near future.
Published by Elsevier B.V.
JF - Journal of hepatology
AU - Matter, Matthias S
AU - Decaens, Thomas
AU - Andersen, Jesper B
AU - Thorgeirsson, Snorri S
AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, MD, USA. ; Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, MD, USA. Electronic address: snorri_thorgeirsson@nih.gov.
Y1 - 2014/04//
PY - 2014
DA - April 2014
SP - 855
EP - 865
VL - 60
IS - 4
KW - TOR Serine-Threonine Kinases
KW - EC 2.7.1.1
KW - Sirolimus
KW - W36ZG6FT64
KW - Index Medicus
KW - Rapalogs
KW - mTOR
KW - Second generation mTOR inhibitors
KW - Rapamycin
KW - HCC
KW - Animals
KW - Liver Neoplasms, Experimental -- metabolism
KW - Humans
KW - Sirolimus -- pharmacology
KW - Signal Transduction -- drug effects
KW - Liver Neoplasms, Experimental -- therapy
KW - Clinical Trials as Topic
KW - Chemoembolization, Therapeutic
KW - Liver Neoplasms, Experimental -- prevention & control
KW - Models, Biological
KW - Liver Transplantation
KW - Liver Neoplasms -- metabolism
KW - Carcinoma, Hepatocellular -- metabolism
KW - TOR Serine-Threonine Kinases -- antagonists & inhibitors
KW - Liver Neoplasms -- therapy
KW - Carcinoma, Hepatocellular -- drug therapy
KW - Liver Neoplasms -- drug therapy
KW - Carcinoma, Hepatocellular -- therapy
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-05-11
N1 - Date created - 2014-03-18
N1 - Date revised - 2017-01-14
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.jhep.2013.11.031
ER -
TY - JOUR
T1 - Expression and Targeting of Secreted Proteins from Chlamydia trachomatis
AN - 1516760278; 19446493
AB - Chlamydia trachomatis is an obligate intracellular pathogen that replicates in a vacuole termed the inclusion. Many of the interactions of chlamydiae with the host cell are dependent upon bacterial protein synthesis and presumably exposure of these proteins to the cytosol. Because of the dearth of genetic tools for chlamydiae, previous studies examining secreted proteins required the use of heterologous bacterial systems. Recent advances in genetic manipulation of chlamydia now allow for transformation of the bacteria with plasmids. We describe here a shuttle vector system, pBOMB4, that permits expression of recombinant proteins under constitutive or conditional promoter control. We show that the inclusion membrane protein IncD is secreted in a type III-dependent manner from Yersinia pseudotuberculosis and also secreted from C. trachomatis in infected cells where it localizes appropriately to the inclusion membrane. IncD truncated of the first 30 amino acids containing the secretion signal is no longer secreted and is retained by the bacteria. Cytosolic exposure of secreted proteins can be confirmed by using CyaA, GSK, or microinjection assays. A protein predicted to be retained within the bacteria, NrdB is indeed localized to the chlamydia. In addition, we have shown that the chlamydial effector protein, CPAF, which is secreted into the host cell cytosol by a Sec-dependent pathway, also accesses the cytosol when expressed from this system. These assays should prove useful to assess the secretion of other chlamydial proteins that are potentially exposed to the cytosol of the host cell.
JF - Journal of Bacteriology
AU - Bauler, Laura D
AU - Hackstadt, Ted
Y1 - 2014/04//
PY - 2014
DA - April 2014
SP - 1325
EP - 1334
PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL - 196
IS - 7
SN - 0021-9193, 0021-9193
KW - Microbiology Abstracts B: Bacteriology
KW - Transformation
KW - Protein biosynthesis
KW - Amino acids
KW - Secretion
KW - Chlamydia trachomatis
KW - Yersinia pseudotuberculosis
KW - Membrane proteins
KW - shuttle vectors
KW - Pathogens
KW - Plasmids
KW - Microinjection
KW - Promoters
KW - secretion signals
KW - Vacuoles
KW - Cytosol
KW - Pseudotuberculosis
KW - J 02310:Genetics & Taxonomy
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1516760278?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Bacteriology&rft.atitle=Expression+and+Targeting+of+Secreted+Proteins+from+Chlamydia+trachomatis&rft.au=Bauler%2C+Laura+D%3BHackstadt%2C+Ted&rft.aulast=Bauler&rft.aufirst=Laura&rft.date=2014-04-01&rft.volume=196&rft.issue=7&rft.spage=1325&rft.isbn=&rft.btitle=&rft.title=Journal+of+Bacteriology&rft.issn=00219193&rft_id=info:doi/10.1128%2FJB.01290-13
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-01
N1 - Number of references - 78
N1 - Last updated - 2016-08-03
N1 - SubjectsTermNotLitGenreText - Transformation; Amino acids; Protein biosynthesis; Secretion; Pathogens; shuttle vectors; Membrane proteins; Microinjection; Plasmids; Promoters; secretion signals; Vacuoles; Cytosol; Pseudotuberculosis; Yersinia pseudotuberculosis; Chlamydia trachomatis
DO - http://dx.doi.org/10.1128/JB.01290-13
ER -
TY - JOUR
T1 - Perfluoroalkyl Substances During Pregnancy and Validated Preeclampsia Among Nulliparous Women in the Norwegian Mother and Child Cohort Study
AN - 1516754492; 19531753
AB - Perfluoroalkyl substances (PFAS) are persistent and ubiquitous environmental contaminants, and human exposure to these substances may be related to preeclampsia, a common pregnancy complication. Previous studies have found serum concentrations of PFAS to be positively associated with pregnancy-induced hypertension and preeclampsia in a population with high levels of exposure to perfluorooctanoate. Whether this association exists among pregnant women with background levels of PFAS exposure is unknown. Using data from the Norwegian Mother and Child Cohort Study conducted by the Norwegian Institute of Public Health, we carried out a study of nulliparous pregnant women enrolled in 2003-2007 (466 cases, 510 noncases) to estimate associations between PFAS concentrations and an independently validated diagnosis of preeclampsia. We measured levels of 9 PFAS in maternal plasma extracted midpregnancy; statistical analyses were restricted to 7 PFAS that were quantifiable in more than 50% of samples. In proportional hazards models adjusted for maternal age, prepregnancy body mass index (weight (kg)/height (m) super(2)), educational level, and smoking status, we observed no strongly positive associations between PFAS levels and preeclampsia. We found an inverse association between preeclampsia and the highest quartile of perfluoroundecanoic acid concentration relative to the lowest quartile (hazard ratio = 0.55, 95% confidence interval: 0.38, 0.81). Overall, our findings do not support an increased risk of preeclampsia among nulliparous Norwegian women with background levels of PFAS exposure.
JF - American Journal of Epidemiology
AU - Starling, Anne P
AU - Engel, Stephanie M
AU - Richardson, David B
AU - Baird, Donna D
AU - Haug, Line S
AU - Stuebe, Alison M
AU - Klungsoeyr, Kari
AU - Harmon, Quaker
AU - Becher, Georg
AU - Thomsen, Cathrine
AU - Sabaredzovic, Azemira
AU - Eggesboe, Merete
AU - Hoppin, Jane A
AU - Travlos, Gregory S
AU - Wilson, Ralph E
AU - Trogstad, Lill I
AU - Magnus, Per
AU - Longnecker, Matthew P
AD - Correspondence to Dr. Matthew P. Longnecker, NIEHS, Epidemiology Branch, Mail Drop A3-05, P.O. Box 12233, Research Triangle Park, NC 27709-2233., longnec1@niehs.nih.gov
Y1 - 2014/04/01/
PY - 2014
DA - 2014 Apr 01
SP - 824
EP - 833
PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL - 179
IS - 7
SN - 0002-9262, 0002-9262
KW - Risk Abstracts
KW - Smoking
KW - Age
KW - Complications
KW - Body mass
KW - Females
KW - Norway
KW - Pregnancy
KW - Hypertension
KW - Public health
KW - R2 23060:Medical and environmental health
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1516754492?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Epidemiology&rft.atitle=Perfluoroalkyl+Substances+During+Pregnancy+and+Validated+Preeclampsia+Among+Nulliparous+Women+in+the+Norwegian+Mother+and+Child+Cohort+Study&rft.au=Starling%2C+Anne+P%3BEngel%2C+Stephanie+M%3BRichardson%2C+David+B%3BBaird%2C+Donna+D%3BHaug%2C+Line+S%3BStuebe%2C+Alison+M%3BKlungsoeyr%2C+Kari%3BHarmon%2C+Quaker%3BBecher%2C+Georg%3BThomsen%2C+Cathrine%3BSabaredzovic%2C+Azemira%3BEggesboe%2C+Merete%3BHoppin%2C+Jane+A%3BTravlos%2C+Gregory+S%3BWilson%2C+Ralph+E%3BTrogstad%2C+Lill+I%3BMagnus%2C+Per%3BLongnecker%2C+Matthew+P&rft.aulast=Starling&rft.aufirst=Anne&rft.date=2014-04-01&rft.volume=179&rft.issue=7&rft.spage=824&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Epidemiology&rft.issn=00029262&rft_id=info:doi/10.1093%2Faje%2Fkwt432
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-01
N1 - Last updated - 2014-05-15
N1 - SubjectsTermNotLitGenreText - Smoking; Age; Complications; Body mass; Females; Public health; Hypertension; Pregnancy; Norway
DO - http://dx.doi.org/10.1093/aje/kwt432
ER -
TY - JOUR
T1 - Genetic assessment of environmental features that influence deer dispersal: implications for prion-infected populations
AN - 1516749053; 19508046
AB - The landscape can influence host dispersal and density, which in turn, affect infectious disease transmission, spread, and persistence. Understanding how the landscape influences wildlife dispersal and pathogen epidemiology can enhance the efficacy of disease management in natural populations. We applied landscape genetics to examine relationships among landscape variables, dispersal of white-tailed deer hosts and transmission/spread of chronic wasting disease (CWD), a fatal prion encephalopathy. Our focus was on quantifying movements and population structure of host deer in infected areas as a means of predicting the spread of this pathology and promoting its adaptive management. We analyzed microsatellite genotypes of CWD-infected and uninfected deer from two disease foci (Southern Wisconsin, Northern Illinois). We quantified gene flow and population structure using F sub(ST), assignment tests, and spatial autocorrelation analyses. Gene flow estimates were then contrasted against a suite of landscape variables that potentially mediate deer dispersal. Forest fragmentation and grassland connectivity promoted deer movements while rivers, agricultural fields and large urbanized areas impeded movement. Landscape variables, deer dispersal, and disease transmission covaried significantly and positively in our analyses. Habitats with elevated host gene flow supported the concept of dispersal-mediated CWD transmission by reflecting a concomitant, rapid CWD expansion. Large, interrelated social groups isolated by movement barriers overlapped disease foci, suggesting that philopatry exacerbated CWD transmission. Our results promote adaptive management of CWD by predicting patterns of its spread and identifying habitats at risk for invasion. Further, our landscape genetics approach underscores the significance of topography and host behavior in wildlife disease transmission.
JF - Population Ecology
AU - Kelly, Amy C
AU - Mateus-Pinilla, Nohra E
AU - Brown, William
AU - Ruiz, Marilyn O
AU - Douglas, Marlis R
AU - Douglas, Michael E
AU - Shelton, Paul
AU - Beissel, Tom
AU - Novakofski, Jan
AD - Department of Animal Sciences, University of Illinois, 1503 S. Maryland Dr., Urbana, IL, 61801, USA, kellyac@mail.nih.gov
Y1 - 2014/04//
PY - 2014
DA - Apr 2014
SP - 327
EP - 340
PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL - 56
IS - 2
SN - 1438-3896, 1438-3896
KW - Genetics Abstracts; Virology & AIDS Abstracts; Ecology Abstracts
KW - Forests
KW - Genotypes
KW - Habitat fragmentation
KW - Population ecology
KW - Disease transmission
KW - Transmissible spongiform encephalopathy
KW - Infectious diseases
KW - Gene flow
KW - Prion protein
KW - Encephalopathy
KW - Topography
KW - Rivers
KW - Data processing
KW - Wildlife
KW - Landscape
KW - Microsatellites
KW - Pathogens
KW - Habitat
KW - Chronic wasting disease
KW - Philopatry
KW - Grasslands
KW - Epidemiology
KW - Population structure
KW - Dispersal
KW - D 04040:Ecosystem and Ecology Studies
KW - G 07750:Ecological & Population Genetics
KW - V 22380:Prions
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1516749053?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aecology&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Population+Ecology&rft.atitle=Genetic+assessment+of+environmental+features+that+influence+deer+dispersal%3A+implications+for+prion-infected+populations&rft.au=Kelly%2C+Amy+C%3BMateus-Pinilla%2C+Nohra+E%3BBrown%2C+William%3BRuiz%2C+Marilyn+O%3BDouglas%2C+Marlis+R%3BDouglas%2C+Michael+E%3BShelton%2C+Paul%3BBeissel%2C+Tom%3BNovakofski%2C+Jan&rft.aulast=Kelly&rft.aufirst=Amy&rft.date=2014-04-01&rft.volume=56&rft.issue=2&rft.spage=327&rft.isbn=&rft.btitle=&rft.title=Population+Ecology&rft.issn=14383896&rft_id=info:doi/10.1007%2Fs10144-013-0427-9
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-01
N1 - Number of references - 83
N1 - Last updated - 2015-08-05
N1 - SubjectsTermNotLitGenreText - Rivers; Data processing; Landscape; Wildlife; Microsatellites; Forests; Pathogens; Genotypes; Habitat; Philopatry; Chronic wasting disease; Habitat fragmentation; Disease transmission; Population ecology; Transmissible spongiform encephalopathy; Grasslands; Infectious diseases; Epidemiology; Gene flow; Prion protein; Population structure; Dispersal; Encephalopathy; Topography
DO - http://dx.doi.org/10.1007/s10144-013-0427-9
ER -
TY - JOUR
T1 - Immune-related conditions and subsequent risk of brain cancer in a cohort of 4.5 million male US veterans
AN - 1516746449; 19543137
AB - Background: Case-control studies have reported an inverse association between self-reported history of allergy and risk of glioma, but cohort data are limited. Our objectives were to evaluate the associations of major groups of medically diagnosed immune-related conditions (allergy/atopy, autoimmune disease, diabetes, infectious/inflammatory disease) and to explore associations with specific conditions in relation to subsequent diagnosis of brain cancer in a large cohort study. Methods: We used hospital discharge records for a cohort of 4.5 million male US veterans, of whom 4383 developed primary brain cancer. Rate ratios (RRs) and 95% confidence intervals (CIs) were calculated using time-dependent Poisson regression. Results: We found a significant trend of decreasing RRs for brain cancer with longer duration of allergy/atopy (P=0.02), but not for other conditions studied. Rate ratios of brain cancer for allergy/atopy and diabetes with duration of 10 or more years were 0.60 (95% CI: 0.43, 0.83) and 0.75 (95% CI: 0.62, 0.93), respectively. Several associations with specific conditions were found, but these did not withstand correction for multiple comparisons. Conclusions: This study lends some support to an inverse association between allergy/atopy and diabetes of long duration and brain cancer risk, but prospective studies with biological samples are needed to uncover the underlying biological mechanisms.
JF - British Journal of Cancer
AU - Cahoon, E K
AU - Inskip, P D
AU - Gridley, G
AU - Brenner, A V
AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD 20850, USA
Y1 - 2014/04/01/
PY - 2014
DA - 2014 Apr 01
SP - 1825
EP - 1833
PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL - 110
IS - 7
SN - 0007-0920, 0007-0920
KW - Immunology Abstracts; Risk Abstracts
KW - Historical account
KW - Data processing
KW - Males
KW - Autoimmune diseases
KW - Brain
KW - Allergies
KW - Cancer
KW - Diabetes mellitus
KW - Brain tumors
KW - Health risks
KW - USA
KW - Hypersensitivity
KW - Atopy
KW - Inflammatory diseases
KW - Glioma
KW - Hospitals
KW - F 06915:Cancer Immunology
KW - R2 23060:Medical and environmental health
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1516746449?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+Journal+of+Cancer&rft.atitle=Immune-related+conditions+and+subsequent+risk+of+brain+cancer+in+a+cohort+of+4.5+million+male+US+veterans&rft.au=Cahoon%2C+E+K%3BInskip%2C+P+D%3BGridley%2C+G%3BBrenner%2C+A+V&rft.aulast=Cahoon&rft.aufirst=E&rft.date=2014-04-01&rft.volume=110&rft.issue=7&rft.spage=1825&rft.isbn=&rft.btitle=&rft.title=British+Journal+of+Cancer&rft.issn=00070920&rft_id=info:doi/10.1038%2Fbjc.2014.97
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-01
N1 - Last updated - 2014-07-24
N1 - SubjectsTermNotLitGenreText - Brain tumors; Diabetes mellitus; Hypersensitivity; Data processing; Inflammatory diseases; Atopy; Autoimmune diseases; Brain; Glioma; Hospitals; Historical account; Health risks; Males; Allergies; Cancer; USA
DO - http://dx.doi.org/10.1038/bjc.2014.97
ER -
TY - JOUR
T1 - Population-based absolute risk estimation with survey data
AN - 1516740133; 19506182
AB - Absolute risk is the probability that a cause-specific event occurs in a given time interval in the presence of competing events. We present methods to estimate population-based absolute risk from a complex survey cohort that can accommodate multiple exposure-specific competing risks. The hazard function for each event type consists of an individualized relative risk multiplied by a baseline hazard function, which is modeled nonparametrically or parametrically with a piecewise exponential model. An influence method is used to derive a Taylor-linearized variance estimate for the absolute risk estimates. We introduce novel measures of the cause-specific influences that can guide modeling choices for the competing event components of the model. To illustrate our methodology, we build and validate cause-specific absolute risk models for cardiovascular and cancer deaths using data from the National Health and Nutrition Examination Survey. Our applications demonstrate the usefulness of survey-based risk prediction models for predicting health outcomes and quantifying the potential impact of disease prevention programs at the population level.
JF - Lifetime Data Analysis
AU - Kovalchik, Stephanie A
AU - Pfeiffer, Ruth M
AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, 9609 Medical Center Drive, Bethesda, MD, 20892-9702, USA, pfeiffer@mail.nih.gov
Y1 - 2014/04//
PY - 2014
DA - Apr 2014
SP - 252
EP - 275
PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL - 20
IS - 2
SN - 1380-7870, 1380-7870
KW - Health & Safety Science Abstracts; Risk Abstracts
KW - Health risks
KW - Mortality
KW - Prevention
KW - Prediction models
KW - Population levels
KW - Nutrition
KW - Cancer
KW - H 11000:Diseases/Injuries/Trauma
KW - R2 23060:Medical and environmental health
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1516740133?accountid=14244
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-01
N1 - Number of references - 36
N1 - Last updated - 2014-06-26
N1 - SubjectsTermNotLitGenreText - Mortality; Health risks; Prevention; Prediction models; Population levels; Nutrition; Cancer
DO - http://dx.doi.org/10.1007/s10985-013-9258-4
ER -
TY - JOUR
T1 - PARP1-TDP1 coupling for the repair of topoisomerase I-induced DNA damage.
AN - 1516722995; 24493735
AB - Poly(ADP-ribose) polymerases (PARP) attach poly(ADP-ribose) (PAR) chains to various proteins including themselves and chromatin. Topoisomerase I (Top1) regulates DNA supercoiling and is the target of camptothecin and indenoisoquinoline anticancer drugs, as it forms Top1 cleavage complexes (Top1cc) that are trapped by the drugs. Endogenous and carcinogenic DNA lesions can also trap Top1cc. Tyrosyl-DNA phosphodiesterase 1 (TDP1), a key repair enzyme for trapped Top1cc, hydrolyzes the phosphodiester bond between the DNA 3'-end and the Top1 tyrosyl moiety. Alternative repair pathways for Top1cc involve endonuclease cleavage. However, it is unknown what determines the choice between TDP1 and the endonuclease repair pathways. Here we show that PARP1 plays a critical role in this process. By generating TDP1 and PARP1 double-knockout lymphoma chicken DT40 cells, we demonstrate that TDP1 and PARP1 are epistatic for the repair of Top1cc. The N-terminal domain of TDP1 directly binds the C-terminal domain of PARP1, and TDP1 is PARylated by PARP1. PARylation stabilizes TDP1 together with SUMOylation of TDP1. TDP1 PARylation enhances its recruitment to DNA damage sites without interfering with TDP1 catalytic activity. TDP1-PARP1 complexes, in turn recruit X-ray repair cross-complementing protein 1 (XRCC1). This work identifies PARP1 as a key component driving the repair of trapped Top1cc by TDP1.
JF - Nucleic acids research
AU - Das, Benu Brata
AU - Huang, Shar-yin N
AU - Murai, Junko
AU - Rehman, Ishita
AU - Amé, Jean-Christophe
AU - Sengupta, Souvik
AU - Das, Subhendu K
AU - Majumdar, Papiya
AU - Zhang, Hongliang
AU - Biard, Denis
AU - Majumder, Hemanta K
AU - Schreiber, Valérie
AU - Pommier, Yves
AD - Developmental Therapeutics Branch and Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-4255, USA, Laboratory of Molecular Biology, Indian Association for the Cultivation of Science, Jadavpur, Kolkata 700032, India, Biotechnology and Cell Signaling, UMR7242 CNRS, Université de Strasbourg, Laboratory of Excellence Medalis, ESBS, Blvd Sébastien Brant, CS 10413, 67412 Illkirch, France, CEA-DSV-iMETI-SEPIA, BP6, 92265 Fontenay-aux-Roses cedex, France and Laboratory of Molecular Parasitology, Indian Institute of Chemical Biology, Kolkata 700032, India.
Y1 - 2014/04//
PY - 2014
DA - April 2014
SP - 4435
EP - 4449
VL - 42
IS - 7
KW - DNA-Binding Proteins
KW - 0
KW - X-ray repair cross complementing protein 1
KW - Poly(ADP-ribose) Polymerases
KW - EC 2.4.2.30
KW - Phosphoric Diester Hydrolases
KW - EC 3.1.4.-
KW - DNA Topoisomerases, Type I
KW - EC 5.99.1.2
KW - Index Medicus
KW - Animals
KW - Humans
KW - Cell Line, Tumor
KW - Sumoylation
KW - Protein Interaction Domains and Motifs
KW - Epistasis, Genetic
KW - DNA Topoisomerases, Type I -- metabolism
KW - Phosphoric Diester Hydrolases -- genetics
KW - Poly(ADP-ribose) Polymerases -- genetics
KW - DNA Repair
KW - Poly(ADP-ribose) Polymerases -- chemistry
KW - DNA Damage
KW - Phosphoric Diester Hydrolases -- metabolism
KW - Poly(ADP-ribose) Polymerases -- metabolism
KW - Phosphoric Diester Hydrolases -- chemistry
KW - DNA-Binding Proteins -- metabolism
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1516722995?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nucleic+acids+research&rft.atitle=PARP1-TDP1+coupling+for+the+repair+of+topoisomerase+I-induced+DNA+damage.&rft.au=Das%2C+Benu+Brata%3BHuang%2C+Shar-yin+N%3BMurai%2C+Junko%3BRehman%2C+Ishita%3BAm%C3%A9%2C+Jean-Christophe%3BSengupta%2C+Souvik%3BDas%2C+Subhendu+K%3BMajumdar%2C+Papiya%3BZhang%2C+Hongliang%3BBiard%2C+Denis%3BMajumder%2C+Hemanta+K%3BSchreiber%2C+Val%C3%A9rie%3BPommier%2C+Yves&rft.aulast=Das&rft.aufirst=Benu&rft.date=2014-04-01&rft.volume=42&rft.issue=7&rft.spage=4435&rft.isbn=&rft.btitle=&rft.title=Nucleic+acids+research&rft.issn=1362-4962&rft_id=info:doi/10.1093%2Fnar%2Fgku088
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-07-08
N1 - Date created - 2014-04-15
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/nar/gku088
ER -
TY - JOUR
T1 - A quantitative high-resolution genetic profile rapidly identifies sequence determinants of hepatitis C viral fitness and drug sensitivity.
AN - 1515643204; 24722365
AB - Widely used chemical genetic screens have greatly facilitated the identification of many antiviral agents. However, the regions of interaction and inhibitory mechanisms of many therapeutic candidates have yet to be elucidated. Previous chemical screens identified Daclatasvir (BMS-790052) as a potent nonstructural protein 5A (NS5A) inhibitor for Hepatitis C virus (HCV) infection with an unclear inhibitory mechanism. Here we have developed a quantitative high-resolution genetic (qHRG) approach to systematically map the drug-protein interactions between Daclatasvir and NS5A and profile genetic barriers to Daclatasvir resistance. We implemented saturation mutagenesis in combination with next-generation sequencing technology to systematically quantify the effect of every possible amino acid substitution in the drug-targeted region (domain IA of NS5A) on replication fitness and sensitivity to Daclatasvir. This enabled determination of the residues governing drug-protein interactions. The relative fitness and drug sensitivity profiles also provide a comprehensive reference of the genetic barriers for all possible single amino acid changes during viral evolution, which we utilized to predict clinical outcomes using mathematical models. We envision that this high-resolution profiling methodology will be useful for next-generation drug development to select drugs with higher fitness costs to resistance, and also for informing the rational use of drugs based on viral variant spectra from patients.
JF - PLoS pathogens
AU - Qi, Hangfei
AU - Olson, C Anders
AU - Wu, Nicholas C
AU - Ke, Ruian
AU - Loverdo, Claude
AU - Chu, Virginia
AU - Truong, Shawna
AU - Remenyi, Roland
AU - Chen, Zugen
AU - Du, Yushen
AU - Su, Sheng-Yao
AU - Al-Mawsawi, Laith Q
AU - Wu, Ting-Ting
AU - Chen, Shu-Hua
AU - Lin, Chung-Yen
AU - Zhong, Weidong
AU - Lloyd-Smith, James O
AU - Sun, Ren
AD - Department of Molecular and Medical Pharmacology, University of California Los Angeles, Los Angeles, California, United States of America. ; The Molecular Biology Institute, University of California Los Angeles, Los Angeles, California, United States of America. ; Department of Ecology and Evolutionary Biology, University of California Los Angeles, Los Angeles, California, United States of America. ; Department of Molecular, Cell and Developmental Biology, University of California Los Angeles, Los Angeles, California, United States of America. ; Department of Human Genetics, University of California Los Angeles, Los Angeles, California, United States of America. ; Institute of Information Science, Academia Sinica, Taipei, Taiwan; Institute of Biomedical Informatics, National Yang-Ming University, Taipei, Taiwan. ; Institute of Information Science, Academia Sinica, Taipei, Taiwan. ; Department of Infectious Diseases, Novartis Institutes for BioMedical Research, Emeryville, California, United States of America. ; Department of Ecology and Evolutionary Biology, University of California Los Angeles, Los Angeles, California, United States of America; Fogarty International Center, National Institutes of Health, Bethesda, Maryland, United States of America. ; Department of Molecular and Medical Pharmacology, University of California Los Angeles, Los Angeles, California, United States of America; The Molecular Biology Institute, University of California Los Angeles, Los Angeles, California, United States of America; School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Y1 - 2014/04//
PY - 2014
DA - April 2014
SP - 1
VL - 10
IS - 4
KW - BMS-790052
KW - 0
KW - Imidazoles
KW - NS-5 protein, hepatitis C virus
KW - Viral Nonstructural Proteins
KW - Index Medicus
KW - Viral Nonstructural Proteins -- genetics
KW - Humans
KW - Viral Nonstructural Proteins -- metabolism
KW - Cell Line
KW - Hepacivirus -- physiology
KW - Gene Expression Profiling
KW - Virus Replication -- genetics
KW - Hepatitis C -- drug therapy
KW - Imidazoles -- pharmacology
KW - Virus Replication -- drug effects
KW - Genetic Fitness
KW - Drug Resistance, Viral -- genetics
KW - Hepatitis C -- metabolism
KW - Hepatitis C -- genetics
KW - Hepatitis C -- pathology
KW - Drug Resistance, Viral -- drug effects
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1515643204?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PLoS+pathogens&rft.atitle=A+quantitative+high-resolution+genetic+profile+rapidly+identifies+sequence+determinants+of+hepatitis+C+viral+fitness+and+drug+sensitivity.&rft.au=Qi%2C+Hangfei%3BOlson%2C+C+Anders%3BWu%2C+Nicholas+C%3BKe%2C+Ruian%3BLoverdo%2C+Claude%3BChu%2C+Virginia%3BTruong%2C+Shawna%3BRemenyi%2C+Roland%3BChen%2C+Zugen%3BDu%2C+Yushen%3BSu%2C+Sheng-Yao%3BAl-Mawsawi%2C+Laith+Q%3BWu%2C+Ting-Ting%3BChen%2C+Shu-Hua%3BLin%2C+Chung-Yen%3BZhong%2C+Weidong%3BLloyd-Smith%2C+James+O%3BSun%2C+Ren&rft.aulast=Qi&rft.aufirst=Hangfei&rft.date=2014-04-01&rft.volume=10&rft.issue=4&rft.spage=e1004064&rft.isbn=&rft.btitle=&rft.title=PLoS+pathogens&rft.issn=1553-7374&rft_id=info:doi/10.1371%2Fjournal.ppat.1004064
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-12-10
N1 - Date created - 2014-04-11
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Cell Host Microbe. 2011 Jan 20;9(1):32-45 [21238945]
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J Biol Chem. 2011 Apr 1;286(13):11290-8 [21297162]
Virology. 2011 May 25;414(1):10-8 [21513964]
Proc Natl Acad Sci U S A. 2011 Jun 21;108(25):10290-5 [21646519]
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J Virol. 2011 Sep;85(17):8870-83 [21697487]
PLoS One. 2011;6(10):e26300 [22022594]
Hepatology. 2011 Dec;54(6):1924-35 [21809362]
Hepatology. 2011 Dec;54(6):1956-65 [21837752]
N Engl J Med. 2012 Jan 19;366(3):216-24 [22256805]
Antimicrob Agents Chemother. 2012 Mar;56(3):1588-90 [22203595]
Antimicrob Agents Chemother. 2012 Mar;56(3):1350-8 [22214777]
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Lancet Infect Dis. 2012 Sep;12(9):671-7 [22714001]
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Virus Res. 2012 Dec;170(1-2):1-14 [23009750]
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Hepatology. 2013 Jul;58(1):428-38 [23467911]
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J Virol. 2009 May;83(9):4395-403 [19244328]
Proc Natl Acad Sci U S A. 2009 May 5;106(18):7577-82 [19376974]
J Virol. 2010 Jan;84(1):482-91 [19812153]
Nature. 2010 May 6;465(7294):96-100 [20410884]
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Antimicrob Agents Chemother. 2010 Sep;54(9):3641-50 [20585111]
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Nat Methods. 2010 Sep;7(9):741-6 [20711194]
Gastroenterology. 2011 Mar;140(3):1032-42 [21111742]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1371/journal.ppat.1004064
ER -
TY - JOUR
T1 - Activation of peroxisome proliferator-activated receptor-β/δ (PPAR-β/δ) inhibits human breast cancer cell line tumorigenicity.
AN - 1514432594; 24464939
AB - The effect of activation and overexpression of the nuclear receptor PPAR-β/δ in human MDA-MB-231 (estrogen receptor-negative; ER(-)) and MCF7 (estrogen-receptor-positive; ER(+)) breast cancer cell lines was examined. Target gene induction by ligand activation of PPAR-β/δ was increased by overexpression of PPAR-β/δ compared with controls. Overexpression of PPAR-β/δ caused a decrease in cell proliferation in MCF7 and MDA-MB-231 cells compared with controls, whereas ligand activation of PPAR-β/δ further inhibited proliferation of MCF7 but not MDA-MB-231 cells. Overexpression and/or ligand activation of PPAR-β/δ in MDA-MB-231 or MCF7 cells had no effect on experimental apoptosis. Decreased clonogenicity was observed in both MDA-MB-231 and MCF7 overexpressing PPAR-β/δ in response to ligand activation of PPAR-β/δ as compared with controls. Ectopic xenografts developed from MDA-MB-231 and MCF7 cells overexpressing PPAR-β/δ were significantly smaller, and ligand activation of PPAR-β/δ caused an even greater reduction in tumor volume as compared with controls. Interestingly, the decrease in MDA-MB-231 tumor size after overexpressing PPAR-β/δ and ligand activation of PPAR-β/δ correlated with increased necrosis. These data show that ligand activation and/or overexpression of PPAR-β/δ in two human breast cancer cell lines inhibits relative breast cancer tumorigenicity and provide further support for the development of ligands for PPAR-β/δ to specifically inhibit breast carcinogenesis. These new cell-based models will be invaluable tools for delineating the role of PPAR-β/δ in breast cancer and evaluating the effects of PPAR-β/δ agonists.
JF - Molecular cancer therapeutics
AU - Yao, Pei-Li
AU - Morales, Jose L
AU - Zhu, Bokai
AU - Kang, Boo-Hyon
AU - Gonzalez, Frank J
AU - Peters, Jeffrey M
AD - Authors' Affiliations: Department of Veterinary and Biomedical Sciences and The Center of Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, Pennsylvania; and Non-clinical Research Institute, Chemon, Jeil-Ri, Yangji-Myeon, Cheoin-Gu, Yongin-Si, Gyeonggi-Do, Korea; and Laboratory of Metabolism, National Cancer Institute, Bethesda, Maryland.
Y1 - 2014/04//
PY - 2014
DA - April 2014
SP - 1008
EP - 1017
VL - 13
IS - 4
KW - ANGPTL4 protein, human
KW - 0
KW - Angiopoietins
KW - PPAR delta
KW - PPAR-beta
KW - Index Medicus
KW - Gene Expression Regulation, Neoplastic
KW - Animals
KW - Apoptosis -- genetics
KW - Humans
KW - MCF-7 Cells
KW - Mice, Nude
KW - Mice
KW - Mammary Neoplasms, Experimental
KW - Cell Line, Tumor
KW - Cell Proliferation
KW - Female
KW - PPAR-beta -- metabolism
KW - Breast Neoplasms -- pathology
KW - Angiopoietins -- genetics
KW - Breast Neoplasms -- metabolism
KW - PPAR delta -- metabolism
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1514432594?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+cancer+therapeutics&rft.atitle=Activation+of+peroxisome+proliferator-activated+receptor-%CE%B2%2F%CE%B4+%28PPAR-%CE%B2%2F%CE%B4%29+inhibits+human+breast+cancer+cell+line+tumorigenicity.&rft.au=Yao%2C+Pei-Li%3BMorales%2C+Jose+L%3BZhu%2C+Bokai%3BKang%2C+Boo-Hyon%3BGonzalez%2C+Frank+J%3BPeters%2C+Jeffrey+M&rft.aulast=Yao&rft.aufirst=Pei-Li&rft.date=2014-04-01&rft.volume=13&rft.issue=4&rft.spage=1008&rft.isbn=&rft.btitle=&rft.title=Molecular+cancer+therapeutics&rft.issn=1538-8514&rft_id=info:doi/10.1158%2F1535-7163.MCT-13-0836
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-12-09
N1 - Date created - 2014-04-08
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Cancer Res. 2005 May 1;65(9):3950-7 [15867396]
Proc Soc Exp Biol Med. 1999 Jun;221(2):87-8 [10352117]
Biochem Biophys Res Commun. 2006 Feb 10;340(2):656-60 [16378595]
Curr Opin Cell Biol. 2007 Dec;19(6):697-704 [18035529]
Toxicology. 2008 Jan 14;243(1-2):236-43 [18054822]
Curr Opin Investig Drugs. 2008 May;9(5):463-9 [18465655]
Biochem Biophys Res Commun. 2008 Jul 4;371(3):456-61 [18442472]
Proc Natl Acad Sci U S A. 2008 May 27;105(21):7546-51 [18495924]
Clin Sci (Lond). 2008 Aug;115(4):107-27 [18616431]
Mol Pharmacol. 2008 Nov;74(5):1429-42 [18687807]
Mol Pharmacol. 2008 Nov;74(5):1269-77 [18701617]
Prostaglandins Other Lipid Mediat. 2009 Apr;88(3-4):97-100 [19101649]
Breast Cancer Res. 2009;11(1):R7 [19187537]
Biochim Biophys Acta. 2009 Dec;1796(2):230-41 [19505534]
Cancer Lett. 2010 Feb 28;288(2):219-25 [19660859]
Curr Opin Lipidol. 2010 Jun;21(3):186-91 [20480546]
Mol Pharmacol. 2010 Sep;78(3):419-30 [20516370]
Nat Biotechnol. 2010 Dec;28(12):1248-50 [21139605]
Cell Signal. 2011 Dec;23(12):2039-50 [21843636]
Mol Carcinog. 2011 Nov;50(11):884-900 [21400612]
Cancer Metastasis Rev. 2011 Dec;30(3-4):619-40 [22037942]
Nat Rev Cancer. 2012 Mar;12(3):181-95 [22318237]
BMC Genomics. 2012;13:665 [23176727]
Biochemistry. 2013 Jun 18;52(24):4193-203 [23713684]
Cancer Res. 2013 Jul 15;73(14):4349-61 [23811944]
Nature. 2000 Aug 17;406(6797):747-52 [10963602]
Proc Natl Acad Sci U S A. 2001 Sep 11;98(19):10869-74 [11553815]
Proc Natl Acad Sci U S A. 2003 Jul 8;100(14):8418-23 [12829800]
Proc Natl Acad Sci U S A. 2003 Dec 23;100(26):15924-9 [14676330]
Cancer Res. 2004 May 1;64(9):3162-70 [15126355]
Blood. 1998 Nov 15;92(10):3780-92 [9808572]
Atherosclerosis. 2005 Jul;181(1):29-37 [15939051]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1158/1535-7163.MCT-13-0836
ER -
TY - JOUR
T1 - LGR5 positivity defines stem-like cells in colorectal cancer.
AN - 1514432490; 24282287
AB - Like normal colorectal epithelium, colorectal carcinomas (CRCs) are organized hierarchically and include populations of cells with stem-like properties. Leucine-rich-repeat-containing G-protein-coupled receptor 5 (LGR5) is associated with these stem cells in normal colorectal epithelium; however, the precise function of LGR5 in CRC remains largely unknown. Here, we analyzed the functional and molecular consequences of short hairpin RNA-mediated silencing of LGR5 in CRC cell lines SW480 and HT-29. Additionally, we exposed Lgr5-EGFP-IRES-CreERT2 mice to azoxymethane/dextrane sodium sulfate (AOM/DSS), which induces inflammation-driven colon tumors. Tumors were then flow-sorted into fractions of epithelial cells that expressed high or low levels of Lgr5 and were molecularly characterized using gene expression profiling and array comparative genomic hybridization. Silencing of LGR5 in SW480 CRC cells resulted in a depletion of spheres but did not affect adherently growing cells. Spheres expressed higher levels of several stem cell-associated genes than adherent cells, including LGR5. Silencing of LGR5 reduced proliferation, migration and colony formation in vitro and tumorigenicity in vivo. In accordance with these results, NOTCH signaling was downregulated upon LGR5 silencing. In AOM/DSS-induced colon tumors, Lgr5 high cells showed higher levels of several stem cell-associated genes and higher Wnt signaling than Lgr5 low tumor cells and Lgr5 high normal colon cells. Array comparative genomic hybridization revealed no genomic imbalances in either tumor cell fraction. Our data elucidate mechanisms that define the role of LGR5 as a marker for stem-like cells in CRC.
JF - Carcinogenesis
AU - Hirsch, Daniela
AU - Barker, Nick
AU - McNeil, Nicole
AU - Hu, Yue
AU - Camps, Jordi
AU - McKinnon, Katherine
AU - Clevers, Hans
AU - Ried, Thomas
AU - Gaiser, Timo
AD - Section of Cancer Genomics, Genetics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Y1 - 2014/04//
PY - 2014
DA - April 2014
SP - 849
EP - 858
VL - 35
IS - 4
KW - LGR5 protein, human
KW - 0
KW - Receptors, G-Protein-Coupled
KW - Receptors, Notch
KW - Index Medicus
KW - Gene Silencing
KW - Humans
KW - Cell Line, Tumor
KW - Receptors, Notch -- metabolism
KW - Colorectal Neoplasms -- pathology
KW - Neoplastic Stem Cells -- pathology
KW - Receptors, G-Protein-Coupled -- metabolism
KW - Receptors, G-Protein-Coupled -- genetics
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1514432490?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=LGR5+positivity+defines+stem-like+cells+in+colorectal+cancer.&rft.au=Hirsch%2C+Daniela%3BBarker%2C+Nick%3BMcNeil%2C+Nicole%3BHu%2C+Yue%3BCamps%2C+Jordi%3BMcKinnon%2C+Katherine%3BClevers%2C+Hans%3BRied%2C+Thomas%3BGaiser%2C+Timo&rft.aulast=Hirsch&rft.aufirst=Daniela&rft.date=2014-04-01&rft.volume=35&rft.issue=4&rft.spage=849&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgt377
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-05-27
N1 - Date created - 2014-04-08
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/carcin/bgt377
ER -
TY - JOUR
T1 - The interplay between hypoxia, endothelial and melanoma cells regulates vascularization and cell motility through endothelin-1 and vascular endothelial growth factor.
AN - 1514426591; 24473118
AB - Reciprocal growth factor exchanges between endothelial and malignant cells within the hypoxic microenvironment determine tumor progression. However, the nature of these exchanges has not yet been fully explored. We studied the mutual regulation between endothelial cells (EC), melanoma cells and hypoxia that dictate tumor aggressiveness and angiogenic activity. Here, we investigated the presence of bidirectional autocrine/paracrine endothelin (ET)-1/ET receptor (ETBR) signaling in melanoma cells, blood and lymphatic EC. In all these cells, hypoxia enhanced ET-1 expression, which in turn induced vascular endothelial growth factor (VEGF)-A and VEGF-C secretion, through the hypoxia-inducible growth factor (HIF)-1α and HIF-2α. Autocrine/paracrine exchanges of ET-1, VEGF-A and VEGF-C promoted tumor aggressiveness and morphological changes in blood and lymphatic EC. Furthermore, conditioned media from EC enhanced melanoma cell migration and vessel-like channel formation. This regulation was inhibited by ETBR blockade, by using the selective ETBR antagonist, or ETBR small interfering RNA (siRNA), and by VEGFR-2/-3 antibodies, indicating that ET-1, VEGF-A/VEGF-C, produced by melanoma cells or EC mediated inter-regulation between these cells. Interestingly, HIF-1α/HIF-2α siRNA, impaired this reciprocal regulation, demonstrating the key role of these transcriptional factors in signaling exchanges. In melanoma xenografts, the ETBR antagonist reduced tumor growth and the number of blood and lymphatic vessels. These results reveal an interplay between melanoma cells and EC mediated by ET-1 and VEGF-A/-C and coordinated by the hypoxic microenvironment through HIF-1α/2α transcriptional programs. Thus, targeting ETBR may improve melanoma treatment for tumor and EC, by inhibiting autocrine/paracrine signaling that sustains melanoma progression.
JF - Carcinogenesis
AU - Spinella, Francesca
AU - Caprara, Valentina
AU - Cianfrocca, Roberta
AU - Rosanò, Laura
AU - Di Castro, Valeriana
AU - Garrafa, Emirena
AU - Natali, Pier Giorgio
AU - Bagnato, Anna
AD - Experimental Oncology Department, Regina Elena National Cancer Institute, 00144 Rome.
Y1 - 2014/04//
PY - 2014
DA - April 2014
SP - 840
EP - 848
VL - 35
IS - 4
KW - Endothelin-1
KW - 0
KW - Vascular Endothelial Growth Factor A
KW - Index Medicus
KW - Real-Time Polymerase Chain Reaction
KW - Animals
KW - Humans
KW - Enzyme-Linked Immunosorbent Assay
KW - Mice, Nude
KW - Mice
KW - Human Umbilical Vein Endothelial Cells
KW - Female
KW - Endothelin-1 -- metabolism
KW - Cell Movement
KW - Melanoma -- pathology
KW - Endothelium, Vascular -- pathology
KW - Neovascularization, Pathologic
KW - Cell Hypoxia
KW - Melanoma -- blood supply
KW - Vascular Endothelial Growth Factor A -- metabolism
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=The+interplay+between+hypoxia%2C+endothelial+and+melanoma+cells+regulates+vascularization+and+cell+motility+through+endothelin-1+and+vascular+endothelial+growth+factor.&rft.au=Spinella%2C+Francesca%3BCaprara%2C+Valentina%3BCianfrocca%2C+Roberta%3BRosan%C3%B2%2C+Laura%3BDi+Castro%2C+Valeriana%3BGarrafa%2C+Emirena%3BNatali%2C+Pier+Giorgio%3BBagnato%2C+Anna&rft.aulast=Spinella&rft.aufirst=Francesca&rft.date=2014-04-01&rft.volume=35&rft.issue=4&rft.spage=840&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgu018
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-05-27
N1 - Date created - 2014-04-08
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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Blood. 2010 Nov 18;116(20):4376-84 [20716773]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/carcin/bgu018
ER -
TY - JOUR
T1 - Cigarette smoking and endometrial carcinoma risk: the role of effect modification and tumor heterogeneity
AN - 1512331030; 19380752
AB - Purpose: The inverse relationship between cigarette smoking and endometrial carcinoma risk is well established. We examined effect modification of this relationship and associations with tumor characteristics in the National Institutes of Health-AARP Diet and Health Study. Methods: We examined the association between cigarette smoking and endometrial carcinoma risk among 110,304 women. During 1,029,041 person years of follow-up, we identified 1,476 incident endometrial carcinoma cases. Multivariable Cox proportional hazards regression models were used to estimate relative risks (RRs) and 95 % confidence intervals (CIs) for the association between smoking status, years since smoking cessation, and endometrial carcinoma risk overall and within strata of endometrial carcinoma risk factors. Effect modification was assessed using likelihood ratio test statistics. Smoking associations by histologic subtype/grade and stage at diagnosis were also evaluated. Results: Reduced endometrial carcinoma risk was evident among former (RR 0.89, 95 % CI 0.80, 1.00) and current (RR 0.65, 95 % CI 0.55, 0.78) smokers compared with never smokers. Smoking cessation 1-4 years prior to baseline was significantly associated with endometrial carcinoma risk (RR 0.65, 95 % CI 0.48, 0.89), while cessation greater than or equal to 10 years before baseline was not. The association between smoking and endometrial carcinoma risk was not significantly modified by any endometrial carcinoma risk factor, nor did we observe major differences in risk associations by tumor characteristics. Conclusion: The cigarette smoking-endometrial carcinoma risk relationship was consistent within strata of important endometrial carcinoma risk factors and by clinically relevant tumor characteristics.
JF - Cancer Causes & Control
AU - Felix, Ashley S
AU - Yang, Hannah P
AU - Gierach, Gretchen L
AU - Park, Yikyung
AU - Brinton, Louise A
AD - Hormonal and Reproductive Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, 9609 Medical Center Drive, Bethesda, MD, 20892-9774, USA, ashley.felix@gmail.com
Y1 - 2014/04//
PY - 2014
DA - Apr 2014
SP - 479
EP - 489
PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL - 25
IS - 4
SN - 0957-5243, 0957-5243
KW - Risk Abstracts; Health & Safety Science Abstracts
KW - Risk assessment
KW - Diets
KW - Health risks
KW - Cigarettes
KW - Risk factors
KW - Tumors
KW - Cancer
KW - H 11000:Diseases/Injuries/Trauma
KW - R2 23060:Medical and environmental health
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1512331030?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Causes+%26+Control&rft.atitle=Cigarette+smoking+and+endometrial+carcinoma+risk%3A+the+role+of+effect+modification+and+tumor+heterogeneity&rft.au=Felix%2C+Ashley+S%3BYang%2C+Hannah+P%3BGierach%2C+Gretchen+L%3BPark%2C+Yikyung%3BBrinton%2C+Louise+A&rft.aulast=Felix&rft.aufirst=Ashley&rft.date=2014-04-01&rft.volume=25&rft.issue=4&rft.spage=479&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/10.1007%2Fs10552-014-0350-1
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-01
N1 - Number of references - 62
N1 - Last updated - 2014-05-29
N1 - SubjectsTermNotLitGenreText - Diets; Risk assessment; Health risks; Cigarettes; Risk factors; Tumors; Cancer
DO - http://dx.doi.org/10.1007/s10552-014-0350-1
ER -
TY - JOUR
T1 - Enhancers are major targets for murine leukemia virus vector integration.
AN - 1511393839; 24501411
AB - Retroviral vectors have been used in successful gene therapies. However, in some patients, insertional mutagenesis led to leukemia or myelodysplasia. Both the strong promoter/enhancer elements in the long terminal repeats (LTRs) of murine leukemia virus (MLV)-based vectors and the vector-specific integration site preferences played an important role in these adverse clinical events. MLV integration is known to prefer regions in or near transcription start sites (TSS). Recently, BET family proteins were shown to be the major cellular proteins responsible for targeting MLV integration. Although MLV integration sites are significantly enriched at TSS, only a small fraction of the MLV integration sites (<15%) occur in this region. To resolve this apparent discrepancy, we created a high-resolution genome-wide integration map of more than one million integration sites from CD34(+) hematopoietic stem cells transduced with a clinically relevant MLV-based vector. The integration sites form ∼60,000 tight clusters. These clusters comprise ∼1.9% of the genome. The vast majority (87%) of the integration sites are located within histone H3K4me1 islands, a hallmark of enhancers. The majority of these clusters also have H3K27ac histone modifications, which mark active enhancers. The enhancers of some oncogenes, including LMO2, are highly preferred targets for integration without in vivo selection.
We show that active enhancer regions are the major targets for MLV integration; this means that MLV preferentially integrates in regions that are favorable for viral gene expression in a variety of cell types. The results provide insights for MLV integration target site selection and also explain the high risk of insertional mutagenesis that is associated with gene therapy trials using MLV vectors.
JF - Journal of virology
AU - De Ravin, Suk See
AU - Su, Ling
AU - Theobald, Narda
AU - Choi, Uimook
AU - Macpherson, Janet L
AU - Poidinger, Michael
AU - Symonds, Geoff
AU - Pond, Susan M
AU - Ferris, Andrea L
AU - Hughes, Stephen H
AU - Malech, Harry L
AU - Wu, Xiaolin
AD - Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Y1 - 2014/04//
PY - 2014
DA - April 2014
SP - 4504
EP - 4513
VL - 88
IS - 8
KW - Histones
KW - 0
KW - Index Medicus
KW - Animals
KW - Genome, Human
KW - Cells, Cultured
KW - Humans
KW - Histones -- metabolism
KW - Mice
KW - Genetic Therapy
KW - Hematopoietic Stem Cells -- virology
KW - Mutagenesis, Insertional
KW - Histones -- genetics
KW - Leukemia Virus, Murine -- physiology
KW - Leukemia Virus, Murine -- genetics
KW - Genetic Vectors -- physiology
KW - Enhancer Elements, Genetic
KW - Genetic Vectors -- genetics
KW - Virus Integration
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Enhancers+are+major+targets+for+murine+leukemia+virus+vector+integration.&rft.au=De+Ravin%2C+Suk+See%3BSu%2C+Ling%3BTheobald%2C+Narda%3BChoi%2C+Uimook%3BMacpherson%2C+Janet+L%3BPoidinger%2C+Michael%3BSymonds%2C+Geoff%3BPond%2C+Susan+M%3BFerris%2C+Andrea+L%3BHughes%2C+Stephen+H%3BMalech%2C+Harry+L%3BWu%2C+Xiaolin&rft.aulast=De+Ravin&rft.aufirst=Suk&rft.date=2014-04-01&rft.volume=88&rft.issue=8&rft.spage=4504&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=1098-5514&rft_id=info:doi/10.1128%2FJVI.00011-14
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-06-24
N1 - Date created - 2014-03-27
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Genome Res. 2007 Aug;17(8):1186-94 [17545577]
Annu Rev Biochem. 2007;76:75-100 [17362198]
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Cell. 2008 Nov 14;135(4):649-61 [18992931]
Blood. 2009 May 21;113(21):5104-10 [19286997]
Genome Biol. 2008;9(9):R137 [18798982]
Hum Mol Genet. 2009 Oct 15;18(R2):R195-201 [19808796]
Blood. 2010 Jan 28;115(4):783-91 [19965657]
Bioinformatics. 2010 Mar 15;26(6):841-2 [20110278]
Blood. 2010 Aug 12;116(6):900-8 [20457870]
Nat Biotechnol. 2010 Oct;28(10):1045-8 [20944595]
Blood. 2010 Dec 16;116(25):5507-17 [20864581]
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Retrovirology. 2008;5:48 [18554410]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1128/JVI.00011-14
ER -
TY - JOUR
T1 - Pentraxins and IgA share a binding hot-spot on FcαRI.
AN - 1510111583; 24407959
AB - The pentraxins, C-reactive protein (CRP), and serum amyloid P component (SAP) have previously been shown to function as innate opsonins through interactions with Fcγ receptors. The molecular details of these interactions were elucidated by the crystal structure of SAP in complex with FcγRIIA. More recently, pentraxins were shown to bind and activate FcαRI (CD89), the receptor for IgA. Here, we used mutations of the receptor based on a docking model to further examine pentraxin recognition by FcαRI. The solution binding of pentraxins to six FcαRI alanine cluster mutants revealed that mutations Y35A and R82A, on the C-and F-strands of the D1 domain, respectively, markedly reduced receptor binding to CRP and SAP. These residues are in the IgA-binding site of the receptor, and thus, significantly affected receptor binding to IgA. The shared pentraxin and IgA-binding site on FcαRI is further supported by the results of a solution binding competition assay. In addition to the IgA-binding site, pentraxins appear to interact with a broader region of the receptor as the mutation in the C'-strand (R48A/E49A) enhanced pentraxin binding. Unlike Fcγ receptors, the H129A/I130A and R178A mutations on the BC- and FG-loops of D2 domain, respectively, had little effect on FcαRI binding to the pentraxins. In conclusion, our data suggest that the pentraxins recognize a similar site on FcαRI as IgA. © 2014 The Protein Society.
JF - Protein science : a publication of the Protein Society
AU - Lu, Jinghua
AU - Marjon, Kristopher D
AU - Mold, Carolyn
AU - Marnell, Lorraine
AU - Du Clos, Terry W
AU - Sun, Peter
AD - Structural Immunology Section, Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland, 20852.
Y1 - 2014/04//
PY - 2014
DA - April 2014
SP - 378
EP - 386
VL - 23
IS - 4
KW - Antigens, CD
KW - 0
KW - Fc(alpha) receptor
KW - Immunoglobulin A
KW - Receptors, Fc
KW - Serum Amyloid P-Component
KW - C-Reactive Protein
KW - 9007-41-4
KW - Index Medicus
KW - surface plasmon resonance
KW - site-directed mutagenesis
KW - competition
KW - Neutrophils -- metabolism
KW - Humans
KW - Mutation
KW - Binding Sites
KW - Receptors, Fc -- chemistry
KW - Immunoglobulin A -- chemistry
KW - Antigens, CD -- chemistry
KW - C-Reactive Protein -- chemistry
KW - Antigens, CD -- metabolism
KW - Antigens, CD -- genetics
KW - Receptors, Fc -- metabolism
KW - Serum Amyloid P-Component -- chemistry
KW - Receptors, Fc -- genetics
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Protein+science+%3A+a+publication+of+the+Protein+Society&rft.atitle=Pentraxins+and+IgA+share+a+binding+hot-spot+on+Fc%CE%B1RI.&rft.au=Lu%2C+Jinghua%3BMarjon%2C+Kristopher+D%3BMold%2C+Carolyn%3BMarnell%2C+Lorraine%3BDu+Clos%2C+Terry+W%3BSun%2C+Peter&rft.aulast=Lu&rft.aufirst=Jinghua&rft.date=2014-04-01&rft.volume=23&rft.issue=4&rft.spage=378&rft.isbn=&rft.btitle=&rft.title=Protein+science+%3A+a+publication+of+the+Protein+Society&rft.issn=1469-896X&rft_id=info:doi/10.1002%2Fpro.2419
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-02-07
N1 - Date created - 2014-03-24
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Clin Exp Immunol. 2000 Jul;121(1):106-11 [10886246]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1002/pro.2419
ER -
TY - JOUR
T1 - Aberrant microRNA expression likely controls RAS oncogene activation during malignant transformation of human prostate epithelial and stem cells by arsenic.
AN - 1509415401; 24431212
AB - Inorganic arsenic (iAs), a human carcinogen, potentially targets the prostate. iAs malignantly transforms the RWPE-1 human prostate epithelial line to CAsE-PE cells, and a derivative normal stem cell (SC) line, WPE-stem, to As-Cancer SC (As-CSC) line. MicroRNAs (miRNA) are noncoding but exert negative control on expression by degradation or translational repression of target mRNAs. Aberrant miRNA expression is important in carcinogenesis. A miRNA array of CAsE-PE and As-CSC revealed common altered expression in both for pathways concerning oncogenesis, miRNA biogenesis, cell signaling, proliferation, and tumor metastasis and invasion. The KRAS oncogene is overexpressed in CAsE-PE cells but not by mutation or promoter hypomethylation, and is intensely overexpressed in As-CSC cells. In both transformants, decreased miRNAs targeting KRAS and RAS superfamily members occurred. Reduced miR-134, miR-373, miR-155, miR-138, miR-205, miR-181d, miR-181c, and let-7 in CAsE-PE cells correlated with increased target RAS oncogenes, RAN, RAB27A, RAB22A mRNAs, and KRAS protein. Reduced miR-143, miR-34c-5p, and miR-205 in As-CSC correlated with increased target RAN mRNA, and KRAS, NRAS, and RRAS proteins. The RAS/ERK and PI3K/PTEN/AKT pathways control cell survival, differentiation, and proliferation, and when dysregulated promote a cancer phenotype. iAs transformation increased expression of activated ERK kinase in both transformants and altered components of the PI3K/PTEN/AKT pathway including decreased PTEN and increases in BCL2, BCL-XL, and VEGF in the absence of AKT activation. Thus, dysregulated miRNA expression may be linked to RAS activation in both transformants.
JF - Toxicological sciences : an official journal of the Society of Toxicology
AU - Ngalame, Ntube N O
AU - Tokar, Erik J
AU - Person, Rachel J
AU - Xu, Yuanyuan
AU - Waalkes, Michael P
AD - Inorganic Toxicology Group, National Toxicology Program Laboratory, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709.
Y1 - 2014/04//
PY - 2014
DA - April 2014
SP - 268
EP - 277
VL - 138
IS - 2
KW - Arsenites
KW - 0
KW - Carcinogens, Environmental
KW - KRAS protein, human
KW - MicroRNAs
KW - Proto-Oncogene Proteins
KW - Sodium Compounds
KW - sodium arsenite
KW - 48OVY2OC72
KW - Proto-Oncogene Proteins p21(ras)
KW - EC 3.6.5.2
KW - ras Proteins
KW - Index Medicus
KW - KRAS
KW - prostate cells
KW - arsenic
KW - microRNA
KW - stem/progenitor cells
KW - cancer
KW - Real-Time Polymerase Chain Reaction
KW - Gene Expression -- drug effects
KW - ras Proteins -- genetics
KW - Blotting, Western
KW - Humans
KW - Proto-Oncogene Proteins -- genetics
KW - Male
KW - Cell Line
KW - Prostate -- drug effects
KW - Genes, ras -- drug effects
KW - MicroRNAs -- genetics
KW - Neoplastic Stem Cells -- pathology
KW - Arsenites -- toxicity
KW - Prostate -- metabolism
KW - Carcinogens, Environmental -- toxicity
KW - Neoplastic Stem Cells -- drug effects
KW - Neoplastic Stem Cells -- metabolism
KW - Epithelial Cells -- metabolism
KW - Epithelial Cells -- drug effects
KW - Genes, ras -- genetics
KW - Epithelial Cells -- pathology
KW - Sodium Compounds -- toxicity
KW - Cell Transformation, Neoplastic -- chemically induced
KW - Prostate -- pathology
KW - Cell Transformation, Neoplastic -- genetics
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-11-10
N1 - Date created - 2014-03-21
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Proc Natl Acad Sci U S A. 2006 Feb 14;103(7):2257-61 [16461460]
J Pathol. 2006 Apr;208(5):699-707 [16402365]
Nat Rev Cancer. 2006 Nov;6(11):857-66 [17060945]
Environ Health Perspect. 2007 Feb;115(2):243-7 [17384772]
Cell Res. 2007 Jun;17(6):531-6 [17404601]
Cancer Res. 2007 Jul 1;67(13):6130-5 [17616669]
Carcinogenesis. 2007 Jul;28(7):1379-86 [17341655]
Stem Cells. 2008 Jan;26(1):17-29 [17916804]
Environ Health Perspect. 2008 Feb;116(2):158-64 [18288312]
Cancer Res. 2008 Oct 15;68(20):8278-85 [18922899]
Nature. 2008 Oct 23;455(7216):1124-8 [18806776]
FASEB J. 2009 Mar;23(3):806-12 [18952709]
PLoS One. 2009;4(10):e7542 [19855844]
J Natl Cancer Inst. 2009 Dec 16;101(24):1670-81 [19933942]
Environ Health Perspect. 2010 Jan;118(1):108-15 [20056578]
J Natl Cancer Inst. 2010 May 5;102(9):638-49 [20339138]
Toxicol Sci. 2011 Jan;119(1):73-83 [20937726]
Nat Med. 2011 Feb;17(2):211-5 [21240262]
Mol Cell Biochem. 2011 Apr;350(1-2):207-13 [21197560]
Cancer Res. 2011 Sep 15;71(18):5950-4 [21917736]
J Cell Physiol. 2011 Dec;226(12):3225-32 [21344382]
Nature. 2011 Oct 20;478(7369):399-403 [22012397]
Toxicol Sci. 2012 Jan;125(1):20-9 [22011395]
Mol Biol Rep. 2012 Feb;39(2):1595-9 [21607617]
Expert Opin Ther Targets. 2012 Apr;16 Suppl 2:S17-27 [22443084]
Cancer Res. 2012 Apr 1;72(7):1878-89 [22350410]
Environ Health Perspect. 2012 Jun;120(6):865-71 [22472196]
Cancer Res. 2012 Jul 1;72(13):3393-404 [22719071]
Mol Oncol. 2013 Jun;7(3):531-42 [23384558]
Mol Carcinog. 2001 Feb;30(2):79-87 [11241755]
Cancer Res. 2002 Apr 1;62(7):2175-83 [11929841]
Carcinogenesis. 2002 May;23(5):777-85 [12016150]
J Natl Cancer Inst. 2002 Dec 18;94(24):1888-91 [12488483]
J Cell Biochem. 2004 Jan 1;91(1):13-25 [14689577]
Cell. 2004 Jan 23;116(2):281-97 [14744438]
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Carcinogenesis. 1997 Jun;18(6):1215-23 [9214605]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/toxsci/kfu002
ER -
TY - JOUR
T1 - A copper chelate selectively triggers apoptosis in myeloid-derived suppressor cells in a drug-resistant tumor model and enhances antitumor immune response.
AN - 1509407973; 24611750
AB - Myeloid-derived suppressor cells (MDSCs), one of the major orchestrators of immunosuppressive network are present in the tumor microenvironment suppress antitumor immunity by subverting Th1 response in tumor site and considered as a great obstacle for advancement of different cancer immunotherapeutic protocols. Till date, various pharmacological approaches have been explored to modulate the suppressive functions of MDSCs in vivo. The present study describes our endeavor to explore a possibility of eradicating MDSCs by the application of a copper chelate, namely copper N-(2-hydroxy acetophenone) glycinate (CuNG), previously found to be a potential immunomodulator that can elicit antitumorogenic Th1 response in doxorubicin-resistant EAC (EAC/Dox) bearing mice. Herein, we demonstrated that CuNG treatment could reduce Gr-1+CD11b+ MDSC accumulation in ascitic fluid and spleen of EAC/Dox tumor model. Furthermore, we found that CuNG mediated reduction in MDSCs is associated with induction of Th1 response and reduction in Treg cells. Moreover, we observed that CuNG could deplete MDSCs by inducing Fas-FasL mediated apoptotic cell death where death receptor Fas expression is enhanced in MDSCs and FasL is provided by activated T cells. However, MDSC expansion from bone marrow cells and their differentiation was not affected by CuNG. Altogether, these findings suggest that the immunomodulatory property of CuNG is attributed to, at least in part, by its selective cytotoxic action on MDSCs. So, this preclinical study unveils a new mechanism of regulating MDSC levels in drug-resistant cancer model and holds promise of translating the findings into clinical settings.
JF - Immunopharmacology and immunotoxicology
AU - Chakraborty, Paramita
AU - Das, Satyajit
AU - Banerjee, Kaushik
AU - Sinha, Abhinaba
AU - Roy, Susmita
AU - Chatterjee, Mitali
AU - Choudhuri, Soumitra Kumar
AD - Department of In Vitro Carcinogenesis and Cellular Chemotherapy, Chittaranjan National Cancer Institute , Kolkata, West Bengal , India and.
Y1 - 2014/04//
PY - 2014
DA - April 2014
SP - 165
EP - 175
VL - 36
IS - 2
KW - Antigens, CD95
KW - 0
KW - Antineoplastic Agents
KW - Chelating Agents
KW - Copper
KW - 789U1901C5
KW - Doxorubicin
KW - 80168379AG
KW - Index Medicus
KW - Bone Marrow Cells -- drug effects
KW - Th1 Cells -- immunology
KW - Animals
KW - T-Lymphocytes, Regulatory -- drug effects
KW - CD4-Positive T-Lymphocytes -- immunology
KW - Cell Line, Tumor
KW - Mice
KW - CD4-Positive T-Lymphocytes -- drug effects
KW - Antigens, CD95 -- immunology
KW - Lymphocyte Activation -- drug effects
KW - Bone Marrow Cells -- metabolism
KW - Doxorubicin -- pharmacology
KW - Lymphocyte Activation -- immunology
KW - Th1 Cells -- drug effects
KW - T-Lymphocytes, Regulatory -- immunology
KW - Chelating Agents -- pharmacology
KW - Antineoplastic Agents -- immunology
KW - Apoptosis -- drug effects
KW - Myeloid Cells -- immunology
KW - Apoptosis -- immunology
KW - Myeloid Cells -- drug effects
KW - Copper -- pharmacology
KW - Copper -- immunology
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-11-10
N1 - Date created - 2014-03-20
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.3109/08923973.2014.897727
ER -
TY - JOUR
T1 - Safety and efficacy evaluation of albumin-bound paclitaxel.
AN - 1508942012; 24559090
AB - Nanoparticle albumin-bound paclitaxel (nab-paclitaxel) is a novel solvent-free formulation of paclitaxel, which was developed to avoid toxicities associated with Cremophor EL® vehicle used in solvent-based paclitaxel. It is approved as monotherapy for treatment of metastatic breast cancer (MBC) in Europe and the US; in combination therapy for non-small-cell lung cancer (NSCLC) and for first-line treatment of advanced pancreatic cancer (PC) only in the US. The European Medicines Agency has recently released only a positive opinion for use of nab-paclitaxel in PC.
This review reports the clinical findings and the safety data of nab-paclitaxel for MBC, NSCLC and PC. In MBC, nab-paclitaxel has demonstrated a good safety and an efficacy profile compared with other taxanes, but no strong data on overall survival are available. Considering the role of markers or predictive factors for nab-paclitaxel effectiveness in the metastatic setting would be useful. In PC, nab-paclitaxel and gemcitabine represent a new therapeutic choice with significant improvement in survival. In a Phase III study with NSCLC patients, nab-paclitaxel showed better results in a subgroup of patients with squamous histology, for whom results with conventional therapies are still poor and improved therapeutic options are needed.
JF - Expert opinion on drug safety
AU - Cecco, Sara
AU - Aliberti, Maria
AU - Baldo, Paolo
AU - Giacomin, Elisa
AU - Leone, Roberto
AD - CRO Aviano National Cancer Institute, Hospital Pharmacy , Via F. Gallini, 2, 33081, Aviano , Italy.
Y1 - 2014/04//
PY - 2014
DA - April 2014
SP - 511
EP - 520
VL - 13
IS - 4
KW - Albumin-Bound Paclitaxel
KW - 0
KW - Albumins
KW - Antineoplastic Agents
KW - Paclitaxel
KW - P88XT4IS4D
KW - Index Medicus
KW - Albumins -- adverse effects
KW - Clinical Trials, Phase III as Topic
KW - Humans
KW - Albumins -- therapeutic use
KW - Neoplasms -- drug therapy
KW - Paclitaxel -- adverse effects
KW - Paclitaxel -- therapeutic use
KW - Antineoplastic Agents -- therapeutic use
KW - Antineoplastic Agents -- adverse effects
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Expert+opinion+on+drug+safety&rft.atitle=Safety+and+efficacy+evaluation+of+albumin-bound+paclitaxel.&rft.au=Cecco%2C+Sara%3BAliberti%2C+Maria%3BBaldo%2C+Paolo%3BGiacomin%2C+Elisa%3BLeone%2C+Roberto&rft.aulast=Cecco&rft.aufirst=Sara&rft.date=2014-04-01&rft.volume=13&rft.issue=4&rft.spage=511&rft.isbn=&rft.btitle=&rft.title=Expert+opinion+on+drug+safety&rft.issn=1744-764X&rft_id=info:doi/10.1517%2F14740338.2014.893293
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-11-10
N1 - Date created - 2014-03-19
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1517/14740338.2014.893293
ER -
TY - JOUR
T1 - Phase I/II study of erlotinib and temsirolimus for patients with recurrent malignant gliomas: North American Brain Tumor Consortium trial 04-02.
AN - 1508677717; 24470557
AB - Inhibition of epidermal growth factor receptor (EGFR) and the mechanistic target of rapamycin (mTOR) may have synergistic antitumor effects in high-grade glioma patients.
We conducted a phase I/II study of the EGFR inhibitor erlotinib (150 mg/day) and the mTOR inhibitor temsirolimus. Patients initially received temsirolimus 50 mg weekly, and the dose adjusted based on toxicities. In the phase II component, the primary endpoint was 6-month progression-free survival (PFS6) among glioblastoma patients. Twenty-two patients enrolled in phase I, 47 in phase II. Twelve phase I patients treated at the maximum tolerated dosage were included in the phase II cohort for analysis. The maximum tolerated dosage was 15 mg temsirolimus weekly with erlotinib 150 mg daily. Dose-limiting toxicities were rash and mucositis. Among 42 evaluable glioblastoma patients, 12 (29%) achieved stable disease, but there were no responses, and PFS6 was 13%. Among 16 anaplastic glioma patients, 1 (6%) achieved complete response, 1 (6%) partial response, and 2 (12.5%) stable disease, with PFS6 of 8%. Tumor levels of both drugs were low, and posttreatment tissue in 3 patients showed no reduction in the mTOR target phosphorylated (phospho-)S6(S235/236) but possible compensatory increase in phospho-Akt(S473). Presence of EGFR variant III, phospho-EGFR, and EGFR amplification did not correlate with survival, but patients with elevated phospho-extracellular signal-regulated kinase or reduced phosphatase and tensin homolog protein expression had decreased progression-free survival at 4 months.
Because of increased toxicity, the maximum tolerated dosage of temsirolimus in combination with erlotinib proved lower than expected. Insufficient tumor drug levels and redundant signaling pathways may partly explain the minimal antitumor activity noted.
JF - Neuro-oncology
AU - Wen, Patrick Y
AU - Chang, Susan M
AU - Lamborn, Kathleen R
AU - Kuhn, John G
AU - Norden, Andrew D
AU - Cloughesy, Timothy F
AU - Robins, H Ian
AU - Lieberman, Frank S
AU - Gilbert, Mark R
AU - Mehta, Minesh P
AU - Drappatz, Jan
AU - Groves, Morris D
AU - Santagata, Sandro
AU - Ligon, Azra H
AU - Yung, W K Alfred
AU - Wright, John J
AU - Dancey, Janet
AU - Aldape, Kenneth D
AU - Prados, Michael D
AU - Ligon, Keith L
AD - Center for Neuro-Oncology, Dana Farber/Brigham and Women's Cancer Center, Boston, Massachusetts (P.Y.W., A.D.N., J.D.); Department of Neurosurgery, University of California, San Francisco, San Francisco, California (S.M.C., K.R.L., M.D.P.); University of Texas Health Science Center, San Antonio, Texas (J.G.K.); Division of Neuro-Oncology, Department of Neurology, University of California, Los Angeles, Los Angeles, California (T.F.C.); University of Wisconsin, Madison Wisconsin (H.I.R., M.P.M.); Neurooncology Program, Division of Hematology/Oncology, University of Pittsburgh Medical Center Cancer Pavilion, Pittsburgh, Pennsylvania (F.S.L.); Division of Neuro-Oncology, MD Anderson Cancer Center, Houston, Texas (M.R.G., M.D.G., W.K.A.Y., K.D.A.); Center for Molecular Oncologic Pathology, Dana Farber/Brigham and Women's Cancer Center, Boston, Massachusetts (S.S., A.H.L.); Department of Pathology, Brigham and Women's Hospital, Boston, Massachusetts (S.S., A.H.L., K.L.L.); Investigational Drug Branch, Cancer Therapy Evaluation Program, National Cancer Institute, Bethesda, Maryland (J.D.*, J.J.W.).
Y1 - 2014/04//
PY - 2014
DA - April 2014
SP - 567
EP - 578
VL - 16
IS - 4
KW - Quinazolines
KW - 0
KW - temsirolimus
KW - 624KN6GM2T
KW - Erlotinib Hydrochloride
KW - DA87705X9K
KW - Sirolimus
KW - W36ZG6FT64
KW - Index Medicus
KW - epidermal growth factor
KW - clinical trial
KW - anaplastic glioma
KW - glioblastoma
KW - erlotinib
KW - Young Adult
KW - Sirolimus -- administration & dosage
KW - Neoplasm Staging
KW - Humans
KW - Prognosis
KW - Aged
KW - Tissue Distribution
KW - Quinazolines -- administration & dosage
KW - Survival Rate
KW - Adult
KW - Follow-Up Studies
KW - Middle Aged
KW - Female
KW - Male
KW - Sirolimus -- analogs & derivatives
KW - Brain Neoplasms -- pathology
KW - Glioma -- pathology
KW - Glioma -- drug therapy
KW - Brain Neoplasms -- drug therapy
KW - Neoplasm Recurrence, Local -- drug therapy
KW - Brain Neoplasms -- mortality
KW - Antineoplastic Combined Chemotherapy Protocols -- pharmacokinetics
KW - Glioma -- mortality
KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use
KW - Neoplasm Recurrence, Local -- pathology
KW - Neoplasm Recurrence, Local -- mortality
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-11-06
N1 - Date created - 2014-03-18
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/neuonc/not247
ER -
TY - JOUR
T1 - Species and gender differences in the carcinogenic activity of trimethylolpropane triacrylate in rats and mice.
AN - 1508423030; 24503412
AB - Trimethylolpropane triacrylate (TMPTA) is a multifunctional monomer with industrial applications. To determine the carcinogenic potential, male and female F344/N rats and B6C3F1/N mice were administered TMPTA (0, 0.3, 1.0, or 3.0mg/kg) in acetone dermally for 2 years. There were no differences in the body weights and survival in the treated animals compared to controls. Nonneoplastic skin lesions at the site of application included epidermal hyperplasia and hyperkeratosis in both rats and mice. There were no incidences of tumors at the site of application in rats and mice. Rare malignant liver neoplasms were observed in female mice that included hepatoblastoma in the 0.3 and 3.0mg/kg groups, and hepatocholangiocarcinoma in the 1.0 and 3.0mg/kg groups. The incidences of uterine stromal polyp and stromal polyp or stromal sarcoma (combined) in female mice occurred with positive trends and the incidences were significantly increased in the 3.0mg/kg group. A marginal increase in the incidences of malignant mesothelioma in male rats may have been related to TMPTA treatment. In conclusion, our studies show that TMPTA is a dermal irritant in both rats and mice of either sex. Increased incidences of tumor formation were observed in female mice and male rats.
Published by Elsevier Ltd.
JF - Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
AU - Surh, Inok
AU - Rao, Deepa B
AU - Cesta, Mark F
AU - Hébert, Charles D
AU - Mann, Jill F
AU - Cunny, Helen
AU - Kissling, Grace E
AU - Malarkey, David
AU - Chhabra, Rajendra S
AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA. Electronic address: surhi@niehs.nih.gov. ; National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA; Integrated Laboratory Systems, Inc., Research Triangle Park, NC 27709, USA. ; National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA. ; Southern Research Institute, Birmingham, AL 35255, USA.
Y1 - 2014/04//
PY - 2014
DA - April 2014
SP - 254
EP - 261
VL - 66
KW - Acrylates
KW - 0
KW - Carcinogens
KW - trimethylolpropane triacrylate
KW - 4B67KGL96S
KW - Index Medicus
KW - Skin
KW - Carcinogenicity
KW - Uterine
KW - Trimethylolpropane triacrylate
KW - Liver
KW - Rats
KW - Animals
KW - Rats, Inbred F344
KW - Mice
KW - Species Specificity
KW - Male
KW - Female
KW - Sex Factors
KW - Carcinogens -- toxicity
KW - Acrylates -- toxicity
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-02-05
N1 - Date created - 2014-03-17
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.fct.2014.01.048
ER -
TY - JOUR
T1 - Adjuvant high-dose chemotherapy with autologous hematopoietic stem cell support for high-risk primary breast cancer: results from the Italian national registry.
AN - 1508414648; 24374214
AB - The efficacy of high-dose chemotherapy (HDC) and autologous hemopoietic progenitor cell transplantation (AHPCT) for breast cancer (BC) patients has been an area of intense controversy among the medical oncology community. The aim of this study was to assess toxicity and efficacy of this procedure in a large cohort of high-risk primary BC patients who underwent AHPCT in Italy. A total of 1183 patients receiving HDC for high-risk BC (HRBC) (>3 positive nodes) were identified in the Italian registry. The median age was 46 years, 62% of patients were premenopausal at treatment, 60.1% had endocrine-responsive tumors, and 20.7% had a human epidermal growth factor receptor 2 (HER2)-positive tumor. The median number of positive lymph nodes (LN) at surgery was 15, with 71.5% of patients having ≥ 10 positive nodes. Seventy-three percent received an alkylating agent-based HDC as a single procedure, whereas 27% received epirubicin or mitoxantrone-containing HDC, usually within a multitransplantation program. The source of stem cells was peripheral blood in the vast majority of patients. Transplantation-related mortality was .8%, whereas late cardiac and secondary tumor-related mortality were around 1%, overall. With a median follow-up of 79 months, median disease-free and overall survival (OS) in the entire population were 101 and 134 months, respectively. Subgroup analysis demonstrated that OS was significantly better in patients with endocrine-responsive tumors and in patients receiving multiple transplantation procedures. HER2 status did not affect survival probability. The size of the primary tumor and number of involved LN negatively affected OS. Adjuvant HDC with AHPCT has a low mortality rate and provides impressive long-term survival rates in patients with high-risk primary BC. Our results suggest that this treatment modality should be proposed in selected HRBC patients and further investigated in clinical trials.
Copyright © 2014 American Society for Blood and Marrow Transplantation. Published by Elsevier Inc. All rights reserved.
JF - Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
AU - Pedrazzoli, Paolo
AU - Martinelli, Giovanni
AU - Gianni, Alessandro Massimo
AU - Da Prada, Gian Antonio
AU - Ballestrero, Alberto
AU - Rosti, Giovanni
AU - Frassineti, Giovanni Luca
AU - Aieta, Michele
AU - Secondino, Simona
AU - Cinieri, Saverio
AU - Fedele, Roberta
AU - Bengala, Carmelo
AU - Bregni, Marco
AU - Grasso, Donatella
AU - De Giorgi, Ugo
AU - Lanza, Francesco
AU - Castagna, Luca
AU - Bruno, Barbara
AU - Martino, Massimo
AU - of Gruppo Italiano per il Trapianto di Midollo Osseo, Cellule staminali emopoietiche e terapia cellulare (GITMO) – Sezione Tumori Solidi
AD - Medical Oncology, IRCCS Foundation, San Matteo Hospital, Pavia, Italy. ; Medical Oncology, European Institute of Oncology, Milan, Italy. ; Medical Oncology, IRCCS Foundation, National Cancer Institute, Milan, Italy. ; Medical Oncology, IRCCS Maugeri Foundation, Pavia, Italy. ; Department of Internal Medicine, University Hospital, Genova, Italy. ; Medical Oncology, Civil Hospital, Ravenna, Italy. ; Department of Medical Oncology, IRCCS Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori, Meldola, Italy. ; Medical Oncology, IRCCS Casa Sollievo della Sofferenza, San Giovanni Rotondo (FG), Italy. ; Medical Oncology, Niguarda Ca', Granda Hospital, Milan, Italy. ; Hematology and Bone Marrow Transplant Unit, Azienda Ospedaliera "BMM", Reggio Calabria, Italy. ; Medical Oncology, University Hospital, Pisa, Italy. ; Hematology Unit, San Raffaele Scientific Institute, Milan, Italy. ; Section of Hematology and Bone Marrow Transplant Unit, Cremona, Italy. ; Hematology Unit, Humanitas Cancer Center, Rozzano, Milan, Italy. ; National Registry GITMO & Data Managing, Ospedale San Martino, Genova, Italy. ; Hematology and Bone Marrow Transplant Unit, Azienda Ospedaliera "BMM", Reggio Calabria, Italy. Electronic address: dr.massimomartino@gmail.com. ; of Gruppo Italiano per il Trapianto di Midollo Osseo, Cellule staminali emopoietiche e terapia cellulare (GITMO) – Sezione Tumori Solidi
Y1 - 2014/04//
PY - 2014
DA - April 2014
SP - 501
EP - 506
VL - 20
IS - 4
KW - Antineoplastic Agents, Alkylating
KW - 0
KW - Epirubicin
KW - 3Z8479ZZ5X
KW - Mitoxantrone
KW - BZ114NVM5P
KW - ERBB2 protein, human
KW - EC 2.7.10.1
KW - Receptor, ErbB-2
KW - Index Medicus
KW - High-dose chemotherapy
KW - Autologous hematopoietic progenitor cell support
KW - High-risk breast cancer
KW - Receptor, ErbB-2 -- genetics
KW - Drug Administration Schedule
KW - Lymphatic Metastasis
KW - Humans
KW - Gene Expression
KW - Mitoxantrone -- administration & dosage
KW - Aged
KW - Antineoplastic Agents, Alkylating -- administration & dosage
KW - Transplantation, Autologous
KW - Italy
KW - Risk
KW - Adult
KW - Receptor, ErbB-2 -- immunology
KW - Middle Aged
KW - Epirubicin -- administration & dosage
KW - Female
KW - Survival Analysis
KW - Registries
KW - Breast Neoplasms -- immunology
KW - Breast Neoplasms -- mortality
KW - Peripheral Blood Stem Cell Transplantation
KW - Breast Neoplasms -- pathology
KW - Antineoplastic Combined Chemotherapy Protocols
KW - Breast Neoplasms -- therapy
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-11-03
N1 - Date created - 2014-03-17
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.bbmt.2013.12.569
ER -
TY - JOUR
T1 - Perilipin 5, a lipid droplet protein adapted to mitochondrial energy utilization.
AN - 1507791951; 24535284
AB - We summarize recent mechanistic and physiological studies related to the role of perilipin 5 (Plin5) in regulating lipid droplet accumulation and protection to fatty acids in tissues with high lipid oxidative metabolism.
Plin5 is a lipid droplet targeting protein that promotes association of lipid droplets with mitochondria and is most highly expressed in oxidative tissues, including cardiac and skeletal muscle. Recent in-vivo and in-vitro data indicate an important role for Plin5 in the regulation of cardiac lipid storage and function. Targeted overexpression of Plin5 in heart causes steatosis, mild mitochondria dysfunction, and hypertrophy in cardiac tissue, but without affecting cardiac function. In contrast, whole body ablation of Plin5 (Plin5 mice) reduces cardiac lipid droplet formation, increases cardiac fatty acid oxidation, and promotes cardiac dysfunction; cardiac defects can be prevented with antioxidative therapy. These data suggest a cytoprotective role for Plin5 to promote lipid storage but to limit fatty acid toxicity, parameters critical for tissues with high lipid oxidative metabolism. In-vivo and in-vitro data suggest that Plin5 is part of a cell-adaptive response to high lipid oxidative metabolism to protect lipid droplet storage against neutral lipases and, so, limit fatty acid accumulation. Although the specific mechanisms that underlie Plin5 lipid droplet storage protection in oxidative tissues remain to be fully elucidated, Plin5 provides a basis for the novel cytoprotective nature of lipid droplets.
JF - Current opinion in lipidology
AU - Kimmel, Alan R
AU - Sztalryd, Carole
AD - aLaboratory of Cellular and Developmental Biology (50/3351), National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland bThe Geriatric Research, Education and Clinical Center, Baltimore Veterans Affairs Healthcare Center, Division of Endocrinology, Department of Medicine, School of Medicine, University of Maryland, Baltimore, Maryland, USA.
Y1 - 2014/04//
PY - 2014
DA - April 2014
SP - 110
EP - 117
VL - 25
IS - 2
KW - Intracellular Signaling Peptides and Proteins
KW - 0
KW - Muscle Proteins
KW - Perilipin-5
KW - Plin5 protein, mouse
KW - Proteins
KW - lipid storage droplet protein 5, mouse
KW - Index Medicus
KW - Animals
KW - Humans
KW - Muscle Proteins -- metabolism
KW - Muscle Proteins -- genetics
KW - Organelles -- metabolism
KW - Intracellular Signaling Peptides and Proteins -- genetics
KW - Intracellular Signaling Peptides and Proteins -- metabolism
KW - Mitochondria -- metabolism
KW - Energy Metabolism
KW - Proteins -- metabolism
KW - Proteins -- genetics
KW - Lipid Metabolism
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-11-05
N1 - Date created - 2014-03-13
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1097/MOL.0000000000000057
ER -
TY - JOUR
T1 - Alterations of the lung methylome in allergic airway hyper-responsiveness.
AN - 1506407114; 24446183
AB - Asthma is a chronic airway disorder characterized by recurrent attacks of breathlessness and wheezing, affecting 300 million people around the world (available at: www.who.int). To date, genetic factors associated with asthma susceptibility have been unable to explain the full etiology of asthma. Recent studies have demonstrated that the epigenetic disruption of gene expression plays an equally important role in the development of asthma through interaction with our environment. We sensitized 6-week-old C57BL/6J mice with house-dust-mite (HDM) extracts intraperitoneally followed by 5 weeks of exposure to HDM challenges (three times a week) intratracheally. HDM-exposed mice showed an increase in airway hyper-responsiveness (AHR) and inflammation together with structural remodeling of the airways. We applied methylated DNA immunoprecipitation-next generation sequencing (MeDIP-seq) for profiling of DNA methylation changes in the lungs in response to HDM. We observed about 20 million reads by a single-run of massive parallel sequencing. We performed bioinformatics and pathway analysis on the raw sequencing data to identify differentially methylated candidate genes in HDM-exposed mice. Specifically, we have revealed that the transforming growth factor beta signaling pathway is epigenetically modulated by chronic exposure to HDM. Here, we demonstrated that a specific allergen may play a role in AHR through an epigenetic mechanism by disrupting the expression of genes in lungs that might be involved in airway inflammation and remodeling. Our findings provide new insights into the potential mechanisms by which environmental allergens induce allergic asthma and such insights may assist in the development of novel preventive and therapeutic options for this debilitative disease.
Copyright © 2014 Wiley Periodicals, Inc.
JF - Environmental and molecular mutagenesis
AU - Cheng, Robert Ys
AU - Shang, Yan
AU - Limjunyawong, Nathachit
AU - Dao, Tyna
AU - Das, Sandhya
AU - Rabold, Richard
AU - Sham, James Sk
AU - Mitzner, Wayne
AU - Tang, Wan-Yee
AD - Radiation Biology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States.
Y1 - 2014/04//
PY - 2014
DA - April 2014
SP - 244
EP - 255
VL - 55
IS - 3
KW - Transforming Growth Factor beta
KW - 0
KW - Index Medicus
KW - house dust mite
KW - airway hyperresponsiveness
KW - asthma
KW - DNA methylation
KW - next generation sequencing
KW - Animals
KW - Pyroglyphidae
KW - Immunoprecipitation
KW - Mice
KW - Computational Biology
KW - Epigenesis, Genetic
KW - Inflammation
KW - Gene Expression Profiling
KW - Cells, Cultured
KW - Bronchoalveolar Lavage Fluid
KW - Mice, Inbred C57BL
KW - Trachea -- metabolism
KW - Transforming Growth Factor beta -- metabolism
KW - Signal Transduction
KW - Male
KW - High-Throughput Nucleotide Sequencing
KW - Lung -- immunology
KW - Hypersensitivity -- immunology
KW - Asthma -- metabolism
KW - DNA Methylation
KW - Lung -- metabolism
KW - Hypersensitivity -- metabolism
KW - Asthma -- immunology
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1506407114?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+and+molecular+mutagenesis&rft.atitle=Alterations+of+the+lung+methylome+in+allergic+airway+hyper-responsiveness.&rft.au=Cheng%2C+Robert+Ys%3BShang%2C+Yan%3BLimjunyawong%2C+Nathachit%3BDao%2C+Tyna%3BDas%2C+Sandhya%3BRabold%2C+Richard%3BSham%2C+James+Sk%3BMitzner%2C+Wayne%3BTang%2C+Wan-Yee&rft.aulast=Cheng&rft.aufirst=Robert&rft.date=2014-04-01&rft.volume=55&rft.issue=3&rft.spage=244&rft.isbn=&rft.btitle=&rft.title=Environmental+and+molecular+mutagenesis&rft.issn=1098-2280&rft_id=info:doi/10.1002%2Fem.21851
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-05-01
N1 - Date created - 2014-03-10
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1002/em.21851
ER -
TY - JOUR
T1 - High miR-21 expression from FFPE tissues is associated with poor survival and response to adjuvant chemotherapy in colon cancer
AN - 1505334743; 19297133
AB - Colon cancer (CC) is a leading cause of cancer mortality. Novel biomarkers are needed to identify CC patients at high risk of recurrence and those who may benefit from therapeutic intervention. The aim of this study is to investigate if miR-21 expression from RNA isolated from formalin-fixed paraffin-embedded (FFPE) tissue sections is associated with prognosis and therapeutic outcome for patients with CC. The expression of miR-21 was measured by quantitative reverse transcriptase-polymerase chain reaction in a Japanese cohort (stage I-IV, n = 156) and a German cohort (stage II, n = 145). High miR-21 expression in tumors was associated with poor survival in both the stage II/III Japanese (p = 0.0008) and stage II German (p = 0.047) cohorts. These associations were independent of other clinical covariates in multivariable models. Receipt of adjuvant chemotherapy was not beneficial in patients with high miR-21 in either cohort. In the Japanese cohort, high miR-21 expression was significantly associated with poor therapeutic outcome (p = 0.0001) and adjuvant therapy was associated with improved survival in patients with low miR-21 (p = 0.001). These results suggest that miR-21 is a promising biomarker to identify patients with poor prognosis and can be accurately measured in FFPE tissues. The expression of miR-21 may also identify patients who will benefit from adjuvant chemotherapy. What's new? While many stage II colorectal cancer patients benefit from adjuvant therapy, others may be harmed, making the decision to use additional chemotherapy in these populations controversial. This study describes a candidate biomarker, miR-21, that could help overcome this problem. High expression of miR-21 in formalin-fixed paraffin-embedded (FFPE) tissues was associated with poor survival in two independent cohorts of colon cancer patients from Japan and Germany. Low miR-21 expression, on the other hand, was associated with improved survival with adjuvant therapy.
JF - International Journal of Cancer
AU - Oue, Naohide
AU - Anami, Katsuhiro
AU - Schetter, Aaron J
AU - Moehler, Markus
AU - Okayama, Hirokazu
AU - Khan, Mohammed A
AU - Bowman, Elise D
AU - Mueller, Annett
AU - Schad, Arno
AU - Shimomura, Manabu
AU - Hinoi, Takao
AU - Aoyagi, Kazuhiko
AU - Sasaki, Hiroki
AU - Okajima, Masazumi
AU - Ohdan, Hideki
AU - Galle, Peter R
AU - Yasui, Wataru
AU - Harris, Curtis C
AD - Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD.
Y1 - 2014/04//
PY - 2014
DA - Apr 2014
SP - 1926
EP - 1934
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 134
IS - 8
SN - 0020-7136, 0020-7136
KW - Health & Safety Science Abstracts; Risk Abstracts
KW - Bioindicators
KW - Tissues
KW - Mortality
KW - Chemotherapy
KW - Survival
KW - Intervention
KW - Tumors
KW - Cancer
KW - Health risks
KW - Colorectal carcinoma
KW - Germany
KW - Japan
KW - H 11000:Diseases/Injuries/Trauma
KW - R2 23060:Medical and environmental health
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1505334743?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Cancer&rft.atitle=High+miR-21+expression+from+FFPE+tissues+is+associated+with+poor+survival+and+response+to+adjuvant+chemotherapy+in+colon+cancer&rft.au=Oue%2C+Naohide%3BAnami%2C+Katsuhiro%3BSchetter%2C+Aaron+J%3BMoehler%2C+Markus%3BOkayama%2C+Hirokazu%3BKhan%2C+Mohammed+A%3BBowman%2C+Elise+D%3BMueller%2C+Annett%3BSchad%2C+Arno%3BShimomura%2C+Manabu%3BHinoi%2C+Takao%3BAoyagi%2C+Kazuhiko%3BSasaki%2C+Hiroki%3BOkajima%2C+Masazumi%3BOhdan%2C+Hideki%3BGalle%2C+Peter+R%3BYasui%2C+Wataru%3BHarris%2C+Curtis+C&rft.aulast=Oue&rft.aufirst=Naohide&rft.date=2014-04-01&rft.volume=134&rft.issue=8&rft.spage=1926&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.28522
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-03-01
N1 - Last updated - 2014-06-26
N1 - SubjectsTermNotLitGenreText - Bioindicators; Mortality; Tissues; Health risks; Chemotherapy; Colorectal carcinoma; Intervention; Survival; Tumors; Cancer; Germany; Japan
DO - http://dx.doi.org/10.1002/ijc.28522
ER -
TY - JOUR
T1 - Telmisartan ameliorates glutamate-induced neurotoxicity: roles of AT(1) receptor blockade and PPARγ activation.
AN - 1504149624; 24316465
AB - Sartans (Angiotensin II AT(1) Receptor Blockers, ARBs) are powerful neuroprotective agents in vivo and protect against IL-1β neurotoxicity in vitro. The purpose of this research was to determine the extent of sartan neuroprotection against glutamate excitotoxicity, a common cause of neuronal injury and apoptosis. The results show that sartans are neuroprotective, significantly reducing glutamate-induced neuronal injury and apoptosis in cultured rat primary cerebellar granule cells (CGCs). Telmisartan was the most potent sartan studied, with an order of potency telmisartan > candesartan > losartan > valsartan. Mechanisms involved reduction of pro-apoptotic caspase-3 activation, protection of the survival PI3K/Akt/GSK-3β pathway and prevention of glutamate-induced ERK1/2 activation. NMDA receptor stimulation was essential for glutamate-induced cell injury and apoptosis. Participation of AT(1A) receptor was supported by glutamate-induced upregulation of AT(1A) gene expression and AT(1) receptor binding. Conversely, AT(1B) or AT(2) receptors played no role. Glutamate-induced neuronal injury and the neuroprotective effect of telmisartan were decreased, but not abolished, in CGCs obtained from AT(1A) knock-out mice. This indicates that although AT(1) receptors are necessary for glutamate to exert its full neurotoxic potential, part of the neuroprotective effect of telmisartan is independent of AT(1) receptor blockade. PPARγ activation was also involved in the neuroprotective effects of telmisartan, as telmisartan enhanced PPARγ nuclear translocation and the PPARγ antagonist GW9662 partially reversed the neuroprotective effects of telmisartan. The present results substantiate the therapeutic use of sartans, in particular telmisartan, in neurodegenerative diseases and traumatic brain disorders where glutamate neurotoxicity plays a significant role. Published by Elsevier Ltd.
JF - Neuropharmacology
AU - Wang, Juan
AU - Pang, Tao
AU - Hafko, Roman
AU - Benicky, Julius
AU - Sanchez-Lemus, Enrique
AU - Saavedra, Juan M
AD - Section on Pharmacology, Division of Intramural Research Programs, National Institute of Mental Health, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, 20892, USA. Electronic address: jw543@georgetown.edu. ; Section on Pharmacology, Division of Intramural Research Programs, National Institute of Mental Health, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, 20892, USA; New Drug Screening Center, China Pharmaceutical University, Nanjing 210009, PR China. ; Section on Pharmacology, Division of Intramural Research Programs, National Institute of Mental Health, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, 20892, USA. ; Section on Pharmacology, Division of Intramural Research Programs, National Institute of Mental Health, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, 20892, USA. Electronic address: jb2304@georgetown.edu. ; Section on Pharmacology, Division of Intramural Research Programs, National Institute of Mental Health, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, 20892, USA. Electronic address: scientificsupport@mesoscale.com. ; Section on Pharmacology, Division of Intramural Research Programs, National Institute of Mental Health, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, 20892, USA; Department of Pharmacology and Physiology, Georgetown University Medical Center, Washington, DC 20057, USA. Electronic address: jms522@georgetown.edu.
Y1 - 2014/04//
PY - 2014
DA - April 2014
SP - 249
EP - 261
VL - 79
KW - Agtr1a protein, mouse
KW - 0
KW - Angiotensin II Type 1 Receptor Blockers
KW - Benzimidazoles
KW - Benzoates
KW - Neuroprotective Agents
KW - PPAR gamma
KW - Receptor, Angiotensin, Type 1
KW - Glutamic Acid
KW - 3KX376GY7L
KW - telmisartan
KW - U5SYW473RQ
KW - Index Medicus
KW - Apoptosis
KW - Angiotensin II AT(1) Receptor Blockers
KW - Neuroprotection
KW - Telmisartan
KW - PPARγ
KW - Glutamate neurotoxicity
KW - Animals
KW - Apoptosis -- physiology
KW - Mice
KW - Mice, Transgenic
KW - Angiotensin II Type 1 Receptor Blockers -- pharmacology
KW - Cerebellum -- metabolism
KW - Mice, Knockout
KW - Rats
KW - Rats, Sprague-Dawley
KW - Cells, Cultured
KW - Cerebellum -- drug effects
KW - Apoptosis -- drug effects
KW - Mice, Inbred C57BL
KW - Female
KW - Male
KW - Glutamic Acid -- toxicity
KW - Receptor, Angiotensin, Type 1 -- genetics
KW - PPAR gamma -- antagonists & inhibitors
KW - Neurons -- drug effects
KW - Benzimidazoles -- pharmacology
KW - Neurons -- physiology
KW - PPAR gamma -- metabolism
KW - Receptor, Angiotensin, Type 1 -- metabolism
KW - Benzoates -- pharmacology
KW - Neuroprotective Agents -- pharmacology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuropharmacology&rft.atitle=Telmisartan+ameliorates+glutamate-induced+neurotoxicity%3A+roles+of+AT%281%29+receptor+blockade+and+PPAR%CE%B3+activation.&rft.au=Wang%2C+Juan%3BPang%2C+Tao%3BHafko%2C+Roman%3BBenicky%2C+Julius%3BSanchez-Lemus%2C+Enrique%3BSaavedra%2C+Juan+M&rft.aulast=Wang&rft.aufirst=Juan&rft.date=2014-04-01&rft.volume=79&rft.issue=&rft.spage=249&rft.isbn=&rft.btitle=&rft.title=Neuropharmacology&rft.issn=1873-7064&rft_id=info:doi/10.1016%2Fj.neuropharm.2013.11.022
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-12-03
N1 - Date created - 2014-03-03
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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Stroke. 2000 Oct;31(10):2478-86 [11022082]
Endocrinology. 2001 Sep;142(9):3880-9 [11517166]
J Pharmacol Exp Ther. 2002 May;301(2):494-500 [11961048]
J Neurotrauma. 2002 May;19(5):627-38 [12042097]
Stroke. 2002 Sep;33(9):2297-303 [12215602]
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Cerebellum. 2002 Jan-Mar;1(1):41-55 [12879973]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.neuropharm.2013.11.022
ER -
TY - JOUR
T1 - 9-Cis retinoic acid protects against methamphetamine-induced neurotoxicity in nigrostriatal dopamine neurons.
AN - 1503552675; 23884514
AB - Methamphetamine (MA) is a drug of abuse as well as a dopaminergic neurotoxin. 9-Cis retinoic acid (9cRA), a biologically active derivative of vitamin A, has protective effects against damage caused by H(2)O(2) and oxygen-glucose deprivation in vitro as well as infarction and terminal deoxynucleotidyl transferase-mediated dNTP nick-end labeling (TUNEL) labeling in ischemic brain. The purpose of this study was to examine if there was a protective role for 9cRA against MA toxicity in nigrostriatal dopaminergic neurons. Primary dopaminergic neurons, prepared from rat embryonic ventral mesencephalic tissue, were treated with MA. High doses of MA decreased tyrosine hydroxylase (TH) immunoreactivity while increasing TUNEL labeling. These toxicities were significantly reduced by 9cRA. 9cRA also inhibited the export of Nur77 from nucleus to cytosol, a response that activates apoptosis. The interaction of 9cRA and MA in vivo was next examined in adult rats. 9cRA was delivered intracerebroventricularly; MA was given (5 mg/kg, 4×) one day later. Locomotor behavior was measured 2 days after surgery for a period of 48 h. High doses of MA significantly reduced locomotor activity and TH immunoreactivity in striatum. Administration of 9cRA antagonized these changes. Previous studies have shown that 9cRA can induce bone morphogenetic protein-7 (BMP7) expression and that administration of BMP7 attenuates MA toxicity. We demonstrated that MA treatment significantly reduced BMP7 mRNA expression in nigra. Noggin (a BMP antagonist) antagonized 9cRA-induced behavioral recovery and 9cRA-induced normalization of striatal TH levels. Our data suggest that 9cRA has a protective effect against MA-mediated neurodegeneration in dopaminergic neurons via upregulation of BMP.
JF - Neurotoxicity research
AU - Reiner, David J
AU - Yu, Seong-Jin
AU - Shen, Hui
AU - He, Yi
AU - Bae, Eunkyung
AU - Wang, Yun
AD - Neural Protection and Regeneration Section, Intramural Research Program, National Institute on Drug Abuse, NIH, Baltimore, MD, 21224, USA.
Y1 - 2014/04//
PY - 2014
DA - April 2014
SP - 248
EP - 261
VL - 25
IS - 3
KW - Bmp7 protein, rat
KW - 0
KW - Bone Morphogenetic Protein 7
KW - Carrier Proteins
KW - Neuroprotective Agents
KW - Nr4a1 protein, rat
KW - Nuclear Receptor Subfamily 4, Group A, Member 1
KW - RNA, Messenger
KW - noggin protein
KW - 148294-77-3
KW - alitretinoin
KW - 1UA8E65KDZ
KW - Methamphetamine
KW - 44RAL3456C
KW - Tretinoin
KW - 5688UTC01R
KW - Tyrosine 3-Monooxygenase
KW - EC 1.14.16.2
KW - Index Medicus
KW - Animals
KW - Bone Morphogenetic Protein 7 -- metabolism
KW - Tyrosine 3-Monooxygenase -- metabolism
KW - Carrier Proteins -- metabolism
KW - Nerve Degeneration -- physiopathology
KW - Substantia Nigra -- drug effects
KW - Nerve Degeneration -- chemically induced
KW - Nuclear Receptor Subfamily 4, Group A, Member 1 -- metabolism
KW - Motor Activity -- physiology
KW - Rats
KW - Nerve Degeneration -- drug therapy
KW - Substantia Nigra -- physiopathology
KW - Rats, Sprague-Dawley
KW - Corpus Striatum -- physiopathology
KW - RNA, Messenger -- metabolism
KW - Cells, Cultured
KW - Corpus Striatum -- drug effects
KW - Motor Activity -- drug effects
KW - Male
KW - Tretinoin -- pharmacology
KW - Dopaminergic Neurons -- drug effects
KW - Neurotoxicity Syndromes -- prevention & control
KW - Neurotoxicity Syndromes -- physiopathology
KW - Dopaminergic Neurons -- physiology
KW - Neuroprotective Agents -- pharmacology
KW - Methamphetamine -- toxicity
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-11-05
N1 - Date created - 2014-02-27
N1 - Date revised - 2017-01-13
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1007/s12640-013-9413-4
ER -
TY - JOUR
T1 - Molecular cloning and knockdown of galactocerebrosidase in zebrafish: new insights into the pathogenesis of Krabbe's disease.
AN - 1501834079; 24463171
AB - The lysosomal hydrolase galactocerebrosidase (GALC) catalyzes the removal of galactose from galactosylceramide and from other sphingolipids. GALC deficiency is responsible for globoid cell leukodystrophy (GLD), or Krabbe's disease, an early lethal inherited neurodegenerative disorder characterized by the accumulation of the neurotoxic metabolite psychosine in the central nervous system (CNS). The poor outcome of current clinical treatments calls for novel model systems to investigate the biological impact of GALC down-regulation and for the search of novel therapeutic strategies in GLD. Zebrafish (Danio rerio) represents an attractive vertebrate model for human diseases. Here, lysosomal GALC activity was demonstrated in the brain of zebrafish adults and embryos. Accordingly, we identified two GALC co-orthologs (named galca and galcb) dynamically co-expressed in CNS during zebrafish development. Both genes encode for lysosomal enzymes endowed with GALC activity. Single down-regulation of galca or galcb by specific antisense morpholino oligonucleotides results in a partial decrease of GALC activity in zebrafish embryos that was abrogated in double galca/galcb morphants. However, no psychosine accumulation was observed in galca/galcb double morphants. Nevertheless, double galca/galcb knockdown caused reduction and partial disorganization of the expression of the early neuronal marker neuroD and an increase of apoptotic events during CNS development. These observations provide new insights into the pathogenesis of GLD, indicating that GALC loss-of-function may have pathological consequences in developing CNS independent of psychosine accumulation. Also, they underscore the potentiality of the zebrafish system in studying the pathogenesis of lysosomal neurodegenerative diseases, including GLD.
Copyright © 2014 Elsevier B.V. All rights reserved.
JF - Biochimica et biophysica acta
AU - Zizioli, Daniela
AU - Guarienti, Michela
AU - Tobia, Chiara
AU - Gariano, Giuseppina
AU - Borsani, Giuseppe
AU - Bresciani, Roberto
AU - Ronca, Roberto
AU - Giacopuzzi, Edoardo
AU - Preti, Augusto
AU - Gaudenzi, Germano
AU - Belleri, Mirella
AU - Di Salle, Emanuela
AU - Fabrias, Gemma
AU - Casas, Josefina
AU - Ribatti, Domenico
AU - Monti, Eugenio
AU - Presta, Marco
AD - Unit of Biotechnology, Department of Molecular and Translational Medicine, University of Brescia, Brescia, Italy. ; Unit of Oncology and Experimental Immunology, Department of Molecular and Translational Medicine, University of Brescia, Brescia, Italy. ; Unit of Biology and Genetics, Department of Molecular and Translational Medicine, University of Brescia, Brescia, Italy. ; Department of Biology, University of Milan, Milan, Italy. ; Research Unit on Bioactive Molecules (RUBAM), Department of Biomedicinal Chemistry, Institute for Advanced Chemistry of Catalonia (IQAC), Spanish Council for Scientific Research (CSIC), Barcelona, Spain. ; Department of Basic Biomedical Sciences, Unit of Human Anatomy and Histology, University of Bari, Bari, Italy; National Cancer Institute, Giovanni Paolo II, Bari, Italy. ; Unit of Oncology and Experimental Immunology, Department of Molecular and Translational Medicine, University of Brescia, Brescia, Italy. Electronic address: presta@med.unibs.it.
Y1 - 2014/04//
PY - 2014
DA - April 2014
SP - 665
EP - 675
VL - 1842
IS - 4
SN - 0006-3002, 0006-3002
KW - Galactosylceramidase
KW - EC 3.2.1.46
KW - Index Medicus
KW - Krabbe disease
KW - Embryonic development
KW - Sphingolipid
KW - Zebrafish
KW - Brain -- enzymology
KW - Animals
KW - Humans
KW - Brain -- embryology
KW - Disease Models, Animal
KW - Cloning, Molecular
KW - Leukodystrophy, Globoid Cell -- etiology
KW - Galactosylceramidase -- genetics
KW - Zebrafish -- metabolism
KW - Galactosylceramidase -- physiology
KW - Zebrafish -- embryology
KW - Leukodystrophy, Globoid Cell -- enzymology
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-04-23
N1 - Date created - 2014-02-24
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.bbadis.2014.01.008
ER -
TY - JOUR
T1 - Semiparametric Bayesian joint modeling of a binary and continuous outcome with applications in toxicological risk assessment.
AN - 1504450317; 24123309
AB - Many dose-response studies collect data on correlated outcomes. For example, in developmental toxicity studies, uterine weight and presence of malformed pups are measured on the same dam. Joint modeling can result in more efficient inferences than independent models for each outcome. Most methods for joint modeling assume standard parametric response distributions. However, in toxicity studies, it is possible that response distributions vary in location and shape with dose, which may not be easily captured by standard models. To address this issue, we propose a semiparametric Bayesian joint model for a binary and continuous response. In our model, a kernel stick-breaking process prior is assigned to the distribution of a random effect shared across outcomes, which allows flexible changes in distribution shape with dose shared across outcomes. The model also includes outcome-specific fixed effects to allow different location effects. In simulation studies, we found that the proposed model provides accurate estimates of toxicological risk when the data do not satisfy assumptions of standard parametric models. We apply our method to data from a developmental toxicity study of ethylene glycol diethyl ether.
Copyright © 2013 John Wiley & Sons, Ltd.
JF - Statistics in medicine
AU - Hwang, Beom Seuk
AU - Pennell, Michael L
AD - Biostatistics and Bioinformatics Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, U.S.A.
Y1 - 2014/03/30/
PY - 2014
DA - 2014 Mar 30
SP - 1162
EP - 1175
VL - 33
IS - 7
KW - Ethyl Ethers
KW - 0
KW - Ethylene Glycols
KW - ethylene glycol diethyl ether
KW - 629-14-1
KW - Index Medicus
KW - kernel stick-breaking process
KW - nonparametric Bayes
KW - benchmark dose
KW - developmental toxicology study
KW - Animals
KW - Ethylene Glycols -- toxicity
KW - Computer Simulation
KW - Mice
KW - Markov Chains
KW - Uterus -- pathology
KW - Monte Carlo Method
KW - Organ Size
KW - Female
KW - Pregnancy
KW - Ethyl Ethers -- toxicity
KW - Bayes Theorem
KW - Toxicology -- methods
KW - Models, Statistical
KW - Risk Assessment -- methods
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-11-06
N1 - Date created - 2014-03-04
N1 - Date revised - 2017-01-13
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1002/sim.6007
ER -
TY - JOUR
T1 - The steric gate of DNA polymerase ι regulates ribonucleotide incorporation and deoxyribonucleotide fidelity.
AN - 1511822636; 24532793
AB - Accurate DNA synthesis in vivo depends on the ability of DNA polymerases to select dNTPs from a nucleotide pool dominated by NTPs. High fidelity replicative polymerases have evolved to efficiently exclude NTPs while copying long stretches of undamaged DNA. However, to bypass DNA damage, cells utilize specialized low fidelity polymerases to perform translesion DNA synthesis (TLS). Of interest is human DNA polymerase ι (pol ι), which has been implicated in TLS of oxidative and UV-induced lesions. Here, we evaluate the ability of pol ι to incorporate NTPs during DNA synthesis. pol ι incorporates and extends NTPs opposite damaged and undamaged template bases in a template-specific manner. The Y39A "steric gate" pol ι mutant is considerably more active in the presence of Mn(2+) compared with Mg(2+) and exhibits a marked increase in NTP incorporation and extension, and surprisingly, it also exhibits increased dNTP base selectivity. Our results indicate that a single residue in pol ι is able to discriminate between NTPs and dNTPs during DNA synthesis. Because wild-type pol ι incorporates NTPs in a template-specific manner, certain DNA sequences may be "at risk" for elevated mutagenesis during pol ι-dependent TLS. Molecular modeling indicates that the constricted active site of wild-type pol ι becomes more spacious in the Y39A variant. Therefore, the Y39A substitution not only permits incorporation of ribonucleotides but also causes the enzyme to favor faithful Watson-Crick base pairing over mutagenic configurations.
JF - The Journal of biological chemistry
AU - Donigan, Katherine A
AU - McLenigan, Mary P
AU - Yang, Wei
AU - Goodman, Myron F
AU - Woodgate, Roger
AD - From the Laboratory of Genomic Integrity, NICHD and.
Y1 - 2014/03/28/
PY - 2014
DA - 2014 Mar 28
SP - 9136
EP - 9145
VL - 289
IS - 13
KW - DNA Primers
KW - 0
KW - Deoxyribonucleotides
KW - Ribonucleotides
KW - Tyrosine
KW - 42HK56048U
KW - Manganese
KW - 42Z2K6ZL8P
KW - DNA
KW - 9007-49-2
KW - DNA polymerase iota
KW - EC 2.7.7.-
KW - DNA-Directed DNA Polymerase
KW - EC 2.7.7.7
KW - Index Medicus
KW - DNA Synthesis
KW - DNA Repair
KW - Steric Gate Mutant
KW - DNA Polymerase Iota
KW - DNA-binding Protein
KW - Ribonucleotide Incorporation
KW - Y Family DNA Polymerase
KW - Mutagenesis
KW - Enzyme Kinetics
KW - Manganese -- pharmacology
KW - Models, Molecular
KW - DNA Damage
KW - DNA Primers -- genetics
KW - DNA -- metabolism
KW - Humans
KW - Catalytic Domain
KW - Amino Acid Sequence
KW - DNA -- biosynthesis
KW - Base Pairing
KW - Conserved Sequence
KW - DNA -- genetics
KW - Molecular Sequence Data
KW - DNA -- chemistry
KW - Substrate Specificity
KW - Mutation
KW - Ribonucleotides -- metabolism
KW - Deoxyribonucleotides -- metabolism
KW - DNA-Directed DNA Polymerase -- genetics
KW - DNA-Directed DNA Polymerase -- metabolism
KW - DNA-Directed DNA Polymerase -- chemistry
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-05-21
N1 - Date created - 2014-03-31
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1074/jbc.M113.545442
ER -
TY - JOUR
T1 - Epidemiologic contributions to recent cancer trends among HIV-infected people in the United States
AN - 1765982938; PQ0002610751
AB - Objective: HIV-infected people have elevated risk for some cancers. Changing incidence of these cancers over time may reflect changes in three factors: HIV population demographic structure (e.g. age distribution), general population (background) cancer rates, and HIV-associated relative risks. We assessed the contributions of these factors to time trends for 10 cancers during 1996-2010. Design: Population-based registry linkage study. Methods: We applied Poisson models to data from the U.S. HIV/AIDS Cancer Match Study to estimate annual percentage changes (APCs) in incidence rates of AIDS-defining cancers [ADCs: Kaposi sarcoma, non-Hodgkin lymphoma (NHL), and cervical cancer] and seven non-AIDS-defining cancers (NADCs). We evaluated HIV-infected cancer trends with and without adjustment for demographics, trends in background rates, and trends in standardized incidence ratios (SIRs, to capture relative risk). Results: Cancer rates among HIV-infected people rose over time for anal (APC 3.8%), liver (8.5%), and prostate (9.8%) cancers, but declined for Kaposi sarcoma (1996-2000: -29.3%; 2000-2010: -7.8%), NHL (1996-2003: -15.7%; 2003-2010: -5.5%), cervical cancer (-11.1%), Hodgkin lymphoma (-4.0%), and lung cancer (-2.8%). Breast and colorectal cancer incidence did not change over time. Based on comparison to adjusted models, changing demographics contributed to trends for Kaposi sarcoma and breast, colorectal, liver, lung, and prostate cancers (all P < 0.01). Trends in background rates were notable for liver (APC 5.6%) and lung (-3.2%) cancers. SIRs declined for ADCs, Hodgkin lymphoma (APC -3.2%), and lung cancer (-4.4%). Conclusion: Demographic shifts influenced several cancer trends among HIV-infected individuals. Falling relative risks largely explained ADC declines, while background incidence contributed to some NADC trends.
JF - AIDS
AU - Robbins, Hilary A
AU - Shiels, Meredith S
AU - Pfeiffer, Ruth M
AU - Engels, Eric A
AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, Maryland, USA, hilary.robbins@nih.gov
Y1 - 2014/03/27/
PY - 2014
DA - 2014 Mar 27
SP - 881
EP - 890
PB - Lippincott Williams & Wilkins, Inc, 530 Walnut Street Philadelphia PA 19106-3621 United States
VL - 28
IS - 6
SN - 0269-9370, 0269-9370
KW - Health & Safety Science Abstracts; Immunology Abstracts; Virology & AIDS Abstracts
KW - cancer
KW - HIV/AIDS
KW - statistical modeling
KW - trends
KW - United States
KW - Risk assessment
KW - Acquired immune deficiency syndrome
KW - Hodgkin's disease
KW - Cervical cancer
KW - Colorectal cancer
KW - Models
KW - Demography
KW - Non-Hodgkin's lymphoma
KW - adenomatous polyposis coli
KW - Risk factors
KW - Lymphoma
KW - Lung cancer
KW - Age composition
KW - Data processing
KW - Cancer
KW - Health risks
KW - USA
KW - Prostate cancer
KW - Human immunodeficiency virus
KW - Sarcoma
KW - Liver
KW - Breast cancer
KW - Standards
KW - V 22360:AIDS and HIV
KW - H 11000:Diseases/Injuries/Trauma
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1765982938?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS&rft.atitle=Epidemiologic+contributions+to+recent+cancer+trends+among+HIV-infected+people+in+the+United+States&rft.au=Robbins%2C+Hilary+A%3BShiels%2C+Meredith+S%3BPfeiffer%2C+Ruth+M%3BEngels%2C+Eric+A&rft.aulast=Robbins&rft.aufirst=Hilary&rft.date=2014-03-27&rft.volume=28&rft.issue=6&rft.spage=881&rft.isbn=&rft.btitle=&rft.title=AIDS&rft.issn=02699370&rft_id=info:doi/10.1097%2FQAD.0000000000000163
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2016-02-01
N1 - Last updated - 2016-03-17
N1 - SubjectsTermNotLitGenreText - Risk assessment; Age composition; Acquired immune deficiency syndrome; Hodgkin's disease; Data processing; Cervical cancer; Colorectal cancer; Models; Demography; Prostate cancer; adenomatous polyposis coli; Liver; Sarcoma; Breast cancer; Lung cancer; Cancer; Non-Hodgkin's lymphoma; Health risks; Human immunodeficiency virus; Risk factors; Standards; Lymphoma; USA
DO - http://dx.doi.org/10.1097/QAD.0000000000000163
ER -
TY - CPAPER
T1 - Genetic Medicine in Uganda - The Children's National Medical Center and NIH Experience
T2 - 2014 Annual Clinical Genetics Meeting of the American College of Medical Genetics (ACMG 2014)
AN - 1518616882; 6286300
JF - 2014 Annual Clinical Genetics Meeting of the American College of Medical Genetics (ACMG 2014)
AU - Kruszka, Paul
Y1 - 2014/03/25/
PY - 2014
DA - 2014 Mar 25
KW - Uganda
KW - Children
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518616882?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Clinical+Genetics+Meeting+of+the+American+College+of+Medical+Genetics+%28ACMG+2014%29&rft.atitle=Genetic+Medicine+in+Uganda+-+The+Children%27s+National+Medical+Center+and+NIH+Experience&rft.au=Kruszka%2C+Paul&rft.aulast=Kruszka&rft.aufirst=Paul&rft.date=2014-03-25&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Clinical+Genetics+Meeting+of+the+American+College+of+Medical+Genetics+%28ACMG+2014%29&rft.issn=&rft_id=info:doi/
L2 - http://www.acmgmeeting.net/acmg2014/CUSTOM/images/client/2014/2014%20ACMG%20Program%20Guide.pdf
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-23
N1 - Last updated - 2014-04-24
ER -
TY - CPAPER
T1 - Glut1 Deficiency and other Metabolic Causes of Microcephaly - Recognizing Treatable Conditions
T2 - 2014 Annual Clinical Genetics Meeting of the American College of Medical Genetics (ACMG 2014)
AN - 1518616866; 6286410
JF - 2014 Annual Clinical Genetics Meeting of the American College of Medical Genetics (ACMG 2014)
AU - Wolfe, Lynne
Y1 - 2014/03/25/
PY - 2014
DA - 2014 Mar 25
KW - Microencephaly
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518616866?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Clinical+Genetics+Meeting+of+the+American+College+of+Medical+Genetics+%28ACMG+2014%29&rft.atitle=Glut1+Deficiency+and+other+Metabolic+Causes+of+Microcephaly+-+Recognizing+Treatable+Conditions&rft.au=Wolfe%2C+Lynne&rft.aulast=Wolfe&rft.aufirst=Lynne&rft.date=2014-03-25&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Clinical+Genetics+Meeting+of+the+American+College+of+Medical+Genetics+%28ACMG+2014%29&rft.issn=&rft_id=info:doi/
L2 - http://www.acmgmeeting.net/acmg2014/CUSTOM/images/client/2014/2014%20ACMG%20Program%20Guide.pdf
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-23
N1 - Last updated - 2014-04-24
ER -
TY - CPAPER
T1 - The Spectrum of Vascular Anomalies in Disorders of the P13K-AKT Pathway
T2 - 2014 Annual Clinical Genetics Meeting of the American College of Medical Genetics (ACMG 2014)
AN - 1518615274; 6286361
JF - 2014 Annual Clinical Genetics Meeting of the American College of Medical Genetics (ACMG 2014)
AU - Biesecker, Leslie
Y1 - 2014/03/25/
PY - 2014
DA - 2014 Mar 25
KW - Genetics
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518615274?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Clinical+Genetics+Meeting+of+the+American+College+of+Medical+Genetics+%28ACMG+2014%29&rft.atitle=The+Spectrum+of+Vascular+Anomalies+in+Disorders+of+the+P13K-AKT+Pathway&rft.au=Biesecker%2C+Leslie&rft.aulast=Biesecker&rft.aufirst=Leslie&rft.date=2014-03-25&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Clinical+Genetics+Meeting+of+the+American+College+of+Medical+Genetics+%28ACMG+2014%29&rft.issn=&rft_id=info:doi/
L2 - http://www.acmgmeeting.net/acmg2014/CUSTOM/images/client/2014/2014%20ACMG%20Program%20Guide.pdf
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-23
N1 - Last updated - 2014-04-24
ER -
TY - JOUR
T1 - A new approach to radial basis function approximation and its application to QSAR.
AN - 1510105943; 24451033
AB - We describe a novel approach to RBF approximation, which combines two new elements: (1) linear radial basis functions and (2) weighting the model by each descriptor's contribution. Linear radial basis functions allow one to achieve more accurate predictions for diverse data sets. Taking into account the contribution of each descriptor produces more accurate similarity values used for model development. The method was validated on 14 public data sets comprising nine physicochemical properties and five toxicity endpoints. We also compared the new method with five different QSAR methods implemented in the EPA T.E.S.T. program. Our approach, implemented in the program GUSAR, showed a reasonable accuracy of prediction and high coverage for all external test sets, providing more accurate prediction results than the comparison methods and even the consensus of these methods. Using our new method, we have created models for physicochemical and toxicity endpoints, which we have made freely available in the form of an online service at http://cactus.nci.nih.gov/chemical/apps/cap.
JF - Journal of chemical information and modeling
AU - Zakharov, Alexey V
AU - Peach, Megan L
AU - Sitzmann, Markus
AU - Nicklaus, Marc C
AD - CADD Group, Chemical Biology Laboratory, Center for Cancer Research, National Cancer Institute, National Institutes of Health , DHHS, NCI-Frederick, , 376 Boyles St., Frederick, Maryland 21702, United States.
Y1 - 2014/03/24/
PY - 2014
DA - 2014 Mar 24
SP - 713
EP - 719
VL - 54
IS - 3
KW - Index Medicus
KW - Rats
KW - Daphnia -- physiology
KW - Animals
KW - Daphnia -- drug effects
KW - Computer Simulation
KW - Neural Networks (Computer)
KW - Toxicity Tests
KW - Databases, Factual
KW - Cyprinidae -- physiology
KW - Tetrahymena -- drug effects
KW - Tetrahymena -- physiology
KW - Internet
KW - Software
KW - Quantitative Structure-Activity Relationship
KW - Algorithms
KW - Models, Biological
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510105943?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+chemical+information+and+modeling&rft.atitle=A+new+approach+to+radial+basis+function+approximation+and+its+application+to+QSAR.&rft.au=Zakharov%2C+Alexey+V%3BPeach%2C+Megan+L%3BSitzmann%2C+Markus%3BNicklaus%2C+Marc+C&rft.aulast=Zakharov&rft.aufirst=Alexey&rft.date=2014-03-24&rft.volume=54&rft.issue=3&rft.spage=713&rft.isbn=&rft.btitle=&rft.title=Journal+of+chemical+information+and+modeling&rft.issn=1549-960X&rft_id=info:doi/10.1021%2Fci400704f
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-11-24
N1 - Date created - 2014-03-24
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
J Chem Inf Comput Sci. 2004 Sep-Oct;44(5):1763-73 [15446835]
J Comput Aided Mol Des. 1997 Mar;11(2):135-42 [9089431]
SAR QSAR Environ Res. 2007 May-Jun;18(3-4):285-98 [17514571]
Methods Mol Biol. 2008;458:137-58 [19065809]
Chem Res Toxicol. 2009 Dec;22(12):1913-21 [19845371]
Mol Pharm. 2013 Apr 1;10(4):1224-35 [23305561]
J Agric Food Chem. 2011 Apr 13;59(7):2909-17 [20879794]
Eur J Med Chem. 2011 Sep;46(9):4374-82 [21802177]
Future Med Chem. 2012 Oct;4(15):1933-44 [23088274]
Chem Res Toxicol. 2012 Nov 19;25(11):2378-85 [23078046]
SAR QSAR Environ Res. 2009 Oct;20(7-8):679-709 [20024804]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1021/ci400704f
ER -
TY - CPAPER
T1 - Fetal Consequences of In Utero Antiretroviral (ARV) Nucleoside Reverse Transcriptase Inhibitor (NRTI) Exposures in Primates
T2 - 53rd Annual Meeting of the Society of Toxicology (SOT 2014)
AN - 1518614783; 6281379
JF - 53rd Annual Meeting of the Society of Toxicology (SOT 2014)
AU - Poirier, M
AU - Olivero, O
AU - Liu, Y
AU - Divi, R
AU - Woodward, R
Y1 - 2014/03/23/
PY - 2014
DA - 2014 Mar 23
KW - Antiviral agents
KW - Inhibitors
KW - Primates
KW - Antiretroviral agents
KW - Fetuses
KW - nucleoside reverse transcriptase inhibitors
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518614783?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=53rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2014%29&rft.atitle=Fetal+Consequences+of+In+Utero+Antiretroviral+%28ARV%29+Nucleoside+Reverse+Transcriptase+Inhibitor+%28NRTI%29+Exposures+in+Primates&rft.au=Poirier%2C+M%3BOlivero%2C+O%3BLiu%2C+Y%3BDivi%2C+R%3BWoodward%2C+R&rft.aulast=Poirier&rft.aufirst=M&rft.date=2014-03-23&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=53rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2014%29&rft.issn=&rft_id=info:doi/
L2 - http://www.toxicology.org/AI/Pub/Prog/2014Program.pdf
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-23
N1 - Last updated - 2014-04-24
ER -
TY - CPAPER
T1 - From Research to Regulatory Science: Toxicology Careers in Government
T2 - 53rd Annual Meeting of the Society of Toxicology (SOT 2014)
AN - 1518613249; 6281539
JF - 53rd Annual Meeting of the Society of Toxicology (SOT 2014)
AU - Germolec, D
Y1 - 2014/03/23/
PY - 2014
DA - 2014 Mar 23
KW - Careers
KW - Toxicology
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518613249?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=53rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2014%29&rft.atitle=From+Research+to+Regulatory+Science%3A+Toxicology+Careers+in+Government&rft.au=Germolec%2C+D&rft.aulast=Germolec&rft.aufirst=D&rft.date=2014-03-23&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=53rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2014%29&rft.issn=&rft_id=info:doi/
L2 - http://www.toxicology.org/AI/Pub/Prog/2014Program.pdf
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-23
N1 - Last updated - 2014-04-24
ER -
TY - CPAPER
T1 - Leadership--Doing the Right Things
T2 - 53rd Annual Meeting of the Society of Toxicology (SOT 2014)
AN - 1518613130; 6281582
JF - 53rd Annual Meeting of the Society of Toxicology (SOT 2014)
AU - Birnbaum, L
Y1 - 2014/03/23/
PY - 2014
DA - 2014 Mar 23
KW - Rights
KW - Lead
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518613130?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=53rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2014%29&rft.atitle=Leadership--Doing+the+Right+Things&rft.au=Birnbaum%2C+L&rft.aulast=Birnbaum&rft.aufirst=L&rft.date=2014-03-23&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=53rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2014%29&rft.issn=&rft_id=info:doi/
L2 - http://www.toxicology.org/AI/Pub/Prog/2014Program.pdf
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-23
N1 - Last updated - 2014-04-24
ER -
TY - CPAPER
T1 - The Office of Health Assessment and Translation Approach to Evidence Integration for Assessment of Noncancer Health Effects
T2 - 53rd Annual Meeting of the Society of Toxicology (SOT 2014)
AN - 1518611784; 6281524
JF - 53rd Annual Meeting of the Society of Toxicology (SOT 2014)
AU - Rooney, A
AU - Boyles, A
AU - Wolfe, M
AU - Thayer, K
Y1 - 2014/03/23/
PY - 2014
DA - 2014 Mar 23
KW - Integration
KW - Translation
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518611784?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=53rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2014%29&rft.atitle=The+Office+of+Health+Assessment+and+Translation+Approach+to+Evidence+Integration+for+Assessment+of+Noncancer+Health+Effects&rft.au=Rooney%2C+A%3BBoyles%2C+A%3BWolfe%2C+M%3BThayer%2C+K&rft.aulast=Rooney&rft.aufirst=A&rft.date=2014-03-23&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=53rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2014%29&rft.issn=&rft_id=info:doi/
L2 - http://www.toxicology.org/AI/Pub/Prog/2014Program.pdf
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-23
N1 - Last updated - 2014-04-24
ER -
TY - CPAPER
T1 - The Concepts and Methods for Stem Cells
T2 - 53rd Annual Meeting of the Society of Toxicology (SOT 2014)
AN - 1518609471; 6281297
JF - 53rd Annual Meeting of the Society of Toxicology (SOT 2014)
AU - Tokar, E
Y1 - 2014/03/23/
PY - 2014
DA - 2014 Mar 23
KW - Stem cells
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518609471?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=53rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2014%29&rft.atitle=The+Concepts+and+Methods+for+Stem+Cells&rft.au=Tokar%2C+E&rft.aulast=Tokar&rft.aufirst=E&rft.date=2014-03-23&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=53rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2014%29&rft.issn=&rft_id=info:doi/
L2 - http://www.toxicology.org/AI/Pub/Prog/2014Program.pdf
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-23
N1 - Last updated - 2014-04-24
ER -
TY - CPAPER
T1 - Stem Cells in Carcinogenesis
T2 - 53rd Annual Meeting of the Society of Toxicology (SOT 2014)
AN - 1518609431; 6281298
JF - 53rd Annual Meeting of the Society of Toxicology (SOT 2014)
AU - Waalkes, M
Y1 - 2014/03/23/
PY - 2014
DA - 2014 Mar 23
KW - Stem cells
KW - Carcinogenesis
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=53rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2014%29&rft.atitle=Stem+Cells+in+Carcinogenesis&rft.au=Waalkes%2C+M&rft.aulast=Waalkes&rft.aufirst=M&rft.date=2014-03-23&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=53rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2014%29&rft.issn=&rft_id=info:doi/
L2 - http://www.toxicology.org/AI/Pub/Prog/2014Program.pdf
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-23
N1 - Last updated - 2014-04-24
ER -
TY - CPAPER
T1 - Constructing AOPs for Developmental Toxicities
T2 - 53rd Annual Meeting of the Society of Toxicology (SOT 2014)
AN - 1518609386; 6281260
JF - 53rd Annual Meeting of the Society of Toxicology (SOT 2014)
AU - Kleinstreuer, N
Y1 - 2014/03/23/
PY - 2014
DA - 2014 Mar 23
KW - Toxicity
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=53rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2014%29&rft.atitle=Constructing+AOPs+for+Developmental+Toxicities&rft.au=Kleinstreuer%2C+N&rft.aulast=Kleinstreuer&rft.aufirst=N&rft.date=2014-03-23&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=53rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2014%29&rft.issn=&rft_id=info:doi/
L2 - http://www.toxicology.org/AI/Pub/Prog/2014Program.pdf
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-23
N1 - Last updated - 2014-04-24
ER -
TY - CPAPER
T1 - Challenges and Recommendations for Future Asbestos Research
T2 - 53rd Annual Meeting of the Society of Toxicology (SOT 2014)
AN - 1518609358; 6281346
JF - 53rd Annual Meeting of the Society of Toxicology (SOT 2014)
AU - Miller, A
Y1 - 2014/03/23/
PY - 2014
DA - 2014 Mar 23
KW - Asbestos
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518609358?accountid=14244
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L2 - http://www.toxicology.org/AI/Pub/Prog/2014Program.pdf
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-23
N1 - Last updated - 2014-04-24
ER -
TY - CPAPER
T1 - Perinatal Exposures to Environmental Pollutants and Children's Health
T2 - 53rd Annual Meeting of the Society of Toxicology (SOT 2014)
AN - 1518609338; 6281377
JF - 53rd Annual Meeting of the Society of Toxicology (SOT 2014)
AU - Heindel, J
AU - Schug, T
AU - Gray, K
Y1 - 2014/03/23/
PY - 2014
DA - 2014 Mar 23
KW - Pollutants
KW - Perinatal exposure
KW - Children
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L2 - http://www.toxicology.org/AI/Pub/Prog/2014Program.pdf
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-23
N1 - Last updated - 2014-04-24
ER -
TY - JOUR
T1 - Transgenic mice expressing S129 phosphorylation mutations in α-synuclein.
AN - 1506398416; 24486885
AB - Aggregated α-synuclein is a predominant constituent of Lewy bodies, the intracellular protein aggregates seen in Parkinson's disease. While most α-synuclein in the nervous system is unphosphorylated, the majority of α-synuclein in Lewy bodies is phosphorylated at serine 129 (S129). We developed transgenic mice expressing human SNCA with either a phosphomimic (S129D) or a non-phosphorylatable (S129A) mutation, on a mouse Snca knockout background. Transgenic lines with each mutation expressing the human α-synuclein protein at levels ranging from 0.3 to 1.9 fold of endogenous mouse protein were chosen to avoid toxic overexpression effects. We previously demonstrated an altered distribution of presynaptic vesicles in Snca knockout mice, as well as enhanced interaction between presynaptic cytoskeletal proteins and α-synuclein when phosphorylated at S129 or carrying an S129D mutation. We therefore examined α-synuclein's synaptic localization and the distribution of presynaptic vesicles in these mutants. In addition, we evaluated the transgenic lines for reduced colonic motility, an early marker of α-synuclein pathology, and α-synuclein aggregates. No abnormalities were detected in mice expressing either phosphorylation mutant protein as their only α-synuclein protein. These results suggest the S129A and S129D mutations have no obvious effect on α-synuclein function.
Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.
JF - Neuroscience letters
AU - Escobar, Valerie Drews
AU - Kuo, Yien-Ming
AU - Orrison, Bonnie M
AU - Giasson, Benoit I
AU - Nussbaum, Robert L
AD - Department of Medicine, University of California San Francisco, San Francisco, CA 94143, USA; Institute for Human Genetics, University of California San Francisco, San Francisco, CA 94143, USA. ; Genetic Disease Research Branch, NHGRI, National Institutes of Health, Bethesda, MD 20892, USA. ; Department of Pharmacology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA. ; Department of Medicine, University of California San Francisco, San Francisco, CA 94143, USA; Institute for Human Genetics, University of California San Francisco, San Francisco, CA 94143, USA. Electronic address: nussbaumr@humgen.ucsf.edu.
Y1 - 2014/03/20/
PY - 2014
DA - 2014 Mar 20
SP - 96
EP - 100
VL - 563
KW - alpha-Synuclein
KW - 0
KW - Index Medicus
KW - Phosphorylation
KW - Parkinson's disease
KW - Transgenic
KW - α-synuclein
KW - Lewy bodies
KW - Animals
KW - Gastrointestinal Motility
KW - Humans
KW - Brain -- metabolism
KW - Mice, Transgenic
KW - Lewy Bodies -- pathology
KW - Cells, Cultured
KW - Brain -- pathology
KW - Enteric Nervous System -- physiopathology
KW - Colon -- innervation
KW - Lewy Bodies -- metabolism
KW - Synapses -- metabolism
KW - Mutation
KW - Colon -- physiopathology
KW - Male
KW - Female
KW - Neurons -- metabolism
KW - alpha-Synuclein -- metabolism
KW - alpha-Synuclein -- genetics
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuroscience+letters&rft.atitle=Transgenic+mice+expressing+S129+phosphorylation+mutations+in+%CE%B1-synuclein.&rft.au=Escobar%2C+Valerie+Drews%3BKuo%2C+Yien-Ming%3BOrrison%2C+Bonnie+M%3BGiasson%2C+Benoit+I%3BNussbaum%2C+Robert+L&rft.aulast=Escobar&rft.aufirst=Valerie&rft.date=2014-03-20&rft.volume=563&rft.issue=&rft.spage=96&rft.isbn=&rft.btitle=&rft.title=Neuroscience+letters&rft.issn=1872-7972&rft_id=info:doi/10.1016%2Fj.neulet.2014.01.033
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-10-24
N1 - Date created - 2014-03-10
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.neulet.2014.01.033
ER -
TY - CPAPER
T1 - The Evolution of Cancer and Challenges in Drug Development in AIDS Patients
T2 - 115th American Society for Clinical Pharmacology and Therapeutics (ASCPT 2014)
AN - 1518612912; 6284190
JF - 115th American Society for Clinical Pharmacology and Therapeutics (ASCPT 2014)
AU - Little, Richard
Y1 - 2014/03/18/
PY - 2014
DA - 2014 Mar 18
KW - Acquired immune deficiency syndrome
KW - Drug development
KW - Evolution
KW - Cancer
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L2 - http://www.ascpt.org/Portals/8/docs/Meetings/2014%20Annual%20Meeting/Final%20Program%20Proof%204.pdf
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-23
N1 - Last updated - 2014-04-24
ER -
TY - JOUR
T1 - Direction pathway analysis of large-scale proteomics data reveals novel features of the insulin action pathway
AN - 1516739523; 19505087
AB - Motivation:With the advancement of high-throughput techniques, large-scale profiling of biological systems with multiple experimental perturbations is becoming more prevalent. Pathway analysis incorporates prior biological knowledge to analyze genes/proteins in groups in a biological context. However, the hypotheses under investigation are often confined to a 1D space (i.e. up, down, either or mixed regulation). Here, we develop direction pathway analysis (DPA), which can be applied to test hypothesis in a high-dimensional space for identifying pathways that display distinct responses across multiple perturbations.Results:Our DPA approach allows for the identification of pathways that display distinct responses across multiple perturbations. To demonstrate the utility and effectiveness, we evaluated DPA under various simulated scenarios and applied it to study insulin action in adipocytes. A major action of insulin in adipocytes is to regulate the movement of proteins from the interior to the cell surface membrane. Quantitative mass spectrometry-based proteomics was used to study this process on a large-scale. The combined dataset comprises four separate treatments. By applying DPA, we identified that several insulin responsive pathways in the plasma membrane trafficking are only partially dependent on the insulin-regulated kinase Akt. We subsequently validated our findings through targeted analysis of key proteins from these pathways using immunoblotting and live cell microscopy. Our results demonstrate that DPA can be applied to dissect pathway networks testing diverse hypotheses and integrating multiple experimental perturbations.
JF - Bioinformatics
AU - Yang, Pengyi
AU - Patrick, Ellis
AU - Tan, Shi-Xiong
AU - Fazakerley, Daniel J
AU - Burchfield, James
AU - Gribben, Christopher
AU - Prior, Matthew J
AU - James, David E
AU - Hwa Yang, Yee
AD - super(1)Systems Biology Group, Biostatistics Branch, National Institute of Environmental Health Sciences, National Institute of Health, Research Triangle Park, NC 27709, USA, super(2)School of Mathematics and Statistics, University of Sydney, super(3)Diabetes and Obesity Program, Garvan Institute of Medical Research, NSW 2006, Australia and super(4)Metabolism in Human Disease Unit, Institute of Molecular and Cellular Biology, A*Star, 61 Biopolis Drive, Proteos 138673, Singapore
Y1 - 2014/03/15/
PY - 2014
DA - 2014 Mar 15
SP - 808
EP - 814
PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL - 30
IS - 6
SN - 1367-4803, 1367-4803
KW - Biochemistry Abstracts 2: Nucleic Acids; Biotechnology and Bioengineering Abstracts
KW - Immunoblotting
KW - Cell surface
KW - Data processing
KW - Insulin
KW - Computer programs
KW - Plasma membranes
KW - Adipocytes
KW - Microscopy
KW - AKT protein
KW - membrane trafficking
KW - proteomics
KW - Bioinformatics
KW - Internet
KW - N 14810:Methods
KW - W 30960:Bioinformatics & Computer Applications
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-01
N1 - Last updated - 2016-05-13
N1 - SubjectsTermNotLitGenreText - Cell surface; Immunoblotting; Data processing; Insulin; Computer programs; Plasma membranes; Adipocytes; Microscopy; membrane trafficking; AKT protein; Bioinformatics; proteomics; Internet
DO - http://dx.doi.org/10.1093/bioinformatics/btt616
ER -
TY - JOUR
T1 - Targeting hydrogen sulfide as a promising therapeutic strategy for atherosclerosis.
AN - 1516723998; 24491853
AB - Physiological concentrations of nitric oxide (NO) and carbon monoxide (CO) have multiple protective effects in the cardiovascular system. Recent studies have implicated hydrogen sulfide (H2S) as a new member of vasculoprotective gasotransmitter family, behaving similarly to NO and CO. H2S has been demonstrated to inhibit multiple key aspects of atherosclerosis, including atherogenic modification of LDL, monocytes adhesion to the endothelial cells, macrophage-derived foam cell formation and inflammation, smooth muscle cell proliferation, neointimal hyperplasia, vascular calcification, and thrombogenesis. H2S also decreases plasma homocysteine levels in experimental animal models. In the human body, H2S production is predominantly catalyzed by cystathionine-β-synthase (CBS) and cystathionine γ-lyase (CSE). CSE is the primary H2S-producing enzyme in the vasculature. Growing evidence suggests that atherosclerosis is associated with vascular CSE/H2S deficiency and that H2S supplementation by exogenous H2S donors (such as NaHS and GYY4137) attenuates, and H2S synthesis suppression by inhibitors (such as D, L-propargylglycine) aggravates the development of atherosclerotic plaques. However, it remains elusive whether CSE deficiency plays a causative role in atherosclerosis. A recent study (Circulation. 2013; 127: 2523-2534) demonstrates that decreased endogenous H2S production by CSE genetic deletion accelerates atherosclerosis in athero-prone ApoE-/- mice, pinpointing that endogenously produced H2S by CSE activation may be of benefit in the prevention and treatment of atherosclerosis. This study will facilitate the development of H2S-based pharmaceuticals with therapeutic applications in atherosclerosis-related cardiovascular diseases.
Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.
JF - International journal of cardiology
AU - Xu, Suowen
AU - Liu, Zhiping
AU - Liu, Peiqing
AD - Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China; Cardiovascular and Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892-1590, USA. Electronic address: suowen.xu@gmail.com. ; Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China. ; Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China. Electronic address: liupq@mail.sysu.edu.cn.
Y1 - 2014/03/15/
PY - 2014
DA - 2014 Mar 15
SP - 313
EP - 317
VL - 172
IS - 2
KW - GYY 4137
KW - 0
KW - Morpholines
KW - Organothiophosphorus Compounds
KW - Carbon Dioxide
KW - 142M471B3J
KW - Nitric Oxide
KW - 31C4KY9ESH
KW - Cystathionine gamma-Lyase
KW - EC 4.4.1.1
KW - Hydrogen Sulfide
KW - YY9FVM7NSN
KW - Index Medicus
KW - Atherosclerosis
KW - Hydrogen sulfide
KW - Gasotransmitter
KW - Cystathionine γ-lyase
KW - Signal Transduction -- physiology
KW - Animals
KW - Oxidative Stress -- physiology
KW - Humans
KW - Morpholines -- pharmacology
KW - Nitric Oxide -- metabolism
KW - Mice
KW - Organothiophosphorus Compounds -- pharmacology
KW - Carbon Dioxide -- metabolism
KW - Atherosclerosis -- drug therapy
KW - Hydrogen Sulfide -- metabolism
KW - Atherosclerosis -- etiology
KW - Hydrogen Sulfide -- pharmacology
KW - Cystathionine gamma-Lyase -- deficiency
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-01-12
N1 - Date created - 2014-03-05
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.ijcard.2014.01.068
ER -
TY - JOUR
T1 - Gallstones, Cholecystectomy, and Risk of Digestive System Cancers
AN - 1512331318; 19377170
AB - Gallstones and cholecystectomy may be related to digestive system cancer through inflammation, altered bile flux, and changes in metabolic hormone levels. Although gallstones are recognized causes of gallbladder cancer, associations with other cancers of the digestive system are poorly established. We used the Surveillance, Epidemiology, and End Results (SEER)-Medicare linked database (1992-2005), which includes 17 cancer registries that cover approximately 26% of the US population, to identify first primary cancers (n = 236,850) occurring in persons aged greater than or equal to 66 years and 100,000 cancer-free population-based controls frequency-matched by calendar year, age, and gender. Odds ratios and 95% confidence intervals were calculated using logistic regression analysis, adjusting for the matching factors. Gallstones and cholecystectomy were associated with increased risk of noncardia gastric cancer (odds ratio (OR) = 1.21 (95% confidence interval (CI): 1.11, 1.32) and OR = 1.26 (95% CI: 1.13, 1.40), respectively), small-intestine carcinoid (OR = 1.27 (95% CI: 1.01, 1.60) and OR = 1.78 (95% CI: 1.41, 2.25)), liver cancer (OR = 2.35 (95% CI: 2.18, 2.54) and OR = 1.26 (95% CI: 1.12, 1.41)), and pancreatic cancer (OR = 1.24 (95% CI: 1.16, 1.31) and OR = 1.23 (95% CI: 1.15, 1.33)). Colorectal cancer risk associated with gallstones and cholecystectomy decreased with increasing distance from the common bile duct (P-trend < 0.001). Hence, gallstones and cholecystectomy are associated with the risk of cancers occurring throughout the digestive tract.
JF - American Journal of Epidemiology
AU - Nogueira, Leticia
AU - Freedman, Neal D
AU - Engels, Eric A
AU - Warren, Joan L
AU - Castro, Felipe
AU - Koshiol, Jill
AD - Correspondence to Dr. Leticia Nogueira, National Cancer Institute, 9609 Medical Center Drive, MSC 7248, Bethesda, MD 20892., leticia.nogueira@nih.gov
Y1 - 2014/03/15/
PY - 2014
DA - 2014 Mar 15
SP - 731
EP - 739
PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL - 179
IS - 6
SN - 0002-9262, 0002-9262
KW - Health & Safety Science Abstracts; Risk Abstracts
KW - Health risks
KW - Age
KW - Risk factors
KW - Gender
KW - Liver
KW - Pancreatic cancer
KW - Colorectal carcinoma
KW - Digestive system
KW - Hormones
KW - Cancer
KW - H 11000:Diseases/Injuries/Trauma
KW - R2 23060:Medical and environmental health
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Epidemiology&rft.atitle=Gallstones%2C+Cholecystectomy%2C+and+Risk+of+Digestive+System+Cancers&rft.au=Nogueira%2C+Leticia%3BFreedman%2C+Neal+D%3BEngels%2C+Eric+A%3BWarren%2C+Joan+L%3BCastro%2C+Felipe%3BKoshiol%2C+Jill&rft.aulast=Nogueira&rft.aufirst=Leticia&rft.date=2014-03-15&rft.volume=179&rft.issue=6&rft.spage=731&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Epidemiology&rft.issn=00029262&rft_id=info:doi/10.1093%2Faje%2Fkwt322
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-01
N1 - Last updated - 2014-06-26
N1 - SubjectsTermNotLitGenreText - Health risks; Age; Risk factors; Gender; Pancreatic cancer; Liver; Colorectal carcinoma; Hormones; Digestive system; Cancer
DO - http://dx.doi.org/10.1093/aje/kwt322
ER -
TY - JOUR
T1 - Germline variation in NCF4, an innate immunity gene, is associated with an increased risk of colorectal cancer.
AN - 1490742265; 23982929
AB - Chronic inflammation has been implicated in the etiology of colorectal adenoma and cancer; however, few key inflammatory genes mediating this relationship have been identified. In this study, we investigated the association of germline variation in innate immunity genes in relation to the risk of colorectal neoplasia. Our study was based on the analysis of samples collected from the prostate, lung, colorectal and ovarian (PLCO) Cancer Screening Trial. We investigated the association between 196 tag single nucleotide polymorphisms (SNPs) in 20 key innate immunity genes with risk of advanced colorectal adenoma and cancer in 719 adenoma cases, 481 cancer cases and 719 controls. Logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CIs). After Bonferroni correction, the AG/GG genotype of rs5995355, which is upstream of NCF4, was associated with an increased risk of colorectal cancer (OR = 2.43, 95% CI = 1.73-3.39; p < 0.0001). NCF4 is part of the NAPDH complex, a key factor in biochemical pathways and the innate immune response. While not definitive, our analyses suggest that the variant allele does not affect expression of NCF4, but rather modulates activity of the NADPH complex. Additional studies on the functional consequences of rs5995355 in NCF4 may help to clarify the mechanistic link between inflammation and colorectal cancer.
© 2013 UICC.
JF - International journal of cancer
AU - Ryan, Bríd M
AU - Zanetti, Krista A
AU - Robles, Ana I
AU - Schetter, Aaron J
AU - Goodman, Julie
AU - Hayes, Richard B
AU - Huang, Wen-Yi
AU - Gunter, Mark J
AU - Yeager, Meredith
AU - Burdette, Laurie
AU - Berndt, Sonja I
AU - Harris, Curtis C
AD - Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, MD, 20892.
Y1 - 2014/03/15/
PY - 2014
DA - 2014 Mar 15
SP - 1399
EP - 1407
VL - 134
IS - 6
KW - Biomarkers, Tumor
KW - 0
KW - RNA, Messenger
KW - NADP
KW - 53-59-8
KW - NADPH Oxidase
KW - EC 1.6.3.1
KW - NCF4 protein, human
KW - Index Medicus
KW - single nucleotide polymorphism
KW - NCF4
KW - innate immunity
KW - colorectal cancer
KW - Real-Time Polymerase Chain Reaction
KW - Cell Movement
KW - Apoptosis
KW - Neoplasm Staging
KW - Humans
KW - Prognosis
KW - NADP -- metabolism
KW - Aged
KW - Cell Differentiation
KW - Reverse Transcriptase Polymerase Chain Reaction
KW - RNA, Messenger -- genetics
KW - Cell Proliferation
KW - Genotype
KW - Blotting, Western
KW - Risk Factors
KW - Case-Control Studies
KW - Early Detection of Cancer
KW - Middle Aged
KW - Follow-Up Studies
KW - Cell Cycle
KW - Male
KW - Female
KW - Cell Adhesion
KW - Biomarkers, Tumor -- genetics
KW - Colorectal Neoplasms -- pathology
KW - Colorectal Neoplasms -- etiology
KW - Adenoma -- etiology
KW - Immunity, Innate -- genetics
KW - Adenoma -- pathology
KW - Polymorphism, Single Nucleotide -- genetics
KW - NADPH Oxidase -- genetics
KW - Germ-Line Mutation -- genetics
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-02-25
N1 - Date created - 2014-01-06
N1 - Date revised - 2017-01-13
N1 - SuppNotes - Cited By:
J Immunol. 2003 Sep 15;171(6):3010-8 [12960326]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1002/ijc.28457
ER -
TY - JOUR
T1 - Anal microbiota profiles in HIV-positive and HIV-negative MSM
AN - 1765970151; PQ0002559421
AB - Objective: Because differences in anal microbial populations (microbiota) could affect acquisition of HIV or other conditions, especially among MSM, we profiled the microbiota of the anal canal, assessed its stability, and investigated associations with diversity and composition. Design: Microbiota profiles in anal swabs collected from 76 MSM (52 in 1989, swab-1; 66 1-5 years later, swab-2) were compared by HIV status (25 HIV-positive), T-cell subsets, and questionnaire data. Methods: Bacterial 16S rRNA genes were amplified, sequenced (Illumina MiSeq), and clustered into species-level operational taxonomic units (QIIME and Greengenes). Regression models and Wilcoxon tests were used for associations with alpha diversity (unique operational taxonomic units, Shannon's index). Composition was compared by Adonis (QIIME). Results: Most anal bacteria were Firmicutes (mean 60.6%, range 21.1-91.1%) or Bacteroidetes (29.4%, 4.1-70.8%). Alpha diversity did not change between the two swabs (N = 42 pairs). In swab-2, HIV-positives had lower alpha diversity (P [< or =] 0.04) and altered composition, with fewer Firmicutes and more Fusobacteria taxa (P [< or =] 0.03), not completely attributable to very low CD4 super(+) cell count (median 232 cells/ mu ), prior AIDS clinical diagnosis (N = 17), or trimethoprim-sulfamethoxazole use (N = 6). Similar but weaker differences were observed in swab-1 (HIV-positive median 580 CD4 super(+) cells/( mu l; no trimethoprim-sulfamethoxazole). Associations with T-cell subsets, smoking, and sexual practices were null or inconsistent. Conclusions: The anal microbiota of MSM was relatively stable over 1-5 years. However, with uncontrolled, advanced HIV infection, the microbiota had altered composition and reduced diversity partially attributable to antibiotics. Investigations of microbial community associations with other immune perturbations and clinical abnormalities are needed.
JF - AIDS
AU - Yu, Guoqin
AU - Fadrosh, Doug
AU - Ma, Bing
AU - Ravel, Jacques
AU - Goedert, James J
AD - Infections and Immunoepidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, goedertj@mail.nih.gov
Y1 - 2014/03/13/
PY - 2014
DA - 2014 Mar 13
SP - 753
EP - 760
PB - Lippincott Williams & Wilkins, Inc, 530 Walnut Street Philadelphia PA 19106-3621 United States
VL - 28
IS - 5
SN - 0269-9370, 0269-9370
KW - Health & Safety Science Abstracts; Immunology Abstracts; Virology & AIDS Abstracts
KW - anal
KW - HIV
KW - human microbiome
KW - MSM
KW - risk factors
KW - sexual activities
KW - Inventories
KW - Acquired immune deficiency syndrome
KW - Data processing
KW - Microbial activity
KW - trimethoprim-sulfamethoxazole
KW - Antibiotics
KW - Firmicutes
KW - Infection
KW - Canals
KW - Smoking
KW - CD4 antigen
KW - Human immunodeficiency virus
KW - Lymphocytes T
KW - Regression analysis
KW - Taxonomy
KW - Taxa
KW - rRNA 16S
KW - V 22360:AIDS and HIV
KW - H 11000:Diseases/Injuries/Trauma
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2016-02-01
N1 - Last updated - 2016-03-17
N1 - SubjectsTermNotLitGenreText - Smoking; Canals; Inventories; Acquired immune deficiency syndrome; CD4 antigen; Data processing; Regression analysis; Lymphocytes T; Antibiotics; trimethoprim-sulfamethoxazole; Infection; rRNA 16S; Human immunodeficiency virus; Taxa; Microbial activity; Taxonomy; Firmicutes
DO - http://dx.doi.org/10.1097/QAD.0000000000000154
ER -
TY - JOUR
T1 - The role of Nrf1 and Nrf2 in the regulation of copper-responsive transcription.
AN - 1499153131; 24462598
AB - Recent evidences indicated Nrf2 is more potent than Nrf1 in the activation of antioxidant genes. However, the roles of Nrf proteins in the regulation of copper-responsive transcription have not been well addressed. We took the toxicogenomic approach and the present network and Gene Ontology analyses results showed that Nrf1 and Nrf2 are distinctively involved in copper-responsive transcriptional regulation in HepG2 transcriptome. Cells deficient in either Nrf1 or Nrf2 were more susceptible to copper exposure than wild type cells. Nrf1 and Nrf2 null cells were transfected with the luciferase reporters containing either ARE(s) or a combination of ARE(s) and MREs, and then treated with copper. In Nrf2-null (Nrf2(-/-)) cells, copper did not activate transcription of reporter genes, whereas Nrf1 deficiency did not affect copper-inducible activation. Ectopic expression of Nrf2 restored copper-inducible transcription in Nrf2(-/-) cells. However, the changes in the intrinsic mRNA levels of MT-1 in Nrf null cells following copper treatment showed that Nrf1 and Nrf2 equally contributed to MT-1 activation after 4h, while Nrf1involved more than Nrf2 following 24h exposure. These results suggest that while Nrf2 is crucial for MRE/ARE-mediated transcription in response to copper, Nrf1 may activate MT-1 expression by a mechanism different from that Nrf2 employs. Copyright © 2014 Elsevier Inc. All rights reserved.
JF - Experimental cell research
AU - Song, Min Ok
AU - Mattie, Michael D
AU - Lee, Chang-Ho
AU - Freedman, Jonathan H
AD - Department of Biology, College of Natural Sciences, Gangneung-Wonju National University, Gangwon-do 210-702, Republic of Korea. Electronic address: rotisong@gmail.com. ; Nicholas School of the Environment, Box 90328, Duke University, Durham, NC 27708, USA. Electronic address: mmattie@agensys.com. ; Department of Biology, College of Natural Sciences, Gangneung-Wonju National University, Gangwon-do 210-702, Republic of Korea. ; Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA.
Y1 - 2014/03/10/
PY - 2014
DA - 2014 Mar 10
SP - 39
EP - 50
VL - 322
IS - 1
KW - NF-E2-Related Factor 2
KW - 0
KW - Nfe2l2 protein, mouse
KW - Nrf1 protein, mouse
KW - Nuclear Respiratory Factor 1
KW - metallothionein-1, mouse
KW - Copper
KW - 789U1901C5
KW - Metallothionein
KW - 9038-94-2
KW - Index Medicus
KW - Nrf1
KW - ARE
KW - Metallothionein-1
KW - Transcription
KW - Nrf2
KW - Gene Expression Profiling
KW - Animals
KW - Transcription, Genetic -- drug effects
KW - Hep G2 Cells
KW - Cells, Cultured
KW - Humans
KW - Gene Regulatory Networks
KW - Metallothionein -- genetics
KW - Mice
KW - Metallothionein -- metabolism
KW - Mice, Knockout
KW - NF-E2-Related Factor 2 -- physiology
KW - NF-E2-Related Factor 2 -- genetics
KW - Nuclear Respiratory Factor 1 -- genetics
KW - Gene Expression Regulation -- drug effects
KW - Nuclear Respiratory Factor 1 -- physiology
KW - Copper -- pharmacology
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-04-22
N1 - Date created - 2014-02-17
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Toxicol Appl Pharmacol. 2010 Apr 1;244(1):4-15 [20122947]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.yexcr.2014.01.013
ER -
TY - JOUR
T1 - Intakes of folate, methionine, vitamin B6, and vitamin B12 with risk of esophageal and gastric cancer in a large cohort study.
AN - 1504732509; 24481406
AB - Nutrients in the one-carbon metabolism pathway may be involved in carcinogenesis. Few cohort studies have investigated the intakes of folate and related nutrients in relation to gastric and esophageal cancer.
We prospectively examined the association between self-reported intakes of folate, methionine, vitamin B6, and vitamin B12 and gastric and esophageal cancer in 492,293 men and women. We observed an elevated risk of esophageal squamous cell carcinoma with low intake of folate (relative risk (95% confidence interval): Q1 vs Q3, 1.91 (1.17, 3.10)), but no association with high intake. Folate intake was not associated with esophageal adenocarcinoma, gastric cardia adenocarcinoma, or non-cardia gastric adenocarcinoma. The intakes of methionine, vitamin B6, and vitamin B12 were not associated with esophageal and gastric cancer.
Low intake of folate was associated with increased risk of esophageal squamous cell carcinoma.
JF - British journal of cancer
AU - Xiao, Q
AU - Freedman, N D
AU - Ren, J
AU - Hollenbeck, A R
AU - Abnet, C C
AU - Park, Y
AD - Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland, USA. ; National Office for Cancer Prevention and Control, National Cancer Center, Beijing, China. ; AARP, Washington, District of Columbia, USA.
Y1 - 2014/03/04/
PY - 2014
DA - 2014 Mar 04
SP - 1328
EP - 1333
VL - 110
IS - 5
KW - Vitamin B 6
KW - 8059-24-3
KW - Folic Acid
KW - 935E97BOY8
KW - Methionine
KW - AE28F7PNPL
KW - Vitamin B 12
KW - P6YC3EG204
KW - Index Medicus
KW - Risk
KW - Carcinoma, Squamous Cell -- epidemiology
KW - Humans
KW - Cohort Studies
KW - Middle Aged
KW - United States -- epidemiology
KW - Male
KW - Female
KW - Vitamin B 6 -- administration & dosage
KW - Methionine -- administration & dosage
KW - Diet -- statistics & numerical data
KW - Vitamin B 12 -- administration & dosage
KW - Stomach Neoplasms -- epidemiology
KW - Folic Acid -- administration & dosage
KW - Esophageal Neoplasms -- epidemiology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+journal+of+cancer&rft.atitle=Intakes+of+folate%2C+methionine%2C+vitamin+B6%2C+and+vitamin+B12+with+risk+of+esophageal+and+gastric+cancer+in+a+large+cohort+study.&rft.au=Xiao%2C+Q%3BFreedman%2C+N+D%3BRen%2C+J%3BHollenbeck%2C+A+R%3BAbnet%2C+C+C%3BPark%2C+Y&rft.aulast=Xiao&rft.aufirst=Q&rft.date=2014-03-04&rft.volume=110&rft.issue=5&rft.spage=1328&rft.isbn=&rft.btitle=&rft.title=British+journal+of+cancer&rft.issn=1532-1827&rft_id=info:doi/10.1038%2Fbjc.2014.17
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-06-23
N1 - Date created - 2014-03-05
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
J Nutr. 2003 Nov;133(11 Suppl 1):3748S-3753S [14608109]
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J Natl Cancer Inst. 1988 Dec 21;80(20):1620-5 [3193480]
J Nutr. 1990 Nov;120 Suppl 11:1508-11 [2243297]
Cancer Epidemiol Biomarkers Prev. 1994 Jul-Aug;3(5):393-8 [7920206]
J Natl Cancer Inst. 1995 Jan 18;87(2):104-9 [7707381]
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Nutr Cancer. 2005;52(2):138-46 [16201845]
Gastroenterology. 2006 Oct;131(4):1271-83 [17030196]
Am J Clin Nutr. 2007 Aug;86(2):271-3 [17684194]
Public Health Nutr. 2008 Feb;11(2):183-95 [17610761]
Gastroenterol Clin North Am. 2009 Mar;38(1):27-57, vii [19327566]
Am J Clin Nutr. 2010 Jun;91(6):1708-15 [20410093]
J Natl Cancer Inst. 2010 Sep 8;102(17):1344-53 [20716718]
J Nutr. 2011 Feb;141(2):274-83 [21178085]
Am J Epidemiol. 2011 May 15;173(10):1171-82 [21447479]
Nutr J. 2011;10:137 [22185224]
Asian Pac J Cancer Prev. 2011;12(8):2019-23 [22292644]
Int J Obes (Lond). 2013 Mar;37(3):448-54 [22546778]
Clin Gastroenterol Hepatol. 2013 Sep;11(9):1130-1136.e2 [23591281]
Cancer. 2000 Feb 15;88(4):737-48 [10679641]
Am J Epidemiol. 2000 Aug 1;152(3):279-86 [10933275]
Int J Cancer. 2001 Aug 1;93(3):417-23 [11433408]
Am J Epidemiol. 1986 Jul;124(1):17-27 [3521261]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1038/bjc.2014.17
ER -
TY - JOUR
T1 - Commentary: When to start and what to use in children - recommendations and rationale
AN - 1768567825; PQ0002676694
AB - The 2013 WHO consolidated guidelines recommend treating all HIV-infected children under the age of 5 years regardless of CD4 super(+) T-cell count or WHO clinical stage, and treating children aged 5 years and older according to the same criteria as for adults: WHO clinical stage 3 or 4 or CD4 super(+) T-cell count of 500cells/ mu l or less [1]. Guideline recommendations for what drugs to use for initial antiretroviral therapy (ART) vary by age group: less than 3 years, 3-10 years and above 10 years.
JF - AIDS
AU - Siberry, George
AU - Tindyebwa, Denis
AD - Maternal and Pediatric Infectious Disease (MPID) Branch, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, USA, siberryg@mail.nih.gov
Y1 - 2014/03//
PY - 2014
DA - March 2014
SP - S133
EP - S135
PB - Lippincott Williams & Wilkins, Inc, 530 Walnut Street Philadelphia PA 19106-3621 United States
VL - 28
SN - 0269-9370, 0269-9370
KW - Health & Safety Science Abstracts; Immunology Abstracts; Virology & AIDS Abstracts
KW - Acquired immune deficiency syndrome
KW - Age
KW - Human immunodeficiency virus
KW - Guidelines
KW - Age groups
KW - Children
KW - Antiretroviral agents
KW - Drugs
KW - H 4000:Food and Drugs
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1768567825?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS&rft.atitle=Commentary%3A+When+to+start+and+what+to+use+in+children+-+recommendations+and+rationale&rft.au=Siberry%2C+George%3BTindyebwa%2C+Denis&rft.aulast=Siberry&rft.aufirst=George&rft.date=2014-03-01&rft.volume=28&rft.issue=&rft.spage=S133&rft.isbn=&rft.btitle=&rft.title=AIDS&rft.issn=02699370&rft_id=info:doi/10.1097%2FQAD.0000000000000241
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2016-02-01
N1 - Last updated - 2016-03-17
N1 - SubjectsTermNotLitGenreText - Age; Acquired immune deficiency syndrome; Guidelines; Age groups; Children; Drugs; Antiretroviral agents; Human immunodeficiency virus
DO - http://dx.doi.org/10.1097/QAD.0000000000000241
ER -
TY - JOUR
T1 - Parenting with bipolar disorder: Coping with risk of mood disorders to children
AN - 1692286372; 201504953
AB - Children of individuals with bipolar disorder (BPD) have increased risk for mood disorders and other adverse psychosocial outcomes due to genetic and environmental risk. Though parents with BPD are aware of increased risk to children, little is known about efforts undertaken in response or their perceived utility. Among parents who self-report with BPD, this study identifies key variables associated with parental coping with children's risk of mood disorders; and explores the relationship between monitoring children's moods and perceived coping efficacy. In this U.S. study, active parental coping with, and cognitive distancing from, child's risk were measured using novel scales. Parents (n = 266) who self-identified as having BPD completed a web-based survey. They had at least one unaffected child. Most participants endorsed monitoring their children's moods. Monitoring was associated with increased perceived control over the child's well-being (p < 0.005), but not feeling less worried. Active parental coping with risk to children was positively associated with active coping with own illness (Beta = 0.25, p = 0.001), family history (Beta = 0.24, p = 0.001), and self-report of current depression (Beta = 0.16, p = 0.037), explaining 13.8% of the variance (F = 8.81, p < 0.001). Cognitive distancing from the child's risk was positively associated with confidence in diagnosis (Beta = 0.25, p = 0.001), and negatively associated with self-report of current mania (Beta = -0.19, p = 0.007), perceiving BPD as genetic (Beta = -0.26, p < 0.001) and having more children (Beta = -0.20, p = 0.004); explaining 16.2% of the variance (F = 8.63, p < 0.001). Parents' adaptation to their own BPD was modestly correlated with active coping with child's risk (r = 0.15, p < 0.05) but not with cognitive distancing. The findings support the importance of understanding causal attributions and the value of genetic education and counseling for parents with BPD. Further research is necessary to elucidate the psychological benefits of active coping versus cognitive distancing from child's risk, and explore additional variables that predict parental coping with children's risk of mood disorders. [Copyright Elsevier Ltd.]
JF - Social Science & Medicine
AU - Peay, Holly Landrum
AU - Rosenstein, Donald L
AU - Biesecker, Barbara Bowles
AD - Social and Behavioral Research Branch, National Human Genome Research Institute, NHGRI Building 31, Room B1B36 31 Center Drive, MSC 2073, Bethesda, MD 20892, USA
Y1 - 2014/03//
PY - 2014
DA - March 2014
SP - 194
EP - 200
PB - Elsevier Science, Amsterdam The Netherlands
VL - 104
SN - 0277-9536, 0277-9536
KW - Bipolar disorder Coping Parent Risk Genetic Children Mood disorder United States
KW - Values
KW - Genetics
KW - Emotions
KW - Risk
KW - Affective Illness
KW - Coping
KW - Parents
KW - Children
KW - Cognition
KW - article
KW - 6140: illness & health care
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1692286372?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Asocialservices&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Social+Science+%26+Medicine&rft.atitle=Parenting+with+bipolar+disorder%3A+Coping+with+risk+of+mood+disorders+to+children&rft.au=Peay%2C+Holly+Landrum%3BRosenstein%2C+Donald+L%3BBiesecker%2C+Barbara+Bowles&rft.aulast=Peay&rft.aufirst=Holly&rft.date=2014-03-01&rft.volume=104&rft.issue=&rft.spage=194&rft.isbn=&rft.btitle=&rft.title=Social+Science+%26+Medicine&rft.issn=02779536&rft_id=info:doi/10.1016%2Fj.socscimed.2013.10.022
LA - English
DB - Social Services Abstracts
N1 - Date revised - 2015-07-01
N1 - Last updated - 2016-09-28
N1 - CODEN - SSCMAW
N1 - SubjectsTermNotLitGenreText - Children; Risk; Parents; Coping; Emotions; Cognition; Genetics; Affective Illness; Values
DO - http://dx.doi.org/10.1016/j.socscimed.2013.10.022
ER -
TY - JOUR
T1 - Influencing the World Versus Adjusting to Constraints
AN - 1673613031
AB - Although higher social class carries mental and physical health benefits, these advantages are less robust among members of racial and ethnic minority groups than among European Americans. We explore whether differential reactions to discrimination may be a factor in explaining why. Working-class and middle-class Latino American women engaged in an evaluative interaction with a European American woman who rejected them and held either prejudiced or unprejudiced attitudes. We examined how participants responded to this rejection by measuring neuroendocrine reactivity, executive functioning, and the affective content of their verbal responses during the interaction. Among middleclass Latinas, rejection from a prejudiced, compared to unprejudiced, out-group member was associated with less adaptive stress responses, greater cognitive depletion, and more feelings of uncertainty. In contrast, among working-class Latinas, neuroendocrine, cognitive, and affective responses were similar across the two sources of rejection. Results suggest that social class is an important moderator of responses to discrimination.
JF - Social Psychological & Personality Science
AU - Townsend, Sarah S M
AU - Eliezer, Dina
AU - Major, Brenda
AU - Mendes, Wendy Berry
AD - Department of Management and Organizations, Kellogg School of Management, Northwestern University, Evanston, IL 60208, USA ; National Institutes of Health, Bethesda, MD, USA ; University of California, Santa Barbara, CA, USA ; University of California, San Francisco, CA, USA ; Department of Management and Organizations, Kellogg School of Management, Northwestern University, Evanston, IL 60208, USA
Y1 - 2014/03//
PY - 2014
DA - Mar 2014
SP - 226
EP - 234
CY - Thousand Oaks
PB - SAGE PUBLICATIONS, INC.
VL - 5
IS - 2
SN - 1948-5506
KW - Psychology
KW - socioeconomic status
KW - prejudice
KW - stress reactions
KW - neuroendocrinology
KW - Affective responses
KW - Women
KW - American people
KW - Attitudes
KW - Depletion
KW - Discrimination
KW - Executive function
KW - Health status
KW - Mental health
KW - Middle class people
KW - Minority groups
KW - Reactivity
KW - Rejection
KW - Social class
KW - Social rejection
KW - Uncertainty
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1673613031?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Social+Psychological+%26+Personality+Science&rft.atitle=Influencing+the+World+Versus+Adjusting+to+Constraints%3A+Social+Class+Moderates+Responses+to+Discrimination&rft.au=Townsend%2C+Sarah+S+M%3BEliezer%2C+Dina%3BMajor%2C+Brenda%3BMendes%2C+Wendy+Berry&rft.aulast=Townsend&rft.aufirst=Sarah+S&rft.date=2014-03-01&rft.volume=5&rft.issue=2&rft.spage=226&rft.isbn=&rft.btitle=&rft.title=Social+Psychological+%26+Personality+Science&rft.issn=19485506&rft_id=info:doi/10.1177%2F1948550613490968
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Date revised - 2015-03-31
N1 - Last updated - 2016-05-12
DO - http://dx.doi.org/10.1177/1948550613490968
ER -
TY - JOUR
T1 - Investigating the mechanisms of ribonucleotide excision repair in Escherichia coli
AN - 1668262104; PQ0001243194
AB - Low fidelity Escherichia coli DNA polymerase V (pol V/UmuD'2C) is best characterized for its ability to perform translesion synthesis (TLS). However, in recA730 lexA(Def) strains, the enzyme is expressed under optimal conditions allowing it to compete with the cell's replicase for access to undamaged chromosomal DNA and leads to a substantial increase in spontaneous mutagenesis. We have recently shown that a Y11A substitution in the "steric gate" residue of UmuC reduces both base and sugar selectivity of pol V, but instead of generating an increased number of spontaneous mutations, strains expressing umuC_Y11A are poorly mutable in vivo. This phenotype is attributed to efficient RNase HII-initiated repair of the misincorporated ribonucleotides that concomitantly removes adjacent misincorporated deoxyribonucleotides. We have utilized the ability of the pol V steric gate mutant to promote incorporation of large numbers of errant ribonucleotides into the E. coli genome to investigate the fundamental mechanisms underlying ribonucleotide excision repair (RER). Here, we demonstrate that RER is normally facilitated by DNA polymerase I (pol I) via classical "nick translation". In vitro, pol I displaces 1-3 nucleotides of the RNA/DNA hybrid and through its 5' arrow right 3' (exo/endo) nuclease activity releases ribo- and deoxyribonucleotides from DNA. In vivo, umuC_Y11A-dependent mutagenesis changes significantly in polymerase-deficient, or proofreading-deficient polA strains, indicating a pivotal role for pol I in ribonucleotide excision repair (RER). However, there is also considerable redundancy in the RER pathway in E. coli. Pol I's strand displacement and FLAP-exo/endonuclease activities can be facilitated by alternate enzymes, while the DNA polymerization step can be assumed by high-fidelity pol III. We conclude that RNase HII and pol I normally act to minimize the genomic instability that is generated through errant ribonucleotide incorporation, but that the "nick-translation" activities encoded by the single pol I polypeptide can be undertaken by a variety of back-up enzymes.
JF - Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis
AU - Vaisman, Alexandra
AU - McDonald, John P
AU - Noll, Stephan
AU - Huston, Donald
AU - Loeb, Gregory
AU - Goodman, Myron F
AU - Woodgate, Roger
AD - Laboratory of Genomic Integrity, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892-3371, USA
Y1 - 2014/03//
PY - 2014
DA - March 2014
SP - 21
EP - 33
PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands
VL - 761
SN - 0027-5107, 0027-5107
KW - Microbiology Abstracts B: Bacteriology; Biochemistry Abstracts 2: Nucleic Acids
KW - pol DNA polymerase
KW - nt nucleotide
KW - RER ribonucleotide excision repair
KW - Top1 topoisomerase 1
KW - Y-family DNA polymerase
KW - Steric gate mutant
KW - Ribonucleotide excision repair
KW - UmuC: spontaneous mutagenesis
KW - RNase H
KW - Genomes
KW - Translation
KW - Sugar
KW - Polymerization
KW - Enzymes
KW - Nuclease
KW - deoxyribonucleotides
KW - Nucleotides
KW - replicase
KW - Mutagenesis
KW - ribonuclease H2
KW - Fidelity
KW - Genomic instability
KW - RNA
KW - Hybrids
KW - DNA-directed DNA polymerase
KW - ribonucleotides
KW - Escherichia coli
KW - Ribonuclease
KW - Endonuclease
KW - Mutation
KW - J 02410:Animal Diseases
KW - N 14830:RNA
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1668262104?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Mutation+Research%2FFundamental+and+Molecular+Mechanisms+of+Mutagenesis&rft.atitle=Investigating+the+mechanisms+of+ribonucleotide+excision+repair+in+Escherichia+coli&rft.au=Vaisman%2C+Alexandra%3BMcDonald%2C+John+P%3BNoll%2C+Stephan%3BHuston%2C+Donald%3BLoeb%2C+Gregory%3BGoodman%2C+Myron+F%3BWoodgate%2C+Roger&rft.aulast=Vaisman&rft.aufirst=Alexandra&rft.date=2014-03-01&rft.volume=761&rft.issue=&rft.spage=21&rft.isbn=&rft.btitle=&rft.title=Mutation+Research%2FFundamental+and+Molecular+Mechanisms+of+Mutagenesis&rft.issn=00275107&rft_id=info:doi/10.1016%2Fj.mrfmmm.2014.01.005
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-03-01
N1 - Last updated - 2016-08-17
N1 - SubjectsTermNotLitGenreText - Genomes; Sugar; Translation; Polymerization; Nuclease; Enzymes; replicase; Nucleotides; deoxyribonucleotides; Mutagenesis; ribonuclease H2; Fidelity; Genomic instability; RNA; DNA-directed DNA polymerase; Hybrids; ribonucleotides; Ribonuclease; Endonuclease; Mutation; Escherichia coli
DO - http://dx.doi.org/10.1016/j.mrfmmm.2014.01.005
ER -
TY - JOUR
T1 - Cerebral tubercular thrombophlebitis presenting as venous infarct: Magnetic resonance imaging and pathologic correlation
AN - 1668257725; PQ0001246003
AB - Central nervous system involvement by tuberculosis to produce basal meningitis, hydrocephalus, arteritis and infarcts is well-known, the brunt of the pathology being borne by the arterial vasculature to produce neurological sequelae. However, tuberculous thrombophlebitis causing venous infarction is exceedingly rare. We present imaging and pathological features of two autopsy proven cases of tuberculous thrombophlebitis with venous infarcts involving superficial venous system in one and deep venous system in the other. This is the first study presenting radiopathologic correlation of this rare complication. Tuberculous thrombophlebitis should be suspected if basal exudates and multiple white matter T2 hyperintensities are seen on neuroimaging and the imaging protocol should include both magnetic resonance arteriogram and venogram.
JF - Annals of Indian Academy of Neurology
AU - Mangalore, Sandhya
AU - Desai, Sunali
AU - Mahadevan, Anita
AU - Kovoor, Jerry M E
AU - Vasudev, M K
AU - Tally, Arun Bhagwandas
AU - Shankar, Susarla Krishna
AD - Department of Neuroimaging and Interventional Radiology, National Institute of Mental Health and Neurosciences, Bengaluru, Karnataka, India
Y1 - 2014/03//
PY - 2014
DA - Mar 2014
SP - 130
EP - 134
PB - Medknow Publications Pvt. Ltd., A-108/109 Kanara Business Center Mumbai 400075 India
VL - 17
IS - 1
SN - 0972-2327, 0972-2327
KW - Microbiology Abstracts B: Bacteriology; CSA Neurosciences Abstracts
KW - Central nervous system tuberculosis
KW - Magnetic resonance imaging
KW - thrombophlebitis
KW - venous infarct
KW - Autopsy
KW - Central nervous system
KW - Neuroimaging
KW - Mycobacterium
KW - Neurological complications
KW - Substantia alba
KW - Meningitis
KW - Exudates
KW - N.M.R.
KW - Tuberculosis
KW - Hydrocephalus
KW - Arteritis
KW - Infarction
KW - Thrombophlebitis
KW - J 02490:Miscellaneous
KW - N3 11027:Neurology & neuropathology
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1668257725?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+Indian+Academy+of+Neurology&rft.atitle=Cerebral+tubercular+thrombophlebitis+presenting+as+venous+infarct%3A+Magnetic+resonance+imaging+and+pathologic+correlation&rft.au=Mangalore%2C+Sandhya%3BDesai%2C+Sunali%3BMahadevan%2C+Anita%3BKovoor%2C+Jerry+M+E%3BVasudev%2C+M+K%3BTally%2C+Arun+Bhagwandas%3BShankar%2C+Susarla+Krishna&rft.aulast=Mangalore&rft.aufirst=Sandhya&rft.date=2014-03-01&rft.volume=17&rft.issue=1&rft.spage=130&rft.isbn=&rft.btitle=&rft.title=Annals+of+Indian+Academy+of+Neurology&rft.issn=09722327&rft_id=info:doi/10.4103%2F09722327.128587
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-03-01
N1 - Last updated - 2015-11-16
N1 - SubjectsTermNotLitGenreText - Central nervous system; Autopsy; Neuroimaging; Magnetic resonance imaging; Substantia alba; Neurological complications; Meningitis; Exudates; Tuberculosis; N.M.R.; Arteritis; Hydrocephalus; Infarction; Thrombophlebitis; Mycobacterium
DO - http://dx.doi.org/10.4103/09722327.128587
ER -
TY - JOUR
T1 - Plasmid-mediated transformation tropism of chlamydial biovars
AN - 1654678503; 21296957
AB - Chlamydia trachomatis and C. muridarum are human and mouse pathogens, respectively, which show high conservation of gene order and content. Both species contain a common 7.5-kb plasmid that is an important virulence factor. Recently described transformation systems have been used to characterize C. trachomatis L2 plasmid gene functions; however, similar studies have not been reported for C. trachomatis ocular tropic serovar A or the mouse strain, C. muridarum. Here, we have conducted genetic experiments with C. trachomatis serovar A and C. muridarum and report the following: (1) successful transformation of C. muridarum and C. trachomatis serovar A is restricted to a shuttle vector with a C. muridarum or C. trachomatis serovar A plasmid backbone, respectively; (2) transformation of plasmid-deficient C. muridarum with the C. muridarum-based shuttle vector complement glycogen accumulation and inclusion morphology; and (3) C. muridarum plasmid-encoded Pgp4 is a regulator of chromosomal ( glgA ) and plasmid ( pgp3 ) virulence genes. In summary, our findings show a previously unrecognized and unexpected role for the chlamydial plasmid in its transformation tropism and confirm the plasmids regulatory role of virulence genes in C. muridarum. This study is the first to show that plasmid mediated transformation of chlamydiae is biovar-specific; a tropism that provides experimental evidence for a co-evolutionary relationship between plasmid and chromosomal genes.
JF - Pathogens and Disease
AU - Song, Lihua
AU - Carlson, John H
AU - Zhou, Bing
AU - Virtaneva, Kimmo
AU - Whitmire, William M
AU - Sturdevant, Gail L
AU - Porcella, Stephen F
AU - McClarty, Grant
AU - Caldwell, Harlan D
AD - Laboratory of Intracellular Parasites, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT, USA.
Y1 - 2014/03//
PY - 2014
DA - Mar 2014
SP - 189
EP - 193
PB - Wiley Subscription Services, Inc., 1105 N Market St Wilmington DE 19801 England
VL - 70
IS - 2
SN - 2049-632X, 2049-632X
KW - Microbiology Abstracts B: Bacteriology
KW - Transformation
KW - Gene order
KW - virulence factors
KW - Tropism
KW - Chlamydia trachomatis
KW - shuttle vectors
KW - Pathogens
KW - Plasmids
KW - Glycogen
KW - J 02320:Cell Biology
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1654678503?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pathogens+and+Disease&rft.atitle=Plasmid-mediated+transformation+tropism+of+chlamydial+biovars&rft.au=Song%2C+Lihua%3BCarlson%2C+John+H%3BZhou%2C+Bing%3BVirtaneva%2C+Kimmo%3BWhitmire%2C+William+M%3BSturdevant%2C+Gail+L%3BPorcella%2C+Stephen+F%3BMcClarty%2C+Grant%3BCaldwell%2C+Harlan+D&rft.aulast=Song&rft.aufirst=Lihua&rft.date=2014-03-01&rft.volume=70&rft.issue=2&rft.spage=189&rft.isbn=&rft.btitle=&rft.title=Pathogens+and+Disease&rft.issn=2049632X&rft_id=info:doi/10.1111%2F2049-632X.12104
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-02-01
N1 - Last updated - 2015-11-16
N1 - SubjectsTermNotLitGenreText - Transformation; Gene order; virulence factors; Tropism; Pathogens; shuttle vectors; Plasmids; Glycogen; Chlamydia trachomatis
DO - http://dx.doi.org/10.1111/2049-632X.12104
ER -
TY - JOUR
T1 - Dendrimers as high relaxivity MR contrast agents
AN - 1635018981; 21008404
AB - Dendrimers are versatile macromolecules with tremendous potential as magnetic resonance imaging (MRI) contrast agents. Dendrimer-based agents provide distinct advantages over low-molecular-weight gadolinium chelates, including enhanced r 1 relaxivity due to slow rotational dynamics, tunable pharmacokinetics that can be adapted for blood pool, liver, kidney, and lymphatic imaging, the ability to be a drug carrier, and flexibility for labeling due to their inherent multivalency. Clinical applications are increasingly being developed, particularly in lymphatic imaging. Herein we present a broad overview of dendrimer-based MRI contrast agents with attention to the unique chemistry and physical properties as well as emerging clinical applications. For further resources related to this article, please visit the WIREs website . Conflict of interest: The authors have declared no conflicts of interest for this article.
JF - Wiley Interdisciplinary Reviews: Nanomedicine and Nanobiotechnology
AU - Longmire, Michelle R
AU - Ogawa, Mikako
AU - Choyke, Peter L
AU - Kobayashi, Hisataka
AD - Molecular Imaging Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Y1 - 2014/03//
PY - 2014
DA - March 2014
SP - 155
EP - 162
PB - Wiley-Blackwell, Baffins Lane Chichester W. Sussex PO19 1UD United Kingdom
VL - 6
IS - 2
SN - 1939-5116, 1939-5116
KW - Biotechnology and Bioengineering Abstracts
KW - Drug delivery
KW - Macromolecules
KW - Gadolinium
KW - Magnetic resonance imaging
KW - Therapeutic applications
KW - Pharmacokinetics
KW - Blood
KW - Reviews
KW - Computed tomography
KW - Liver
KW - Kidney
KW - Contrast media
KW - Chelates
KW - nanotechnology
KW - W 30910:Imaging
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1635018981?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Wiley+Interdisciplinary+Reviews%3A+Nanomedicine+and+Nanobiotechnology&rft.atitle=Dendrimers+as+high+relaxivity+MR+contrast+agents&rft.au=Longmire%2C+Michelle+R%3BOgawa%2C+Mikako%3BChoyke%2C+Peter+L%3BKobayashi%2C+Hisataka&rft.aulast=Longmire&rft.aufirst=Michelle&rft.date=2014-03-01&rft.volume=6&rft.issue=2&rft.spage=155&rft.isbn=&rft.btitle=&rft.title=Wiley+Interdisciplinary+Reviews%3A+Nanomedicine+and+Nanobiotechnology&rft.issn=19395116&rft_id=info:doi/10.1002%2Fwnan.1250
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-12-01
N1 - Last updated - 2016-08-03
N1 - SubjectsTermNotLitGenreText - Drug delivery; Macromolecules; Magnetic resonance imaging; Gadolinium; Therapeutic applications; Pharmacokinetics; Blood; Reviews; Computed tomography; Contrast media; Kidney; Liver; Chelates; nanotechnology
DO - http://dx.doi.org/10.1002/wnan.1250
ER -
TY - JOUR
T1 - Cumulative Proportion of Responders Analysis (CPRA) as a Tool to Assess Treatment Outcome in Alcohol Clinical Trials
AN - 1550984222; 201425362
AB - Objective: Several definitions of treatment response have been proposed for alcohol clinical trials (e.g., abstinence and no heavy drinking). However, each of these outcomes allows only one definition of successful response. In contrast, the cumulative proportion of responders analysis (CPRA) includes all of the possible drinking response cutoff points, providing a more complete picture of the therapeutic effects of a treatment. CPRA has been used to examine the efficacy of analgesics but not alcohol pharmacotherapy. To demonstrate its potential utility, we conducted CPRA in two large alcohol treatment trials: the COMBINE (Combined Pharmacotherapies and Behavioral Interventions for Alcohol Dependence) trial (naltrexone) and a multisite topiramate trial. CPRA was used to demonstrate the efficacy of naltrexone and topiramate on continuous measures of in-treatment drinkingheavy drinking days and drinks per dayand their reductions from pretreatment. Method: All possible cutoff points were portrayed for each measure. We provide graphs to illustrate the effects of the active medications compared with placebo and examined them statistically over a number of salient drinking outcomes to evaluate their efficacy. Results: Treatment group responder curves were not parallel across the entire range of cutoff points; rather, they separated only at lower levels of drinking. In general, effect sizes increased by 0.10-0.15 when going from the lowest drinking level cutoff (i.e., abstinence and no heavy drinking) to the cutoff associated with the maximal treatment effect. Conclusions: CPRA may be useful in designing subsequent trials and helping to illustrate for treatment providers the likelihood of treatment success given various definitions of a positive response. Adapted from the source document.
JF - Journal of Studies on Alcohol and Drugs
AU - Falk, Daniel E
AU - Litten, Raye Z
AU - Anton, Raymond F
AU - Kranzler, Henry R
AU - Johnson, Bankole A
AD - Division of Treatment and Recovery Research, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland; National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, 5635 Fishers Lane, Room 2040, Rockville, MD 20852 falkde@mail.nih.gov
Y1 - 2014/03//
PY - 2014
DA - March 2014
SP - 335
EP - 346
PB - Center of Alcohol Studies, Rutgers, The State University of New Jersey, Piscataway
VL - 75
IS - 2
SN - 1937-1888, 1937-1888
KW - Clinical outcomes
KW - Alcohol consumption
KW - Pharmacology
KW - Efficacy
KW - Naltrexone
KW - Clinical trials
KW - article
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1550984222?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Studies+on+Alcohol+and+Drugs&rft.atitle=Cumulative+Proportion+of+Responders+Analysis+%28CPRA%29+as+a+Tool+to+Assess+Treatment+Outcome+in+Alcohol+Clinical+Trials&rft.au=Falk%2C+Daniel+E%3BLitten%2C+Raye+Z%3BAnton%2C+Raymond+F%3BKranzler%2C+Henry+R%3BJohnson%2C+Bankole+A&rft.aulast=Falk&rft.aufirst=Daniel&rft.date=2014-03-01&rft.volume=75&rft.issue=2&rft.spage=335&rft.isbn=&rft.btitle=&rft.title=Journal+of+Studies+on+Alcohol+and+Drugs&rft.issn=19371888&rft_id=info:doi/
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Date revised - 2014-08-01
N1 - Last updated - 2016-09-27
N1 - SubjectsTermNotLitGenreText - Alcohol consumption; Efficacy; Naltrexone; Pharmacology; Clinical outcomes; Clinical trials
ER -
TY - JOUR
T1 - Accuracy and efficacy of percutaneous biopsy and ablation using robotic assistance under computed tomography guidance: a phantom study
AN - 1544002737; 19326088
AB - Objective: To compare the accuracy of a robotic interventional radiologist (IR) assistance platform with a standard freehand technique for computed-tomography (CT)-guided biopsy and simulated radiofrequency ablation (RFA). Methods: The accuracy of freehand single-pass needle insertions into abdominal phantoms was compared with insertions facilitated with the use of a robotic assistance platform (n=20 each). Post-procedural CTs were analysed for needle placement error. Percutaneous RFA was simulated by sequentially placing five 17-gauge needle introducers into 5-cm diameter masses (n=5) embedded within an abdominal phantom. Simulated ablations were planned based on pre-procedural CT, before multi-probe placement was executed freehand. Multi-probe placement was then performed on the same 5-cm mass using the ablation planning software and robotic assistance. Post-procedural CTs were analysed to determine the percentage of untreated residual target. Results: Mean needle tip-to-target errors were reduced with use of the IR assistance platform (both P<0.0001). Reduced percentage residual tumour was observed with treatment planning (P=0.02). Conclusion: Improved needle accuracy and optimised probe geometry are observed during simulated CT-guided biopsy and percutaneous ablation with use of a robotic IR assistance platform. This technology may be useful for clinical CT-guided biopsy and RFA, when accuracy may have an impact on outcome. Key points: : times A recently developed robotic intervention radiology assistance platform facilitates CT-guided interventions. times Improved accuracy of complex needle insertions is achievable. times IR assistance platform use can improve target ablation coverage.
JF - European Radiology
AU - Koethe, Yilun
AU - Xu, Sheng
AU - Velusamy, Gnanasekar
AU - Wood, Bradford J
AU - Venkatesan, Aradhana M
AD - Center for Interventional Oncology, NIH Clinical Center, National Institutes of Health, Bethesda, MD, USA, venkatesana@cc.nih.gov
Y1 - 2014/03//
PY - 2014
DA - Mar 2014
SP - 723
EP - 730
PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL - 24
IS - 3
SN - 0938-7994, 0938-7994
KW - Biotechnology and Bioengineering Abstracts
KW - Computer programs
KW - software
KW - Computed tomography
KW - Probes
KW - robotics
KW - Biopsy
KW - Radiology
KW - W 30910:Imaging
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1544002737?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+Radiology&rft.atitle=Accuracy+and+efficacy+of+percutaneous+biopsy+and+ablation+using+robotic+assistance+under+computed+tomography+guidance%3A+a+phantom+study&rft.au=Koethe%2C+Yilun%3BXu%2C+Sheng%3BVelusamy%2C+Gnanasekar%3BWood%2C+Bradford+J%3BVenkatesan%2C+Aradhana+M&rft.aulast=Koethe&rft.aufirst=Yilun&rft.date=2014-03-01&rft.volume=24&rft.issue=3&rft.spage=723&rft.isbn=&rft.btitle=&rft.title=European+Radiology&rft.issn=09387994&rft_id=info:doi/10.1007%2Fs00330-013-3056-y
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-07-01
N1 - Number of references - 30
N1 - Last updated - 2014-07-10
N1 - SubjectsTermNotLitGenreText - Computer programs; software; Computed tomography; Probes; Biopsy; robotics; Radiology
DO - http://dx.doi.org/10.1007/s00330-013-3056-y
ER -
TY - JOUR
T1 - Alcohol abuse in developed and developing countries in the World Mental Health Surveys: Socially defined consequences or psychiatric disorder?
AN - 1541981377; 201417586
AB - Background Previous single country research has raised concerns that: (1) the DSM-IV diagnosis of alcohol abuse (AA) is met primarily through the hazardous use criterion related to drinking and driving and (2) that the hazardous use and social consequences AA criteria primarily reflect varying socioeconomic and cultural factors rather than psychiatric disorder. Methods Using representative cross-national data from the 21 countries in the World Mental Health surveys, adults meeting DSM-IV lifetime criteria for AA but not dependence from 10 developed (n=46,071) and 11 developing (n=49,761) countries were assessed as meeting AA with the hazardous use or the social consequences criteria. Results Between 29.3% (developed) and 16.2% (developing) of respondents with AA met only the hazardous use criterion. AA cases with and without hazardous use were similar in age-of-onset, course, predictors, and psychopathological consequences in both developed and developing countries. Discussion and Conclusions Despite some associations of the AA criteria with socioeconomic factors, the hazardous use and social consequences criteria were significantly associated with psychiatric predictors and sequelae. The findings indicate that these criteria reflect psychiatric disorder and are appropriate for inclusion as DSM-5 Alcohol Use Disorder criteria. Scientific Significance These findings support a psychiatric rather than a sociocultural view of the hazardous use and social consequences symptoms and provide evidence that they are appropriate diagnostic criteria cross-nationally with utility in a wide range of socioeconomic environments. This suggests consideration for their adoption by ICD-11. Further research is needed on the implications of these results for prevention and treatment. Adapted from the source document.
JF - The American Journal on Addictions
AU - Glantz, Meyer D
AU - Medina-Mora, Maria Elena
AU - Petukhova, Maria
AU - Andrade, Laura Helena
AU - Anthony, James C
AU - de Girolamo, Giovanni
AU - de Graaf, Ron
AU - Degenhardt, Louisa
AU - Demyttenaere, Koen
AU - Florescu, Silvia
AU - Gureje, Oye
AU - Haro, Josep Maria
AU - Horiguchi, Itsuko
AU - Karam, Elie G
AU - Kostyuchenko, Stanislav
AU - Lee, Sing
AU - Lepine, Jean-Pierre
AU - Matschinger, Herbert
AU - Neumark, Yehuda
AU - Posada-Villa, Jose
AU - Sagar, Rajesh
AU - Stein, Dan J
AU - Tomov, Toma
AU - Wells, J Elisabeth
AU - Chatterji, Somnath
AU - Kessler, Ronald C
AD - Division of Epidemiology, Services, and Prevention Research, National Institute on Drug Abuse, National Institutes of Health, Bethesda, Maryland.
Y1 - 2014/03//
PY - 2014
DA - March 2014
SP - 145
EP - 155
PB - Wiley Subscription Services, Inc.
VL - 23
IS - 2
SN - 1055-0496, 1055-0496
KW - Socioeconomic factors
KW - Alcohol abuse
KW - Psychiatric disorders
KW - Mental health
KW - Cultural aspects
KW - Developing countries
KW - article
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541981377?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+American+Journal+on+Addictions&rft.atitle=Alcohol+abuse+in+developed+and+developing+countries+in+the+World+Mental+Health+Surveys%3A+Socially+defined+consequences+or+psychiatric+disorder%3F&rft.au=Glantz%2C+Meyer+D%3BMedina-Mora%2C+Maria+Elena%3BPetukhova%2C+Maria%3BAndrade%2C+Laura+Helena%3BAnthony%2C+James+C%3Bde+Girolamo%2C+Giovanni%3Bde+Graaf%2C+Ron%3BDegenhardt%2C+Louisa%3BDemyttenaere%2C+Koen%3BFlorescu%2C+Silvia%3BGureje%2C+Oye%3BHaro%2C+Josep+Maria%3BHoriguchi%2C+Itsuko%3BKaram%2C+Elie+G%3BKostyuchenko%2C+Stanislav%3BLee%2C+Sing%3BLepine%2C+Jean-Pierre%3BMatschinger%2C+Herbert%3BNeumark%2C+Yehuda%3BPosada-Villa%2C+Jose%3BSagar%2C+Rajesh%3BStein%2C+Dan+J%3BTomov%2C+Toma%3BWells%2C+J+Elisabeth%3BChatterji%2C+Somnath%3BKessler%2C+Ronald+C&rft.aulast=Glantz&rft.aufirst=Meyer&rft.date=2014-03-01&rft.volume=23&rft.issue=2&rft.spage=145&rft.isbn=&rft.btitle=&rft.title=The+American+Journal+on+Addictions&rft.issn=10550496&rft_id=info:doi/10.1111%2Fj.1521-0391.2013.12082.x
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Date revised - 2014-07-01
N1 - Last updated - 2016-09-27
N1 - SubjectsTermNotLitGenreText - Psychiatric disorders; Alcohol abuse; Mental health; Developing countries; Socioeconomic factors; Cultural aspects
DO - http://dx.doi.org/10.1111/j.1521-0391.2013.12082.x
ER -
TY - JOUR
T1 - Implementation of a Tailored Kiosk-Based Injury Prevention Program in Pediatric Primary Care
AN - 1541979627; 201423512
AB - This study identified behavioral and organizational barriers and facilitators related to the implementation of a clinic-based pediatric injury prevention program. Safe N' Sound (SNS), an evidence-based tailored injury prevention program designed for pediatric primary care, was implemented in five pediatric clinics in North Carolina. Office managers participated in structured interviews; health care providers participated in focus groups. Waiting room observations were conducted in participating clinics. Qualitative data captured perceptions of program implementation, including experience in integrating the program into clinical practice, usage by parents and providers, and recommendations for improving implementation. Reported facilitators of program use included usefulness and likeability of customized materials by parents and physicians and alignment with clinic priorities for injury prevention. Barriers included perceived staff burden despite the program's low staff requirements. Consequently, practices experienced difficulty integrating the program into the waiting room environment and within existing staff roles. Recommendations included formalizing staff roles in implementation. Waiting room observations supported greater technology maintenance and staff involvement. Findings suggest a dynamic relationship between program implementation and the adopting organization. In addition to considering characteristics of the intervention, environment, and personnel in intervention development, implementation may require customization to the organization's capacity. [Reprinted by permission of Sage Publications Inc., copyright holder.]
JF - Health Promotion Practice
AU - Tse, Julia
AU - Nansel, Tonja R
AU - Weaver, Nancy L
AU - Williams, Janice
AU - Botello-Harbaum, Maria
AD - Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD, USA
Y1 - 2014/03//
PY - 2014
DA - March 2014
SP - 243
EP - 251
PB - Sage Publications, Thousand Oaks CA
VL - 15
IS - 2
SN - 1524-8399, 1524-8399
KW - injury prevention anticipatory guidance pediatric counseling implementation dissemination evidence-based barriers facilitators
KW - Paediatrics
KW - Injuries
KW - Clinics
KW - Facilitators
KW - Waiting rooms
KW - Preventive programmes
KW - article
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541979627?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Health+Promotion+Practice&rft.atitle=Implementation+of+a+Tailored+Kiosk-Based+Injury+Prevention+Program+in+Pediatric+Primary+Care&rft.au=Tse%2C+Julia%3BNansel%2C+Tonja+R%3BWeaver%2C+Nancy+L%3BWilliams%2C+Janice%3BBotello-Harbaum%2C+Maria&rft.aulast=Tse&rft.aufirst=Julia&rft.date=2014-03-01&rft.volume=15&rft.issue=2&rft.spage=243&rft.isbn=&rft.btitle=&rft.title=Health+Promotion+Practice&rft.issn=15248399&rft_id=info:doi/10.1177%2F1524839913504586
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Date revised - 2014-07-01
N1 - Number of references - 22
N1 - Last updated - 2016-09-27
N1 - SubjectsTermNotLitGenreText - Paediatrics; Injuries; Clinics; Preventive programmes; Waiting rooms; Facilitators
DO - http://dx.doi.org/10.1177/1524839913504586
ER -
TY - JOUR
T1 - Acetaldehyde and the genome: Beyond nuclear DNA adducts and carcinogenesis
AN - 1534857380; 19846875
AB - The designation of acetaldehyde associated with the consumption of alcoholic beverages as "carcinogenic to humans" (Group 1) by the International Agency for Research on Cancer (IARC) has brought renewed attention to the biological effects of acetaldehyde, as the primary oxidative metabolite of alcohol. Therefore, the overall focus of this review is on acetaldehyde and its direct and indirect effects on the nuclear and mitochondrial genome. We first consider different acetaldehyde-DNA adducts, including a critical assessment of the evidence supporting a role for acetaldehyde-DNA adducts in alcohol related carcinogenesis, and consideration of additional data needed to make a conclusion. We also review recent data on the role of the Fanconi anemia DNA repair pathway in protecting against acetaldehyde genotoxicity and carcinogenicity, as well as teratogenicity. We also review evidence from the older literature that acetaldehyde may impact the genome indirectly, via the formation of adducts with proteins that are themselves critically involved in the maintenance of genetic and epigenetic stability. Finally, we note the lack of information regarding acetaldehyde effects on the mitochondrial genome, which is notable since aldehyde dehydrogenase 2 (ALDH2), the primary acetaldehyde metabolic enzyme, is located in the mitochondrion, and roughly 30% of East Asian individuals are deficient in ALDH2 activity due to a genetic variant in the ALDH2 gene. In summary, a comprehensive understanding of all of the mechanisms by which acetaldehyde impacts the function of the genome has implications not only for alcohol and cancer, but types of alcohol related pathologies as well. Environ. Mol. Mutagen. 55:77-91, 2014. copyright 2013 Wiley Periodicals, Inc.
JF - Environmental and Molecular Mutagenesis
AU - Brooks, Philip J
AU - Zakhari, Samir
AD - Division of Metabolism and Health Effects, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland.
Y1 - 2014/03//
PY - 2014
DA - Mar 2014
SP - 77
EP - 91
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 55
IS - 2
SN - 0893-6692, 0893-6692
KW - Toxicology Abstracts; Health & Safety Science Abstracts; Biochemistry Abstracts 2: Nucleic Acids; Genetics Abstracts
KW - Genomes
KW - Mutagens
KW - Pathology
KW - Acetaldehyde
KW - Mitochondria
KW - Metabolites
KW - Mutagenesis
KW - Aldehyde dehydrogenase (NAD)
KW - Carcinogenicity
KW - epigenetics
KW - alcohols
KW - Alcohol
KW - DNA adducts
KW - Alcoholic beverages
KW - Data processing
KW - Genotoxicity
KW - Anemia
KW - Enzymes
KW - DNA repair
KW - Maintenance
KW - Cancer
KW - Biological effects
KW - Reviews
KW - Fanconi syndrome
KW - Carcinogenesis
KW - DNA
KW - Proteins
KW - Teratogenicity
KW - Aldehyde dehydrogenase
KW - H 6000:Natural Disasters/Civil Defense/Emergency Management
KW - X 24380:Social Poisons & Drug Abuse
KW - N 14820:DNA Metabolism & Structure
KW - G 07710:Chemical Mutagenesis & Radiation
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+and+Molecular+Mutagenesis&rft.atitle=Acetaldehyde+and+the+genome%3A+Beyond+nuclear+DNA+adducts+and+carcinogenesis&rft.au=Brooks%2C+Philip+J%3BZakhari%2C+Samir&rft.aulast=Brooks&rft.aufirst=Philip&rft.date=2014-03-01&rft.volume=55&rft.issue=2&rft.spage=77&rft.isbn=&rft.btitle=&rft.title=Environmental+and+Molecular+Mutagenesis&rft.issn=08936692&rft_id=info:doi/10.1002%2Fem.21824
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-01
N1 - Last updated - 2014-10-30
N1 - SubjectsTermNotLitGenreText - Genomes; DNA adducts; Mutagens; Data processing; Alcoholic beverages; Acetaldehyde; Genotoxicity; Mitochondria; Enzymes; Metabolites; DNA repair; Cancer; Mutagenesis; Aldehyde dehydrogenase (NAD); epigenetics; Fanconi syndrome; Reviews; Carcinogenesis; alcohols; Teratogenicity; Aldehyde dehydrogenase; Alcohol; Pathology; Anemia; Maintenance; Biological effects; Carcinogenicity; DNA; Proteins
DO - http://dx.doi.org/10.1002/em.21824
ER -
TY - JOUR
T1 - Effect of acid activated clay minerals on biodegradation of crude oil hydrocarbons
AN - 1534850670; 20038826
AB - The role of acid activated clays and unmodified clays in hydrocarbon removal during biodegradation was investigated in aqueous clay/oil microcosm experiments with a hydrocarbon degrading microorganism community. The clay minerals used for this study were Na-montmorillonite, palygorskite, saponite and kaolinite. The clay mineral samples were treated with hydrochloric acid to produce acid activated clays which were used in this study. The study indicated that acid activated clays and untreated kaolinite were inhibitory to biodegradation of the hydrocarbons via different mechanisms whereas the untreated saponite was neutral to biodegradation of the hydrocarbons. However, untreated palygorskite and Namontmorillonite were stimulatory to biodegradation and appears to do so as a result of the clays' ability to provide high surface area for the accumulation of microbes and nutrients such that the nutrients are within the 'vicinity' of the microbes. Adsorption of hydrocarbons was significant during biodegradation especially with unmodified palygorskite, where there was more than 40% removal of total petroleum hydrocarbons (TPH) by adsorption in the experimental microcosm containing 5:1 ratio (w/w) of clay to oil.
JF - International Biodeterioration & Biodegradation
AU - Ugochukwu, Uzochukwu C
AU - Jones, Martin D
AU - Head, Ian M
AU - Manning, David AC
AU - Fialips, Claire I
AD - School of Civil Engineering and Geosciences, University of Newcastle Upon Tyne, Drummond Building, NEI 7RU, United Kingdom, ugouzochukwu@yahoo.com
Y1 - 2014/03//
PY - 2014
DA - March 2014
SP - 185
EP - 191
PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom
VL - 88
SN - 0964-8305, 0964-8305
KW - Environment Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology; Biotechnology and Bioengineering Abstracts
KW - Acid activated clay
KW - Unmodified clay
KW - Biodegradation
KW - Adsorption
KW - Total petroleum hydrocarbon
KW - Microbial cells
KW - Biodeterioration
KW - Clay
KW - Hydrocarbons
KW - Surface area
KW - Nutrients
KW - kaolinite
KW - Clays
KW - Oil
KW - Crude oil
KW - Petroleum
KW - Microorganisms
KW - Microcosms
KW - Minerals
KW - Hydrochloric acid
KW - Petroleum hydrocarbons
KW - ENA 11:Non-Renewable Resources
KW - W 30950:Waste Treatment & Pollution Clean-up
KW - A 01320:Microbial Degradation
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534850670?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Biodeterioration+%26+Biodegradation&rft.atitle=Effect+of+acid+activated+clay+minerals+on+biodegradation+of+crude+oil+hydrocarbons&rft.au=Ugochukwu%2C+Uzochukwu+C%3BJones%2C+Martin+D%3BHead%2C+Ian+M%3BManning%2C+David+AC%3BFialips%2C+Claire+I&rft.aulast=Ugochukwu&rft.aufirst=Uzochukwu&rft.date=2014-03-01&rft.volume=88&rft.issue=&rft.spage=185&rft.isbn=&rft.btitle=&rft.title=International+Biodeterioration+%26+Biodegradation&rft.issn=09648305&rft_id=info:doi/10.1016%2Fj.ibiod.2013.10.018
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-01
N1 - Last updated - 2016-07-20
N1 - SubjectsTermNotLitGenreText - Biodeterioration; Biodegradation; Hydrocarbons; Surface area; Nutrients; kaolinite; Clays; Oil; Petroleum; Microorganisms; Adsorption; Microcosms; Minerals; Hydrochloric acid; Crude oil; Clay; Petroleum hydrocarbons
DO - http://dx.doi.org/10.1016/j.ibiod.2013.10.018
ER -
TY - JOUR
T1 - THYROID CANCER STUDY AMONG UKRAINIAN CHILDREN EXPOSED TO RADIATION AFTER THE CHORNOBYL ACCIDENT: IMPROVED ESTIMATES OF THE THYROID DOSES TO THE COHORT MEMBERS
AN - 1534846327; 19900498
AB - In collaboration with the Ukrainian Research Center for Radiation Medicine, the U.S. National Cancer Institute initiated a cohort study of children and adolescents exposed to Chornobyl fallout in Ukraine to better understand the long-term health effects of exposure to radioactive iodines. All 13,204 cohort members were subjected to at least one direct thyroid measurement between 30 April and 30 June 1986 and resided at the time of the accident in the northern parts of Kyiv, Zhytomyr, or Chernihiv Oblasts, which were the most contaminated territories of Ukraine as a result of radioactive fallout from the Chornobyl accident. Thyroid doses for the cohort members, which had been estimated following the first round of interviews, were re-evaluated following the second round of interviews. The revised thyroid doses range from 0.35 mGy to 42 Gy, with 95% of the doses between 1 mGy and 4.2 Gy, an arithmetic mean of 0.65 Gy, and a geometric mean of 0.19 Gy. These means are 70% of the previous estimates, mainly because of the use of country-specific thyroid masses. Many of the individual thyroid dose estimates show substantial differences because of the use of an improved questionnaire for the second round of interviews. Limitations of the current set of thyroid dose estimates are discussed. For the epidemiologic study, the most notable improvement is a revised assessment of the uncertainties, as shared and unshared uncertainties in the parameter values were considered in the calculation of the 1,000 stochastic estimates of thyroid dose for each cohort member. This procedure makes it possible to perform a more realistic risk analysis.
JF - Health Physics
AU - Likhtarov, Ilya
AU - Kovgan, Lina
AU - Masiuk, Sergii
AU - Talerko, Mykola
AU - Chepurny, Mykola
AU - Ivanova, Olga
AU - Gerasymenko, Valentina
AU - Boyko, Zulfira
AU - Voilleque, Paul
AU - Drozdovitch, Vladimir
AU - Bouville, Andre
AD - State Institution "National Research Centre for Radiation Medicine," National Academy of Medical Sciences of Ukraine, 53 Melnikova Street, 04050 Kyiv, Ukraine, drozdovv@mail.nih.gov.
Y1 - 2014/03//
PY - 2014
DA - Mar 2014
SP - 370
EP - 396
PB - Williams & Wilkins, 351 W. Camden St. Baltimore MD 21201 United States
VL - 106
IS - 3
SN - 0017-9078, 0017-9078
KW - Risk Abstracts; Health & Safety Science Abstracts
KW - 131I
KW - Chernobyl
KW - dose assessment
KW - thyroid
KW - Risk analysis
KW - Ukraine
KW - Thyroid
KW - Territory
KW - Children
KW - Cancer
KW - Health risks
KW - USA
KW - Accidents
KW - Radiation
KW - Radioactive fallout
KW - Iodine
KW - Adolescents
KW - H 8000:Radiation Safety/Electrical Safety
KW - R2 23060:Medical and environmental health
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534846327?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Health+Physics&rft.atitle=THYROID+CANCER+STUDY+AMONG+UKRAINIAN+CHILDREN+EXPOSED+TO+RADIATION+AFTER+THE+CHORNOBYL+ACCIDENT%3A+IMPROVED+ESTIMATES+OF+THE+THYROID+DOSES+TO+THE+COHORT+MEMBERS&rft.au=Likhtarov%2C+Ilya%3BKovgan%2C+Lina%3BMasiuk%2C+Sergii%3BTalerko%2C+Mykola%3BChepurny%2C+Mykola%3BIvanova%2C+Olga%3BGerasymenko%2C+Valentina%3BBoyko%2C+Zulfira%3BVoilleque%2C+Paul%3BDrozdovitch%2C+Vladimir%3BBouville%2C+Andre&rft.aulast=Likhtarov&rft.aufirst=Ilya&rft.date=2014-03-01&rft.volume=106&rft.issue=3&rft.spage=370&rft.isbn=&rft.btitle=&rft.title=Health+Physics&rft.issn=00179078&rft_id=info:doi/10.1097%2FHP.0b013e31829f3096
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-01
N1 - Last updated - 2015-05-27
N1 - SubjectsTermNotLitGenreText - Health risks; Risk analysis; Accidents; Radiation; Radioactive fallout; Thyroid; Iodine; Territory; Children; Cancer; Adolescents; USA; Ukraine
DO - http://dx.doi.org/10.1097/HP.0b013e31829f3096
ER -
TY - JOUR
T1 - Overfitting, generalization, and MSE in class probability estimation with high-dimensional data
AN - 1534827288; 20037663
AB - Accurate class probability estimation is important for medical decision making but is challenging, particularly when the number of candidate features exceeds the number of cases. Special methods have been developed for nonprobabilistic classification, but relatively little attention has been given to class probability estimation with numerous candidate variables. In this paper, we investigate overfitting in the development of regularized class probability estimators. We investigate the relation between overfitting and accurate class probability estimation in terms of mean square error. Using simulation studies based on real datasets, we found that some degree of overfitting can be desirable for reducing mean square error. We also introduce a mean square error decomposition for class probability estimation that helps clarify the relationship between overfitting and prediction accuracy.
JF - Biometrical Journal
AU - Kim, Kyung In
AU - Simon, Richard
AD - Biometric Research Branch, National Cancer Institute, 9609 Medical Center Dr, MSC 9735 Bethesda, MD 20892-9735, USA.
Y1 - 2014/03//
PY - 2014
DA - Mar 2014
SP - 256
EP - 269
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 56
IS - 2
SN - 0323-3847, 0323-3847
KW - Biotechnology and Bioengineering Abstracts
KW - Decision making
KW - Data processing
KW - Statistics
KW - Classification
KW - Biometrics
KW - Decomposition
KW - W 30900:Methods
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534827288?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biometrical+Journal&rft.atitle=Overfitting%2C+generalization%2C+and+MSE+in+class+probability+estimation+with+high-dimensional+data&rft.au=Kim%2C+Kyung+In%3BSimon%2C+Richard&rft.aulast=Kim&rft.aufirst=Kyung&rft.date=2014-03-01&rft.volume=56&rft.issue=2&rft.spage=256&rft.isbn=&rft.btitle=&rft.title=Biometrical+Journal&rft.issn=03233847&rft_id=info:doi/10.1002%2Fbimj.201300083
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-01
N1 - Last updated - 2014-06-26
N1 - SubjectsTermNotLitGenreText - Decision making; Statistics; Data processing; Classification; Biometrics; Decomposition
DO - http://dx.doi.org/10.1002/bimj.201300083
ER -
TY - JOUR
T1 - ATHENA: the analysis tool for heritable and environmental network associations
AN - 1534822276; 19360573
AB - Motivation: Advancements in high-throughput technology have allowed researchers to examine the genetic etiology of complex human traits in a robust fashion. Although genome-wide association studies have identified many novel variants associated with hundreds of traits, a large proportion of the estimated trait heritability remains unexplained. One hypothesis is that the commonly used statistical techniques and study designs are not robust to the complex etiology that may underlie these human traits. This etiology could include non-linear gene gene or gene environment interactions. Additionally, other levels of biological regulation may play a large role in trait variability.Results: To address the need for computational tools that can explore enormous datasets to detect complex susceptibility models, we have developed a software package called the Analysis Tool for Heritable and Environmental Network Associations (ATHENA). ATHENA combines various variable filtering methods with machine learning techniques to analyze high-throughput categorical (i.e. single nucleotide polymorphisms) and quantitative (i.e. gene expression levels) predictor variables to generate multivariable models that predict either a categorical (i.e. disease status) or quantitative (i.e. cholesterol levels) outcomes. The goal of this article is to demonstrate the utility of ATHENA using simulated and biological datasets that consist of both single nucleotide polymorphisms and gene expression variables to identify complex prediction models. Importantly, this method is flexible and can be expanded to include other types of high-throughput data (i.e. RNA-seq data and biomarker measurements).
JF - Bioinformatics
AU - Holzinger, Emily R
AU - Dudek, Scott M
AU - Frase, Alex T
AU - Pendergrass, Sarah A
AU - Ritchie, Marylyn D
AD - super(1)Inherited Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Baltimore, MD, USA and super(2)Department of Biochemistry and Molecular Biology, Center for Systems Genomics, Pennsylvania State University, University Park, PA, USA
Y1 - 2014/03/01/
PY - 2014
DA - 2014 Mar 01
SP - 698
EP - 705
PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL - 30
IS - 5
SN - 1367-4803, 1367-4803
KW - Biochemistry Abstracts 2: Nucleic Acids; Biotechnology and Bioengineering Abstracts
KW - Etiology
KW - Data processing
KW - Statistical analysis
KW - Cholesterol
KW - Computer applications
KW - biomarkers
KW - Models
KW - Gene expression
KW - Computer programs
KW - software
KW - Single-nucleotide polymorphism
KW - Learning algorithms
KW - Bioinformatics
KW - Internet
KW - Heritability
KW - N 14810:Methods
KW - W 30960:Bioinformatics & Computer Applications
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534822276?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Bioinformatics&rft.atitle=ATHENA%3A+the+analysis+tool+for+heritable+and+environmental+network+associations&rft.au=Holzinger%2C+Emily+R%3BDudek%2C+Scott+M%3BFrase%2C+Alex+T%3BPendergrass%2C+Sarah+A%3BRitchie%2C+Marylyn+D&rft.aulast=Holzinger&rft.aufirst=Emily&rft.date=2014-03-01&rft.volume=30&rft.issue=5&rft.spage=698&rft.isbn=&rft.btitle=&rft.title=Bioinformatics&rft.issn=13674803&rft_id=info:doi/10.1093%2Fbioinformatics%2Fbtt572
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-01
N1 - Last updated - 2016-05-13
N1 - SubjectsTermNotLitGenreText - Etiology; Data processing; Statistical analysis; Cholesterol; Computer applications; biomarkers; Models; Gene expression; Computer programs; software; Single-nucleotide polymorphism; Bioinformatics; Learning algorithms; Heritability; Internet
DO - http://dx.doi.org/10.1093/bioinformatics/btt572
ER -
TY - JOUR
T1 - Discretized Gaussian mixture for genotyping of microsatellite loci containing homopolymer runs
AN - 1534820830; 19360591
AB - Motivation: Inferring lengths of inherited microsatellite alleles with single base pair resolution from short sequence reads is challenging due to several sources of noise caused by the repetitive nature of microsatellites and the technologies used to generate raw sequence data.Results: We have developed a program, GenoTan, using a discretized Gaussian mixture model combined with a rules-based approach to identify inherited variation of microsatellite loci from short sequence reads without paired-end information. It effectively distinguishes length variants from noise including insertion/deletion errors in homopolymer runs by addressing the bidirectional aspect of insertion and deletion errors in sequence reads. Here we first introduce a homopolymer decomposition method which estimates error bias toward insertion or deletion in homopolymer sequence runs. Combining these approaches, GenoTan was able to genotype 94.9% of microsatellite loci accurately from simulated data with 40x sequence coverage quickly while the other programs showed <90% correct calls for the same data and required 5 similar to 30 more computational time than GenoTan. It also showed the highest true-positive rate for real data using mixed sequence data of two Drosophila inbred lines, which was a novel validation approach for genotyping.
JF - Bioinformatics
AU - Tae, Hongseok
AU - Kim, Dong-Yun
AU - McCormick, John
AU - Settlage, Robert E
AU - Garner, Harold R
AD - super(1)Virginia Bioinformatics Institute, Virginia Tech, Blacksburg, VA 24061 and super(2)Office of Biostatistics Research, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
Y1 - 2014/03/01/
PY - 2014
DA - 2014 Mar 01
SP - 652
EP - 659
PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL - 30
IS - 5
SN - 1367-4803, 1367-4803
KW - Biotechnology and Bioengineering Abstracts
KW - Genotyping
KW - Microsatellites
KW - Genotypes
KW - Computer applications
KW - Decomposition
KW - Models
KW - Computer programs
KW - software
KW - Insertion
KW - Inbreeding
KW - Bioinformatics
KW - Drosophila
KW - Internet
KW - W 30960:Bioinformatics & Computer Applications
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534820830?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Bioinformatics&rft.atitle=Discretized+Gaussian+mixture+for+genotyping+of+microsatellite+loci+containing+homopolymer+runs&rft.au=Tae%2C+Hongseok%3BKim%2C+Dong-Yun%3BMcCormick%2C+John%3BSettlage%2C+Robert+E%3BGarner%2C+Harold+R&rft.aulast=Tae&rft.aufirst=Hongseok&rft.date=2014-03-01&rft.volume=30&rft.issue=5&rft.spage=652&rft.isbn=&rft.btitle=&rft.title=Bioinformatics&rft.issn=13674803&rft_id=info:doi/10.1093%2Fbioinformatics%2Fbtt595
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-01
N1 - Last updated - 2014-08-07
N1 - SubjectsTermNotLitGenreText - Computer programs; software; Insertion; Genotyping; Microsatellites; Inbreeding; Genotypes; Bioinformatics; Computer applications; Decomposition; Internet; Models; Drosophila
DO - http://dx.doi.org/10.1093/bioinformatics/btt595
ER -
TY - JOUR
T1 - Serum leptin and loss of control eating in children and adolescents
AN - 1524394920; 19750242
AB - Background: Both insufficiency and resistance to the actions of the adipocyte-derived hormone leptin promote hunger, increased food intake and greater body weight. Some studies suggest that adults reporting binge eating have increased serum leptin compared with those without binge eating, even after adjusting for the greater adiposity that characterizes binge eaters. Pediatric binge or loss of control (LOC) eating are prospective risk factors for excessive weight gain and may predict development of metabolic abnormalities, but whether LOC eating is associated with higher leptin among children is unknown. We therefore examined leptin and LOC eating in a pediatric cohort. Methods: A convenience sample of 506 lean and obese youth (7-18 years) was recruited from Washington, DC and its suburbs. Serum leptin was collected after an overnight fast. Adiposity was measured by dual-energy X-ray absorptiometry or air displacement plethysmography. LOC eating was assessed by interview methodology. Results: Leptin was strongly associated with fat mass (r=0.79, P0.05). The relationship between LOC eating and leptin appeared to be significant for females only (P=0.002). Conclusions: Reports of LOC eating were associated with higher fasting leptin in youth, beyond the contributions of body weight. Prospective studies are required to elucidate whether LOC eating promotes greater leptin or whether greater leptin resistance may promote LOC eating.
JF - International Journal of Obesity
AU - Miller, R
AU - Tanofsky-Kraff, M
AU - Shomaker, L B
AU - Field, S E
AU - Hannallah, L
AU - Reina, S A
AU - Mooreville, M
AU - Sedaka, N
AU - Brady, S M
AU - Condarco, T
AU - Reynolds, J C
AU - Yanovski, S Z
AU - Yanovski, J A
AD - 1] Section on Growth and Obesity, Program in Developmental Endocrinology and Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH), DHHS, Hatfield Clinical Research Center, Bethesda, MD, USA [2] Department of Medical and Clinical Psychology, Uniformed Services University of the Health Sciences, Bethesda, MD, USA
Y1 - 2014/03//
PY - 2014
DA - Mar 2014
SP - 397
EP - 403
PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL - 38
IS - 3
SN - 0307-0565, 0307-0565
KW - Risk Abstracts
KW - Hunger
KW - Obesity
KW - Body weight
KW - Risk factors
KW - Children
KW - Hormones
KW - USA, Washington, D.C.
KW - Suburbs
KW - Adolescents
KW - R2 23060:Medical and environmental health
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1524394920?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Obesity&rft.atitle=Serum+leptin+and+loss+of+control+eating+in+children+and+adolescents&rft.au=Miller%2C+R%3BTanofsky-Kraff%2C+M%3BShomaker%2C+L+B%3BField%2C+S+E%3BHannallah%2C+L%3BReina%2C+S+A%3BMooreville%2C+M%3BSedaka%2C+N%3BBrady%2C+S+M%3BCondarco%2C+T%3BReynolds%2C+J+C%3BYanovski%2C+S+Z%3BYanovski%2C+J+A&rft.aulast=Miller&rft.aufirst=R&rft.date=2014-03-01&rft.volume=38&rft.issue=3&rft.spage=397&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Obesity&rft.issn=03070565&rft_id=info:doi/10.1038%2Fijo.2013.126
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-05-01
N1 - Last updated - 2014-05-29
N1 - SubjectsTermNotLitGenreText - Hunger; Obesity; Body weight; Risk factors; Children; Hormones; Adolescents; Suburbs; USA, Washington, D.C.
DO - http://dx.doi.org/10.1038/ijo.2013.126
ER -
TY - JOUR
T1 - Associations between child disabilities and caregiver discipline and violence in low- and middle-income countries
AN - 1521335782; 4555744
AB - Using nationally representative samples of 45,964 two- to nine-year-old children and their primary caregivers in 17 developing countries, this study examined the relations between children's cognitive, language, sensory, and motor disabilities and caregivers' use of discipline and violence. Primary caregivers reported on their child's disabilities and whether they or anyone in their household had used nonviolent discipline, psychological aggression, and physical violence toward the target child and believed that using corporal punishment is necessary. Logistic regression analyses supported the hypothesis that children with disabilities are treated more harshly than children without disabilities. The findings suggest that policies and interventions are needed to work toward the United Nations' goals of ensuring that children with disabilities are protected from abuse and violence. Reprinted by permission of the University of Chicago Press. © All rights reserved
JF - Child development
AU - Bornstein, Marc H
AU - Hendricks, Charlene
AU - Lansford, Jennifer E
AU - Deater-Deckard, Kirby
AD - National Institutes of Health ; Duke University ; Virginia Polytechnic Institute and State University
Y1 - 2014/03//
PY - 2014
DA - Mar 2014
SP - 513
EP - 531
VL - 85
IS - 2
SN - 0009-3920, 0009-3920
KW - Sociology
KW - Caring
KW - Disability
KW - Aggression
KW - Children
KW - Developing countries
KW - Violence
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1521335782?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Child+development&rft.atitle=Associations+between+child+disabilities+and+caregiver+discipline+and+violence+in+low-+and+middle-income+countries&rft.au=Bornstein%2C+Marc+H%3BHendricks%2C+Charlene%3BLansford%2C+Jennifer+E%3BDeater-Deckard%2C+Kirby&rft.aulast=Bornstein&rft.aufirst=Marc&rft.date=2014-03-01&rft.volume=85&rft.issue=2&rft.spage=513&rft.isbn=&rft.btitle=&rft.title=Child+development&rft.issn=00093920&rft_id=info:doi/10.1111%2Fcdev.12132
LA - English
DB - International Bibliography of the Social Sciences (IBSS)
N1 - Date revised - 2014-05-06
N1 - Last updated - 2014-05-07
N1 - SubjectsTermNotLitGenreText - 2212; 3584 1678; 2039 13521; 13325; 662; 3480 2958 12092
DO - http://dx.doi.org/10.1111/cdev.12132
ER -
TY - JOUR
T1 - Limited HIV-1 Superinfection in Seroconverters from the CAPRISA 004 Microbicide Trial
AN - 1520373038; 19446612
AB - HIV-1 superinfection (SI) occurs when an infected individual acquires a distinct new viral strain. The rate of superinfection may be reflective of the underlying HIV risk in a population. The Centre for the AIDS Programme of Research in South Africa (CAPRISA) 004 clinical trial demonstrated that women who used a tenofovir-containing microbicide gel had lower rates of HIV infection than women using a placebo gel. Women who contracted HIV-1 during the trial were screened for the occurrence of superinfection by next-generation sequencing of the viral gag and env genes. There were two cases (one in each trial arm) of subtype C superinfection identified from the 76 women with primary infection screened at two time points (rate of superinfection, 1.5/100 person-years). Both women experienced a >0.5-log increase in viral load during the window when superinfection occurred. The rate of superinfection was significantly lower than the overall primary HIV incidence in the microbicide trial (incidence rate ratio [IRR], 0.20; P = 0.003). The women who seroconverted during the trial reported a significant increase in sexual contact with their stable partner 4 months after seroconversion (P < 0.001), which may have lowered the risk of superinfection in this population. The lower frequency of SI compared to the primary incidence is in contrast to a report from a general heterosexual African population but agrees with a study of high-risk women in Kenya. A better understanding of the rate of HIV superinfection could have important implications for ongoing HIV vaccine research.
JF - Journal of Clinical Microbiology
AU - Redd, Andrew D
AU - Mullis, Caroline E
AU - Wendel, Sarah K
AU - Sheward, Daniel
AU - Martens, Craig
AU - Bruno, Daniel
AU - Werner, Lise
AU - Garrett, Nigel J
AU - Karim, Quarraisha Abdool
AU - Williamson, Carolyn
AD - Laboratory of Immunoregulation, Division of Intramural Research, NIAID, NIH, Bethesda, Maryland, USA, aredd2@jhmi.edu.
Y1 - 2014/03//
PY - 2014
DA - Mar 2014
SP - 844
EP - 848
PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL - 52
IS - 3
SN - 0095-1137, 0095-1137
KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Virology & AIDS Abstracts
KW - Acquired immune deficiency syndrome
KW - Human immunodeficiency virus
KW - Risk factors
KW - Human immunodeficiency virus 1
KW - Risk groups
KW - Seroconversion
KW - Vaccines
KW - Superinfection
KW - Clinical trials
KW - Gag protein
KW - microbicides
KW - A 01340:Antibiotics & Antimicrobials
KW - V 22360:AIDS and HIV
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1520373038?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Clinical+Microbiology&rft.atitle=Limited+HIV-1+Superinfection+in+Seroconverters+from+the+CAPRISA+004+Microbicide+Trial&rft.au=Redd%2C+Andrew+D%3BMullis%2C+Caroline+E%3BWendel%2C+Sarah+K%3BSheward%2C+Daniel%3BMartens%2C+Craig%3BBruno%2C+Daniel%3BWerner%2C+Lise%3BGarrett%2C+Nigel+J%3BKarim%2C+Quarraisha+Abdool%3BWilliamson%2C+Carolyn&rft.aulast=Redd&rft.aufirst=Andrew&rft.date=2014-03-01&rft.volume=52&rft.issue=3&rft.spage=844&rft.isbn=&rft.btitle=&rft.title=Journal+of+Clinical+Microbiology&rft.issn=00951137&rft_id=info:doi/10.1128%2FJCM.03143-13
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-01
N1 - Number of references - 16
N1 - Last updated - 2015-11-25
N1 - SubjectsTermNotLitGenreText - Acquired immune deficiency syndrome; Risk factors; Seroconversion; Risk groups; Vaccines; Clinical trials; Superinfection; Gag protein; microbicides; Human immunodeficiency virus; Human immunodeficiency virus 1
DO - http://dx.doi.org/10.1128/JCM.03143-13
ER -
TY - JOUR
T1 - Mutagenesis and phenotyping resources in zebrafish for studying development and human disease
AN - 1516739585; 19505047
AB - The zebrafish (Danio rerio) is an important model organism for studying development and human disease. The zebrafish has an excellent reference genome and the functions of hundreds of genes have been tested using both forward and reverse genetic approaches. Recent years have seen an increasing number of large-scale mutagenesis projects and the number of mutants or gene knockouts in zebrafish has increased rapidly, including for the first time conditional knockout technologies. In addition, targeted mutagenesis techniques such as zinc finger nucleases, transcription activator-like effector nucleases and clustered regularly interspaced short sequences (CRISPR) or CRISPR-associated (Cas), have all been shown to effectively target zebrafish genes as well as the first reported germline homologous recombination, further expanding the utility and power of zebrafish genetics. Given this explosion of mutagenesis resources, it is now possible to perform systematic, high-throughput phenotype analysis of all zebrafish gene knockouts.
JF - Briefings in Functional Genomics
AU - Varshney, Gaurav Kumar
AU - Burgess, Shawn Michael
AD - Corresponding author. Shawn Michael Burgess, Developmental Genomics Section, Genome Technology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA., burgess@mail.nih.gov
Y1 - 2014/03//
PY - 2014
DA - March 2014
SP - 82
EP - 94
PB - Oxford University Press, Oxford Journals, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL - 13
IS - 2
SN - 2041-2649, 2041-2649
KW - Genetics Abstracts; ASFA 1: Biological Sciences & Living Resources; Biotechnology and Bioengineering Abstracts
KW - zebrafish
KW - mutagenesis
KW - phenotyping
KW - resources
KW - knockouts
KW - Genomes
KW - Human diseases
KW - Nuclease
KW - Zinc finger proteins
KW - Transcription
KW - Freshwater
KW - Freshwater fish
KW - Phenotypes
KW - Explosions
KW - Models
KW - Mutagenesis
KW - Danio rerio
KW - Phenotyping
KW - Recombination
KW - targeted mutagenesis
KW - homologous recombination
KW - Resource development
KW - Q1 08604:Stock assessment and management
KW - G 07730:Development & Cell Cycle
KW - W 30900:Methods
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1516739585?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Briefings+in+Functional+Genomics&rft.atitle=Mutagenesis+and+phenotyping+resources+in+zebrafish+for+studying+development+and+human+disease&rft.au=Varshney%2C+Gaurav+Kumar%3BBurgess%2C+Shawn+Michael&rft.aulast=Varshney&rft.aufirst=Gaurav&rft.date=2014-03-01&rft.volume=13&rft.issue=2&rft.spage=82&rft.isbn=&rft.btitle=&rft.title=Briefings+in+Functional+Genomics&rft.issn=20412649&rft_id=info:doi/10.1093%2Fbfgp%2Felt042
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-01
N1 - Last updated - 2016-12-22
N1 - SubjectsTermNotLitGenreText - Genomes; Recombination; Human diseases; Transcription; Resource development; Freshwater fish; Phenotypes; Explosions; Mutagenesis; Phenotyping; targeted mutagenesis; Zinc finger proteins; Nuclease; homologous recombination; Models; Danio rerio; Freshwater
DO - http://dx.doi.org/10.1093/bfgp/elt042
ER -
TY - JOUR
T1 - Experience of an information aid for newly diagnosed multiple sclerosis patients: a qualitative study on the SIMS-Trial
AN - 1512193795; 201404444
AB - Background The SIMS-Trial (ISRCTN81072971) proved the effectiveness, in terms of patient's knowledge and care satisfaction, of an add-on information aid (personal interview with a physician using a navigable CD and take-home booklet) in 120 newly diagnosed patients with multiple sclerosis (MS) from five Italian centres. Objective To scrutinize the experience of SIMS-Trial participants in order to gain better understanding of the effectiveness of the information aid and its components. Design We performed (i) nine individual semi-structured interviews with a purposeful sample of SIMS-Trial patients who received the information aid, (ii) focus group meeting (FGM) with the physicians who conducted the personal interview, and (iii) FGM with patients' caring neurologists. Results Patients' experience with the information aid was positive as it enhanced their understanding of their disease, being viewed as a guided tour of their medical condition. The physicians who conducted the personal interviews were also positive in their overall evaluation but noted an initial difficulty in using the CD. The caring neurologists had limited direct experience of the aid, and their views were confined to utility of the information aid in general. All participants considered the combination of personal interview, CD navigation and take-home booklet essential, but urged a more flexible scheduling of the personal interview. It also emerged that some content required revision and that the aid was unsuitable for patients with primary progressive MS. Conclusions The results of the study further support the value of the aid and also provide important indications for improving it and refining indications for use. Adapted from the source document.
JF - Health Expectations
AU - Borreani, Claudia
AU - Giordano, Andrea
AU - Falautano, Monica
AU - Lugaresi, Alessandra
AU - Martinelli, Vittorio
AU - Granella, Franco
AU - Tortorella, Carla
AU - Plasmati, Imma
AU - Radaelli, Marta
AU - Farina, Deborah
AU - Dalla Bella, Eleonora
AU - Bianchi, Elisabetta
AU - Acquarone, Nicola
AU - Miccinesi, Guido
AU - Solari, Alessandra
AD - Psychology Unit, National Cancer Institute Foundation, Milan
Y1 - 2014/03//
PY - 2014
DA - March 2014
SP - 36
EP - 48
PB - Blackwell Publishing, Oxford UK
VL - 17
IS - 1
SN - 1369-6513, 1369-6513
KW - Neurologists
KW - Newly diagnosed
KW - Doctors
KW - Multiple sclerosis
KW - Caring
KW - Navigation
KW - article
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LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Date revised - 2014-04-01
N1 - Last updated - 2016-09-27
N1 - CODEN - HEHPFM
N1 - SubjectsTermNotLitGenreText - Multiple sclerosis; Doctors; Newly diagnosed; Caring; Neurologists; Navigation
DO - http://dx.doi.org/10.1111/j.1369-7625.2011.00736.x
ER -
TY - JOUR
T1 - Subchronic oral toxicity study of decitabine in combination with tetrahydrouridine in CD-1 mice.
AN - 1511820354; 24639139
AB - Decitabine (5-aza-2'-deoxycytidine; DAC) in combination with tetrahydrouridine (THU) is a potential oral therapy for sickle cell disease and β-thalassemia. A study was conducted in mice to assess safety of this combination therapy using oral gavage of DAC and THU administered 1 hour prior to DAC on 2 consecutive days/week for up to 9 weeks followed by a 28-day recovery to support its clinical trials up to 9-week duration. Tetrahydrouridine, a competitive inhibitor of cytidine deaminase, was used in the combination to improve oral bioavailability of DAC. Doses were 167 mg/kg THU followed by 0, 0.2, 0.4, or 1.0 mg/kg DAC; THU vehicle followed by 1.0 mg/kg DAC; or vehicle alone. End points evaluated were clinical observations, body weights, food consumption, clinical pathology, gross/histopathology, bone marrow micronuclei, and toxicokinetics. There were no treatment-related effects noticed on body weight, food consumption, serum chemistry, or urinalysis parameters. Dose- and gender-dependent changes in plasma DAC levels were observed with a Cmax within 1 hour. At the 1 mg/kg dose tested, THU increased DAC plasma concentration (∼ 10-fold) as compared to DAC alone. Severe toxicity occurred in females receiving high-dose 1 mg/kg DAC + THU, requiring treatment discontinuation at week 5. Severity and incidence of microscopic findings increased in a dose-dependent fashion; findings included bone marrow hypocellularity (with corresponding hematologic changes and decreases in white blood cells, red blood cells, hemoglobin, hematocrit, reticulocytes, neutrophils, and lymphocytes), thymic/lymphoid depletion, intestinal epithelial apoptosis, and testicular degeneration. Bone marrow micronucleus analysis confirmed bone marrow cytotoxicity, suppression of erythropoiesis, and genotoxicity. Following the recovery period, a complete or trend toward resolution of these effects was observed. In conclusion, the combination therapy resulted in an increased sensitivity to DAC toxicity correlating with DAC plasma levels, and females are more sensitive compared to their male counterparts.
JF - International journal of toxicology
AU - Terse, Pramod
AU - Engelke, Kory
AU - Chan, Kenneth
AU - Ling, Yonghua
AU - Sharpnack, Douglas
AU - Saunthararajah, Yogen
AU - Covey, Joseph M
AD - Division of Pre-Clinical Innovations, National Center for Advancing Translational Sciences, Bethesda, MD, USA. Email: tersep@mail.nih.gov.
PY - 2014
SP - 75
EP - 85
VL - 33
IS - 2
KW - Antimetabolites
KW - 0
KW - Antimetabolites, Antineoplastic
KW - Tetrahydrouridine
KW - 18771-50-1
KW - decitabine
KW - 776B62CQ27
KW - Azacitidine
KW - M801H13NRU
KW - Index Medicus
KW - combination therapy
KW - hematopoietic tissue
KW - lymphoid tissue
KW - tetrahydrouridine
KW - CD-1 mice
KW - Eating -- drug effects
KW - Bone Marrow Cells -- drug effects
KW - Animals
KW - Micronucleus Tests
KW - Body Weight -- drug effects
KW - Mice
KW - Pharmacokinetics
KW - Male
KW - Female
KW - Blood Cell Count
KW - Antimetabolites -- toxicity
KW - Azacitidine -- toxicity
KW - Azacitidine -- analogs & derivatives
KW - Tetrahydrouridine -- toxicity
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-11-18
N1 - Date created - 2014-03-31
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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Blood. 2000 Oct 1;96(7):2379-84 [11001887]
Blood. 2002 Jun 1;99(11):3905-8 [12010787]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1177/1091581814524994
ER -
TY - JOUR
T1 - Injection parameters and virus dependent choice of promoters to improve neuron targeting in the nonhuman primate brain
AN - 1508762158; 19387222
AB - We, like many others, wish to use modern molecular methods to alter neuronal functionality in primates. For us, this requires expression in a large proportion of the targeted cell population. Long generation times make germline modification of limited use. The size and intricate primate brain anatomy poses additional challenges. We surved methods using lentiviruses and serotypes of adeno-associated viruses (AAVs) to introduce active molecular material into cortical and subcortical regions of old-world monkey brains. Slow injections of AAV2 give well-defined expression of neurons in the cortex surrounding the injection site. Somewhat surprisingly we find that in the monkey the use of cytomegalovirus promoter in lentivirus primarily targets glial cells but few neurons. In contrast, with a synapsin promoter fragment the lentivirus expression is neuron specific at high transduction levels in all cortical layers. We also achieve specific targeting of tyrosine hydroxlase (TH)- rich neurons in the locus coeruleus and substantia nigra with a lentvirus carrying a fragment of the TH promoter. Lentiviruses carrying neuron specific promoters are suitable for both cortical and subcortical injections even when injected quickly.
JF - Gene Therapy
AU - Lerchner, W
AU - Corgiat, B
AU - Der Minassian, V
AU - Saunders, R C
AU - Richmond, B J
AD - Laboratory of Neuropsychology, National Institute of Mental Health/NIMH/DHHS, Bethesda, MD, USA
Y1 - 2014/03//
PY - 2014
DA - Mar 2014
SP - 233
EP - 241
PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL - 21
IS - 3
SN - 0969-7128, 0969-7128
KW - CSA Neurosciences Abstracts; Virology & AIDS Abstracts; Genetics Abstracts; Biotechnology and Bioengineering Abstracts
KW - Synapsin
KW - Substantia nigra
KW - Serotypes
KW - Gene therapy
KW - Locus coeruleus
KW - Glial cells
KW - Brain
KW - Tyrosine
KW - Cytomegalovirus
KW - Primates
KW - Adeno-associated virus
KW - Promoters
KW - Cortex
KW - Lentivirus
KW - Neurons
KW - W 30905:Medical Applications
KW - N3 11023:Neurogenetics
KW - G 07730:Development & Cell Cycle
KW - V 22310:Genetics, Taxonomy & Structure
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gene+Therapy&rft.atitle=Injection+parameters+and+virus+dependent+choice+of+promoters+to+improve+neuron+targeting+in+the+nonhuman+primate+brain&rft.au=Lerchner%2C+W%3BCorgiat%2C+B%3BDer+Minassian%2C+V%3BSaunders%2C+R+C%3BRichmond%2C+B+J&rft.aulast=Lerchner&rft.aufirst=W&rft.date=2014-03-01&rft.volume=21&rft.issue=3&rft.spage=233&rft.isbn=&rft.btitle=&rft.title=Gene+Therapy&rft.issn=09697128&rft_id=info:doi/10.1038%2Fgt.2013.75
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-03-01
N1 - Last updated - 2014-07-10
N1 - SubjectsTermNotLitGenreText - Synapsin; Substantia nigra; Promoters; Cortex; Serotypes; Gene therapy; Locus coeruleus; Glial cells; Neurons; Brain; Tyrosine; Lentivirus; Primates; Cytomegalovirus; Adeno-associated virus
DO - http://dx.doi.org/10.1038/gt.2013.75
ER -
TY - JOUR
T1 - Segmentation of PET Images for Computer-Aided Functional Quantification of Tuberculosis in Small Animal Models
AN - 1508757671; 19399848
AB - Pulmonary infections often cause spatially diffuse and multi-focal radiotracer uptake in positron emission tomography (PET) images, which makes accurate quantification of the disease extent challenging. Image segmentation plays a vital role in quantifying uptake due to the distributed nature of immuno-pathology and associated metabolic activities in pulmonary infection, specifically tuberculosis (TB). For this task, thresholding-based segmentation methods may be better suited over other methods; however, performance of the thresholding-based methods depend on the selection of thresholding parameters, which are often suboptimal. Several optimal thresholding techniques have been proposed in the literature, but there is currently no consensus on how to determine the optimal threshold for precise identification of spatially diffuse and multi-focal radiotracer uptake. In this study, we propose a method to select optimal thresholding levels by utilizing a novel intensity affinity metric within the affinity propagation clustering framework. We tested the proposed method against 70 longitudinal PET images of rabbits infected with TB. The overall dice similarity coefficient between the segmentation from the proposed method and two expert segmentations was found to be syntax error at token \\ with a sensitivity of syntax error at token \\ and a specificity of syntax error at token \\ . High accuracy and heightened efficiency of our proposed method, as compared to other PET image segmentation methods, were reported with various quantification metrics.
JF - IEEE Transactions on Biomedical Engineering
AU - Foster, Brent
AU - Bagci, Ulas
AU - Xu, Ziyue
AU - Dey, Bappaditya
AU - Luna, Brian
AU - Bishai, William
AU - Jain, Sanjay
AU - Mollura, Daniel J
AD - Center for Infectious Disease Imaging (CIDI), Department of Radiology and Imaging Sciences, National Institutes of Health, Bethesda, USA
Y1 - 2014/03//
PY - 2014
DA - Mar 2014
SP - 711
EP - 724
PB - Institute of Electrical and Electronics Engineers, Inc., 345 E. 47th St. NY NY 10017-2394 United States
VL - 61
IS - 3
SN - 0018-9294, 0018-9294
KW - Microbiology Abstracts B: Bacteriology; Biotechnology and Bioengineering Abstracts
KW - Mycobacterium
KW - Lung
KW - Segmentation
KW - Positron emission tomography
KW - Animal models
KW - Image processing
KW - Tuberculosis
KW - Infection
KW - J 02410:Animal Diseases
KW - W 30905:Medical Applications
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=IEEE+Transactions+on+Biomedical+Engineering&rft.atitle=Segmentation+of+PET+Images+for+Computer-Aided+Functional+Quantification+of+Tuberculosis+in+Small+Animal+Models&rft.au=Foster%2C+Brent%3BBagci%2C+Ulas%3BXu%2C+Ziyue%3BDey%2C+Bappaditya%3BLuna%2C+Brian%3BBishai%2C+William%3BJain%2C+Sanjay%3BMollura%2C+Daniel+J&rft.aulast=Foster&rft.aufirst=Brent&rft.date=2014-03-01&rft.volume=61&rft.issue=3&rft.spage=711&rft.isbn=&rft.btitle=&rft.title=IEEE+Transactions+on+Biomedical+Engineering&rft.issn=00189294&rft_id=info:doi/10.1109%2FTBME.2013.2288258
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-03-01
N1 - Last updated - 2015-03-20
N1 - SubjectsTermNotLitGenreText - Lung; Animal models; Positron emission tomography; Segmentation; Image processing; Tuberculosis; Infection; Mycobacterium
DO - http://dx.doi.org/10.1109/TBME.2013.2288258
ER -
TY - JOUR
T1 - Global fold of human cannabinoid type 2 receptor probed by solid-state super(13)C-, super(15)N-MAS NMR and molecular dynamics simulations
AN - 1505345092; 19318207
AB - The global fold of human cannabinoid type 2 (CB sub(2)) receptor in the agonist-bound active state in lipid bilayers was investigated by solid-state super(13)C- and super(15)N magic-angle spinning (MAS) NMR, in combination with chemical-shift prediction from a structural model of the receptor obtained by microsecond-long molecular dynamics (MD) simulations. Uniformly super(13)C- and super(15)N-labeled CB sub(2) receptor was expressed in milligram quantities by bacterial fermentation, purified, and functionally reconstituted into liposomes. super(13)C MAS NMR spectra were recorded without sensitivity enhancement for direct comparison of C sub([alpha]), C sub([beta]), and C==O bands of superimposed resonances with predictions from protein structures generated by MD. The experimental NMR spectra matched the calculated spectra reasonably well indicating agreement of the global fold of the protein between experiment and simulations. In particular, the super(13)C chemical shift distribution of C sub([alpha]) resonances was shown to be very sensitive to both the primary amino acid sequence and the secondary structure of CB sub(2). Thus the shape of the C sub([alpha]) band can be used as an indicator of CB sub(2) global fold. The prediction from MD simulations indicated that upon receptor activation a rather limited number of amino acid residues, mainly located in the extracellular Loop 2 and the second half of intracellular Loop 3, change their chemical shifts significantly ( greater than or equal to 1.5 ppm for carbons and greater than or equal to 5.0 ppm for nitrogens). Simulated two-dimensional super(13)C sub([alpha])(i)-- super(13)C[double horizonal line]O(i) and super(13)C[double horizonal line]O(i)-- super(15)NH(i + 1) dipolar-interaction correlation spectra provide guidance for selective amino acid labeling and signal assignment schemes to study the molecular mechanism of activation of CB sub(2) by solid-state MAS NMR. Proteins 2014; 82:452-465. copyright 2013 Wiley Periodicals, Inc.
JF - Proteins: Structure, Function and Bioinformatics
AU - Kimura, Tomohiro
AU - Vukoti, Krishna
AU - Lynch, Diane L
AU - Hurst, Dow P
AU - Grossfield, Alan
AU - Pitman, Michael C
AU - Reggio, Patricia H
AU - Yeliseev, Alexei A
AU - Gawrisch, Klaus
AD - Laboratory of Membrane Biochemistry and Biophysics, NIAAA, NIH, Bethesda, Maryland, 20892.
Y1 - 2014/03//
PY - 2014
DA - March 2014
SP - 452
EP - 465
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030 United States
VL - 82
IS - 3
SN - 0887-3585, 0887-3585
KW - Biotechnology and Bioengineering Abstracts
KW - cannabinoid receptor
KW - CB sub(2)
KW - GPCR
KW - G protein-coupled receptor
KW - solid-state NMR
KW - molecular dynamics simulation
KW - Molecular modelling
KW - Lipid bilayers
KW - Receptor mechanisms
KW - Fermentation
KW - Secondary structure
KW - Liposomes
KW - Spinning
KW - Protein structure
KW - Carbon
KW - Cannabinoid CB2 receptors
KW - N.M.R.
KW - Bioinformatics
KW - Amino acid sequence
KW - Nitrogen
KW - W 30960:Bioinformatics & Computer Applications
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-03-01
N1 - Last updated - 2016-06-22
N1 - SubjectsTermNotLitGenreText - Molecular modelling; Lipid bilayers; Receptor mechanisms; Fermentation; Secondary structure; Liposomes; Spinning; Protein structure; Carbon; Cannabinoid CB2 receptors; N.M.R.; Bioinformatics; Nitrogen; Amino acid sequence
DO - http://dx.doi.org/10.1002/prot.24411
ER -
TY - JOUR
T1 - Dynamic and inherent B sub(0) correction for DTI using stimulated echo spiral imaging
AN - 1505339627; 19338247
AB - Purpose To present a novel technique for high-resolution stimulated echo diffusion tensor imaging with self-navigated interleaved spirals readout trajectories that can inherently and dynamically correct for image artifacts due to spatial and temporal variations in the static magnetic field (B sub(0)) resulting from eddy currents, tissue susceptibilities, subject/physiological motion, and hardware instabilities. Methods The Hahn spin echo formed by the first two 90 degree radiofrequency pulses is balanced to consecutively acquire two additional images with different echo times and generate an inherent field map, while the diffusion-prepared stimulated echo signal remains unaffected. For every diffusion-encoding direction, an intrinsically registered field map is estimated dynamically and used to effectively and inherently correct for off-resonance artifacts in the reconstruction of the corresponding diffusion-weighted image. Results After correction with the dynamically acquired field maps, local blurring artifacts are specifically removed from individual stimulated echo diffusion-weighted images and the estimated diffusion tensors have significantly improved spatial accuracy and larger fractional anisotropy. Conclusion Combined with the self-navigated interleaved spirals acquisition scheme, our new method provides an integrated high-resolution short-echo time diffusion tensor imaging solution with inherent and dynamic correction for both motion-induced phase errors and off-resonance effects. Magn Reson Med 71:1044-1053, 2014. copyright 2013 Wiley Periodicals, Inc.
JF - Magnetic Resonance in Medicine
AU - Avram, Alexandru V
AU - Guidon, Arnaud
AU - Truong, Trong-Kha
AU - Liu, Chunlei
AU - Song, Allen W
AD - Section on Tissue Biophysics and Biomimetics, NICHD, National Institutes of Health, Bethesda, Maryland, USA.
Y1 - 2014/03//
PY - 2014
DA - Mar 2014
SP - 1044
EP - 1053
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 71
IS - 3
SN - 0740-3194, 0740-3194
KW - Biotechnology and Bioengineering Abstracts
KW - Anisotropy
KW - Magnetic resonance imaging
KW - W 30910:Imaging
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-03-01
N1 - Last updated - 2014-04-03
N1 - SubjectsTermNotLitGenreText - Magnetic resonance imaging
DO - http://dx.doi.org/10.1002/mrm.24767
ER -
TY - JOUR
T1 - The Association between Parity and Birthweight in a Longitudinal Consecutive Pregnancy Cohort
AN - 1505338677; 19285518
AB - Nulliparity is associated with lower birthweight, but few studies have examined how within-mother changes in risk factors impact this association. We used longitudinal electronic medical record data from a hospital-based cohort of consecutive singleton live births from 2002-2010 in Utah. To reduce bias from unobserved pregnancies, primary analyses were limited to 9484 women who entered nulliparous from 2002-2004, with 23 380 pregnancies up to parity 3. Unrestricted secondary analyses used 101 225 pregnancies from 45 212 women with pregnancies up to parity 7. We calculated gestational age and sex-specific birthweight z-scores with nulliparas as the reference. Using linear mixed models, we estimated birthweight z-score by parity adjusting for pregnancy-specific sociodemographics, smoking, alcohol, prepregnancy body mass index, gestational weight gain, and medical conditions. Compared with nulliparas', infants of primiparas were larger by 0.20 unadjusted z-score units [95% confidence interval (CI) 0.18, 0.22]; the adjusted increase was similar at 0.18 z-score units [95% CI 0.15, 0.20]. Birthweight continued to increase up to parity 3, but with a smaller difference (parity 3 vs. 0 beta = 0.27 [95% CI 0.20, 0.34]). In the unrestricted secondary sample, there was significant departure in linearity from parity 1 to 7 (P < 0.001); birthweight increased only up to parity 4 (parity 4 vs. 0 beta = 0.34 [95% CI 0.31, 0.37]). The association between parity and birthweight was non-linear with the greatest increase observed between first- and second-born infants of the same mother. Adjustment for changes in weight or chronic diseases did not change the relationship between parity and birthweight.
JF - Paediatric and Perinatal Epidemiology
AU - Hinkle, Stefanie N
AU - Albert, Paul S
AU - Mendola, Pauline
AU - Sjaarda, Lindsey A
AU - Yeung, Edwina
AU - Boghossian, Nansi S
AU - Laughon, SKatherine
AD - Epidemiology Branch Division of Intramural Population Health Research Eunice Kennedy Shriver National Institute of Child Health and Human Development. National Institutes of Health
Y1 - 2014/03//
PY - 2014
DA - Mar 2014
SP - 106
EP - 115
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 28
IS - 2
SN - 0269-5022, 0269-5022
KW - Risk Abstracts; Health & Safety Science Abstracts
KW - Age
KW - USA, Utah
KW - Parity
KW - R2 23060:Medical and environmental health
KW - H 12000:Epidemiology and Public Health
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Paediatric+and+Perinatal+Epidemiology&rft.atitle=The+Association+between+Parity+and+Birthweight+in+a+Longitudinal+Consecutive+Pregnancy+Cohort&rft.au=Hinkle%2C+Stefanie+N%3BAlbert%2C+Paul+S%3BMendola%2C+Pauline%3BSjaarda%2C+Lindsey+A%3BYeung%2C+Edwina%3BBoghossian%2C+Nansi+S%3BLaughon%2C+SKatherine&rft.aulast=Hinkle&rft.aufirst=Stefanie&rft.date=2014-03-01&rft.volume=28&rft.issue=2&rft.spage=106&rft.isbn=&rft.btitle=&rft.title=Paediatric+and+Perinatal+Epidemiology&rft.issn=02695022&rft_id=info:doi/10.1111%2Fppe.12099
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-03-01
N1 - Last updated - 2014-03-20
N1 - SubjectsTermNotLitGenreText - Parity; USA, Utah
DO - http://dx.doi.org/10.1111/ppe.12099
ER -
TY - JOUR
T1 - Using Weighted Entropy to Rank Chemicals in Quantitative High-Throughput Screening Experiments
AN - 1505336144; 19295923
AB - Quantitative high-throughput screening (qHTS) experiments can simultaneously produce concentration-response profiles for thousands of chemicals. In a typical qHTS study, a large chemical library is subjected to a primary screen to identify candidate hits for secondary screening, validation studies, or prediction modeling. Different algorithms, usually based on the Hill equation logistic model, have been used to classify compounds as active or inactive (or inconclusive). However, observed concentration-response activity relationships may not adequately fit a sigmoidal curve. Furthermore, it is unclear how to prioritize chemicals for follow-up studies given the large uncertainties that often accompany parameter estimates from nonlinear models. Weighted Shannon entropy can address these concerns by ranking compounds according to profile-specific statistics derived from estimates of the probability mass distribution of response at the tested concentration levels. This strategy can be used to rank all tested chemicals in the absence of a prespecified model structure, or the approach can complement existing activity call algorithms by ranking the returned candidate hits. The weighted entropy approach was evaluated here using data simulated from the Hill equation model. The procedure was then applied to a chemical genomics profiling data set interrogating compounds for androgen receptor agonist activity.
JF - Journal of Biomolecular Screening
AU - Shockley, Keith R
AD - The National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA
Y1 - 2014/03//
PY - 2014
DA - Mar 2014
SP - 344
EP - 353
PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom
VL - 19
IS - 3
SN - 1087-0571, 1087-0571
KW - Biotechnology and Bioengineering Abstracts
KW - Algorithms
KW - Entropy
KW - W 30960:Bioinformatics & Computer Applications
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biomolecular+Screening&rft.atitle=Using+Weighted+Entropy+to+Rank+Chemicals+in+Quantitative+High-Throughput+Screening+Experiments&rft.au=Shockley%2C+Keith+R&rft.aulast=Shockley&rft.aufirst=Keith&rft.date=2014-03-01&rft.volume=19&rft.issue=3&rft.spage=344&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biomolecular+Screening&rft.issn=10870571&rft_id=info:doi/10.1177%2F1087057113505325
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-03-01
N1 - Number of references - 1
N1 - Last updated - 2014-03-20
N1 - SubjectsTermNotLitGenreText - Entropy
DO - http://dx.doi.org/10.1177/1087057113505325
ER -
TY - JOUR
T1 - No evidence for synergy between human papillomavirus genotypes for the risk of high-grade squamous intraepithelial lesions in a large population-based study.
AN - 1503542489; 24179110
AB - Multiple human papillomavirus (HPV) genotypes may be independently or synergistically associated with risk of high-grade squamous intraepithelial lesions (HSILs). We evaluated the risk of HSIL in women concomitantly infected with multiple HPV genotypes.
A population-based stratified sample of 59 664 cervical cytology specimens from women residing in New Mexico were evaluated for cytologic abnormalities and HPV genotypes. We calculated the risk of HSIL in women infected with a single HPV genotype and the risk in those infected with multiple HPV genotypes. The highest risk of HSIL was observed for HPV-16 (0.036), followed by HPV-33 (0.028), HPV-58 (0.024), and HPV-18 (0.022). For most types, we observed a greater risk of HSIL in women infected with multiple carcinogenic HPV types. In contrast, the risk of HSIL was similar in women infected with HPV-16 and other types, compared with women infected with HPV-16 only. We observed an increased but plateauing risk of HSIL in women infected with multiple types, compared with those infected with a single type, with risk ratios of 1.5 (95% confidence interval [CI], 1.2-1.8), 1.7 (95% CI, 1.3-2.4), and 1.4 (95% CI, 0.83-2.5) for women infected with 2, 3, and ≥4 genotypes, respectively. In the largest population-based study of HPV genotypes and cytologic outcomes so far, we did not see more than additive effects of HPV types on the risk of HSIL in women infected with multiple types.
JF - The Journal of infectious diseases
AU - Wentzensen, Nicolas
AU - Nason, Martha
AU - Schiffman, Mark
AU - Dodd, Lori
AU - Hunt, William C
AU - Wheeler, Cosette M
AU - New Mexico HPV Pap Registry Steering Committee
AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute. ; New Mexico HPV Pap Registry Steering Committee
Y1 - 2014/03//
PY - 2014
DA - March 2014
SP - 855
EP - 864
VL - 209
IS - 6
KW - Abridged Index Medicus
KW - Index Medicus
KW - human papillomavirus (HPV)
KW - cytology
KW - cervical cancer screening
KW - multiple Infections
KW - New Mexico -- epidemiology
KW - Cross-Sectional Studies
KW - Logistic Models
KW - Humans
KW - Adult
KW - Early Detection of Cancer
KW - Coinfection -- virology
KW - Cervix Uteri -- virology
KW - Coinfection -- epidemiology
KW - Female
KW - Papillomavirus Infections -- epidemiology
KW - Uterine Cervical Neoplasms -- epidemiology
KW - Papillomaviridae -- isolation & purification
KW - Papillomavirus Infections -- virology
KW - Cervical Intraepithelial Neoplasia -- virology
KW - Papillomaviridae -- genetics
KW - Uterine Cervical Neoplasms -- virology
KW - Cervical Intraepithelial Neoplasia -- epidemiology
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-06-24
N1 - Date created - 2014-02-27
N1 - Date revised - 2017-01-13
N1 - SuppNotes - Cited By:
J Natl Cancer Inst. 2011 Sep 21;103(18):1387-96 [21900119]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/infdis/jit577
ER -
TY - JOUR
T1 - Opposing effects of prednisolone treatment on T/NKT cell- and hepatotoxin-mediated hepatitis in mice.
AN - 1503541712; 24115096
AB - Prednisolone is a corticosteroid that has been used to treat inflammatory liver diseases such as autoimmune hepatitis and alcoholic hepatitis. However, the results have been controversial, and how prednisolone affects liver disease progression remains unknown. In the current study we examined the effect of prednisolone treatment on several models of liver injury, including T/NKT cell hepatitis induced by concanavalin A (ConA) and α-galactosylceramide (α-GalCer), and hepatotoxin-mediated hepatitis induced by carbon tetrachloride (CCl4 ) and/or ethanol. Prednisolone administration attenuated ConA- and α-GalCer-induced hepatitis and systemic inflammatory responses. Treating mice with prednisolone also suppressed inflammatory responses in a model of hepatotoxin (CCl4 )-induced hepatitis, but surprisingly exacerbated liver injury and delayed liver repair. In addition, administration of prednisolone also enhanced acetaminophen-, ethanol-, or ethanol plus CCl4 -induced liver injury. Immunohistochemical and flow cytometric analyses demonstrated that prednisolone treatment inhibited hepatic macrophage and neutrophil infiltration in CCl4 -induced hepatitis and suppressed their phagocytic activities in vivo and in vitro. Macrophage and/or neutrophil depletion aggravated CCl4 -induced liver injury and impeded liver regeneration. Finally, conditional disruption of glucocorticoid receptor in macrophages and neutrophils abolished prednisolone-mediated exacerbation of hepatotoxin-induced liver injury. Prednisolone treatment prevents T/NKT cell hepatitis but exacerbates hepatotoxin-induced liver injury by inhibiting macrophage- and neutrophil-mediated phagocytic and hepatic regenerative functions. These findings may not only increase our understanding of the steroid treatment mechanism but also help us to better manage steroid therapy in liver diseases.
Published 2014. This article is a U.S. Government work and is in the public domain in the USA.
JF - Hepatology (Baltimore, Md.)
AU - Kwon, Hyo-Jung
AU - Won, Young-Suk
AU - Park, Ogyi
AU - Feng, Dechun
AU - Gao, Bin
AD - Laboratory of Liver Diseases, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA; College of Veterinary Medicine, Chungnam National University, Yuseong-gu, Daejeon, South Korea.
Y1 - 2014/03//
PY - 2014
DA - March 2014
SP - 1094
EP - 1106
VL - 59
IS - 3
KW - Galactosylceramides
KW - 0
KW - Glucocorticoids
KW - Mitogens
KW - alpha-galactosylceramide
KW - Concanavalin A
KW - 11028-71-0
KW - Prednisolone
KW - 9PHQ9Y1OLM
KW - Carbon Tetrachloride
KW - CL2T97X0V0
KW - Index Medicus
KW - Animals
KW - Liver Regeneration -- drug effects
KW - Neutrophils -- pathology
KW - Concanavalin A -- toxicity
KW - Macrophages -- immunology
KW - Neutrophils -- immunology
KW - Galactosylceramides -- toxicity
KW - Mitogens -- toxicity
KW - Disease Models, Animal
KW - Mice
KW - Liver Regeneration -- immunology
KW - Macrophages -- drug effects
KW - Carbon Tetrachloride -- toxicity
KW - Glucocorticoids -- pharmacology
KW - Mice, Knockout
KW - Neutrophils -- drug effects
KW - Macrophages -- pathology
KW - Mice, Inbred C57BL
KW - Male
KW - Chemical and Drug Induced Liver Injury -- pathology
KW - Prednisolone -- pharmacology
KW - T-Lymphocytes -- drug effects
KW - Killer Cells, Natural -- pathology
KW - T-Lymphocytes -- pathology
KW - Chemical and Drug Induced Liver Injury -- drug therapy
KW - T-Lymphocytes -- immunology
KW - Killer Cells, Natural -- immunology
KW - Killer Cells, Natural -- drug effects
KW - Chemical and Drug Induced Liver Injury -- immunology
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-04-28
N1 - Date created - 2014-02-27
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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Alcohol. 2002 May;27(1):43-6 [12062636]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1002/hep.26748
ER -
TY - JOUR
T1 - Intestinal CYP3A4 protects against lithocholic acid-induced hepatotoxicity in intestine-specific VDR-deficient mice.
AN - 1502996715; 24343899
AB - Vitamin D receptor (VDR) mediates vitamin D signaling involved in bone metabolism, cellular growth and differentiation, cardiovascular function, and bile acid regulation. Mice with an intestine-specific disruption of VDR (Vdr(ΔIEpC)) have abnormal body size, colon structure, and imbalance of bile acid metabolism. Lithocholic acid (LCA), a secondary bile acid that activates VDR, is among the most toxic of the bile acids that when overaccumulated in the liver causes hepatotoxicity. Because cytochrome P450 3A4 (CYP3A4) is a target gene of VDR-involved bile acid metabolism, the role of CYP3A4 in VDR biology and bile acid metabolism was investigated. The CYP3A4 gene was inserted into Vdr(ΔIEpC) mice to produce the Vdr(ΔIEpC)/3A4 line. LCA was administered to control, transgenic-CYP3A4, Vdr(ΔIEpC), and Vdr(ΔIEpC)/3A4 mice, and hepatic toxicity and bile acid levels in the liver, intestine, bile, and urine were measured. VDR deficiency in the intestine of the Vdr(ΔIEpC) mice exacerbates LCA-induced hepatotoxicity manifested by increased necrosis and inflammation, due in part to over-accumulation of hepatic bile acids including taurocholic acid and taurodeoxycholic acid. Intestinal expression of CYP3A4 in the Vdr(ΔIEpC)/3A4 mouse line reduces LCA-induced hepatotoxicity through elevation of LCA metabolism and detoxification, and suppression of bile acid transporter expression in the small intestine. This study reveals that intestinal CYP3A4 protects against LCA hepatotoxicity.
JF - Journal of lipid research
AU - Cheng, Jie
AU - Fang, Zhong-Ze
AU - Kim, Jung-Hwan
AU - Krausz, Kristopher W
AU - Tanaka, Naoki
AU - Chiang, John Y L
AU - Gonzalez, Frank J
AD - Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
Y1 - 2014/03//
PY - 2014
DA - March 2014
SP - 455
EP - 465
VL - 55
IS - 3
KW - Bile Acids and Salts
KW - 0
KW - Receptors, Calcitriol
KW - Lithocholic Acid
KW - 5QU0I8393U
KW - Cholesterol
KW - 97C5T2UQ7J
KW - Cytochrome P-450 CYP3A
KW - EC 1.14.14.1
KW - cytochrome P450 3A4, mouse
KW - Index Medicus
KW - vitamin D receptor
KW - metabolomics
KW - bile acids
KW - Animals
KW - Metabolomics -- methods
KW - Liver -- pathology
KW - Liver -- metabolism
KW - Mice
KW - Bile -- metabolism
KW - Reverse Transcriptase Polymerase Chain Reaction
KW - Mice, Transgenic
KW - Bile Acids and Salts -- metabolism
KW - Mice, Knockout
KW - Cholesterol -- blood
KW - Blotting, Western
KW - Cholesterol -- metabolism
KW - Gallbladder -- metabolism
KW - Male
KW - Receptors, Calcitriol -- deficiency
KW - Chemical and Drug Induced Liver Injury -- etiology
KW - Receptors, Calcitriol -- genetics
KW - Cytochrome P-450 CYP3A -- metabolism
KW - Chemical and Drug Induced Liver Injury -- genetics
KW - Intestines -- metabolism
KW - Cytochrome P-450 CYP3A -- genetics
KW - Cytochrome P-450 CYP3A -- urine
KW - Chemical and Drug Induced Liver Injury -- metabolism
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-10-28
N1 - Date created - 2014-02-26
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1194/jlr.M044420
ER -
TY - JOUR
T1 - Phase I trial of a recombinant yeast-CEA vaccine (GI-6207) in adults with metastatic CEA-expressing carcinoma.
AN - 1500689076; 24327292
AB - Yeast-CEA (GI-6207) is a therapeutic cancer vaccine genetically modified to express recombinant carcinoembryonic antigen (CEA) protein, using heat-killed yeast (Saccharomyces cerevisiae) as a vector. In preclinical studies, yeast-CEA induced a strong immune response to CEA and antitumor responses. Patients received subcutaneous vaccines every 2 weeks for 3 months and then monthly. Patients were enrolled at 3 sequential dose levels: 4, 16, and 40 yeast units (10(7) yeast particles/unit). Eligible patients were required to have serum CEA > 5 ng/mL or > 20 % CEA(+) tumor block, ECOG PS 0-2, and no history of autoimmunity. Restaging scans were performed at 3 months and then bimonthly. Peripheral blood was collected for the analysis of immune response (e.g., by ELISPOT assay). Twenty-five patients with metastatic CEA-expressing carcinomas were enrolled. Median patient age was 52 (range 39-81). A total of 135 vaccines were administered. The vaccine was well tolerated, and the most common adverse event was grade 1/2 injection-site reaction. Five patients had stable disease beyond 3 months (range 3.5-18 months), and each had CEA stabilization while on-study. Some patients showed evidence post-vaccination of increases in antigen-specific CD8(+) T cells and CD4(+) T lymphocytes and decreases in regulatory T cells. Of note, a patient with medullary thyroid cancer had substantial T cell responses and a vigorous inflammatory reaction at sites of metastatic disease. Yeast-CEA vaccination had minimal toxicity and induced some antigen-specific T cell responses and CEA stabilization in a heterogeneous, heavily pre-treated patient population. Further studies are required to determine the clinical benefit of yeast-CEA vaccination.
JF - Cancer immunology, immunotherapy : CII
AU - Bilusic, Marijo
AU - Heery, Christopher R
AU - Arlen, Philip M
AU - Rauckhorst, Myrna
AU - Apelian, David
AU - Tsang, Kwong Y
AU - Tucker, Jo A
AU - Jochems, Caroline
AU - Schlom, Jeffrey
AU - Gulley, James L
AU - Madan, Ravi A
AD - Medical Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Y1 - 2014/03//
PY - 2014
DA - March 2014
SP - 225
EP - 234
VL - 63
IS - 3
KW - Cancer Vaccines
KW - 0
KW - Carcinoembryonic Antigen
KW - Cytokines
KW - Vaccines, DNA
KW - yeast-CEA vaccine
KW - Index Medicus
KW - Genetic Engineering
KW - Enzyme-Linked Immunospot Assay
KW - Humans
KW - Aged
KW - Cytokines -- metabolism
KW - Aged, 80 and over
KW - Cells, Cultured
KW - Genetic Vectors
KW - Adult
KW - Treatment Outcome
KW - Neoplasm Metastasis
KW - Injections, Subcutaneous
KW - Middle Aged
KW - Follow-Up Studies
KW - Male
KW - Female
KW - Carcinoembryonic Antigen -- immunology
KW - Vaccines, DNA -- therapeutic use
KW - Cancer Vaccines -- therapeutic use
KW - CD4-Positive T-Lymphocytes -- immunology
KW - Adenocarcinoma -- immunology
KW - Adenocarcinoma -- therapy
KW - Carcinoembryonic Antigen -- therapeutic use
KW - Colonic Neoplasms -- immunology
KW - Saccharomyces cerevisiae -- genetics
KW - Colonic Neoplasms -- therapy
KW - CD8-Positive T-Lymphocytes -- immunology
KW - Carcinoembryonic Antigen -- genetics
KW - T-Lymphocytes, Regulatory -- immunology
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1500689076?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+immunology%2C+immunotherapy+%3A+CII&rft.atitle=Phase+I+trial+of+a+recombinant+yeast-CEA+vaccine+%28GI-6207%29+in+adults+with+metastatic+CEA-expressing+carcinoma.&rft.au=Bilusic%2C+Marijo%3BHeery%2C+Christopher+R%3BArlen%2C+Philip+M%3BRauckhorst%2C+Myrna%3BApelian%2C+David%3BTsang%2C+Kwong+Y%3BTucker%2C+Jo+A%3BJochems%2C+Caroline%3BSchlom%2C+Jeffrey%3BGulley%2C+James+L%3BMadan%2C+Ravi+A&rft.aulast=Bilusic&rft.aufirst=Marijo&rft.date=2014-03-01&rft.volume=63&rft.issue=3&rft.spage=225&rft.isbn=&rft.btitle=&rft.title=Cancer+immunology%2C+immunotherapy+%3A+CII&rft.issn=1432-0851&rft_id=info:doi/10.1007%2Fs00262-013-1505-8
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-04-29
N1 - Date created - 2014-02-19
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Curr Cancer Drug Targets. 2007 Feb;7(1):31-40 [17305476]
Vaccine. 2007 Feb 9;25(8):1452-63 [17098335]
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Vaccine. 2008 Jan 24;26(4):509-21 [18155327]
Clin Cancer Res. 2008 May 15;14(10):3060-9 [18483372]
Clin Cancer Res. 2008 Jul 1;14(13):4316-25 [18594015]
Vaccine. 2009 Feb 11;27(7):987-94 [19110021]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1007/s00262-013-1505-8
ER -
TY - JOUR
T1 - SALL4 expression in germ cell and non-germ cell tumors: a systematic immunohistochemical study of 3215 cases.
AN - 1499157317; 24525512
AB - The SALL4 transcription factor is associated with embryonic cell pluripotency and has been shown as a useful immunohistochemical marker for germ cell tumors. However, information of SALL4 distribution in normal human tissues and non-germ cell tumors is limited. In this study we examined normal human tissues and 3215 tumors for SALL4 expression using a monoclonal antibody 6E3 and automated immunohistochemistry. In a 10-week embryo, SALL4 was expressed in ovocytes, intestine, kidney, and some hepatocytes. In adult tissues, it was only detected in germ cells. SALL4 was consistently expressed in all germ cell tumors except some trophoblastic tumors and mature components of teratomas, in which it was selectively expressed in intestinal-like and some squamous epithelia. In non-germ cell carcinomas, SALL4 was detected in 20% of cases or more of serous carcinoma of the ovary, urothelial high-grade carcinoma, and gastric adenocarcinoma (especially the intestinal type). SALL4 was only rarely (≤ 5%) expressed in mammary, colorectal, prostatic, and squamous cell carcinomas. Many SALL4-positive carcinomas showed poorly differentiated patterns, and some showed positivity in most tumor cells mimicking the expression in germ cell tumors. SALL4 was commonly expressed in rhabdoid tumors of the kidney and extrarenal sites and in the Wilms tumor. Expression of SALL4 was rare in other mesenchymal and neuroendocrine tumors but was occasionally detected in melanoma, desmoplastic small round cell tumor, epithelioid sarcoma, and rhabdomyosarcoma. All hematopoietic tumors were negative. SALL4 is an excellent marker of nonteratomatous germ cell tumors, but it is also expressed in other tumors, sometimes extensively. Such expression may reflect stem cell-like differentiation and must be considered when using SALL4 as a marker for germ cell tumors. Observed lack of other pluripotency factors, OCT4 and NANOG, in SALL4-positive non-germ cell tumors can also be diagnostically helpful.
JF - The American journal of surgical pathology
AU - Miettinen, Markku
AU - Wang, Zengfeng
AU - McCue, Peter A
AU - Sarlomo-Rikala, Maarit
AU - Rys, Janusz
AU - Biernat, Wojciech
AU - Lasota, Jerzy
AU - Lee, Yi-Shan
AD - *Laboratory of Pathology, National Cancer Institute, Bethesda, MD †Department of Pathology, Cell Biology and Anatomy, Jefferson Medical College of Thomas Jefferson University and University Hospital, Philadelphia, PA ‡Department of Pathology/Haartman Institute and HusLab, Helsinki University Hospital, Helsinki, Finland §Department of Tumor Pathology, Centre of Oncology, Maria Sklodowska-Curie Memorial Institute, Krakow ∥Department of Pathomorphology, Medical University of Gdansk, Gdansk, Poland.
Y1 - 2014/03//
PY - 2014
DA - March 2014
SP - 410
EP - 420
VL - 38
IS - 3
KW - Biomarkers, Tumor
KW - 0
KW - SALL4 protein, human
KW - Transcription Factors
KW - Index Medicus
KW - Humans
KW - Adult
KW - Neoplasm Grading
KW - Cell Differentiation
KW - Predictive Value of Tests
KW - Biopsy
KW - Male
KW - Female
KW - Carcinoma -- pathology
KW - Carcinoma -- chemistry
KW - Neoplasms, Germ Cell and Embryonal -- chemistry
KW - Biomarkers, Tumor -- analysis
KW - Transcription Factors -- analysis
KW - Neoplasms, Germ Cell and Embryonal -- pathology
KW - Immunohistochemistry
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1499157317?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+American+journal+of+surgical+pathology&rft.atitle=SALL4+expression+in+germ+cell+and+non-germ+cell+tumors%3A+a+systematic+immunohistochemical+study+of+3215+cases.&rft.au=Miettinen%2C+Markku%3BWang%2C+Zengfeng%3BMcCue%2C+Peter+A%3BSarlomo-Rikala%2C+Maarit%3BRys%2C+Janusz%3BBiernat%2C+Wojciech%3BLasota%2C+Jerzy%3BLee%2C+Yi-Shan&rft.aulast=Miettinen&rft.aufirst=Markku&rft.date=2014-03-01&rft.volume=38&rft.issue=3&rft.spage=410&rft.isbn=&rft.btitle=&rft.title=The+American+journal+of+surgical+pathology&rft.issn=1532-0979&rft_id=info:doi/10.1097%2FPAS.0000000000000116
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-04-10
N1 - Date created - 2014-02-14
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Mod Pathol. 2006 Dec;19(12):1585-92 [16998462]
Blood. 2006 Oct 15;108(8):2726-35 [16763212]
Proc Natl Acad Sci U S A. 2007 Oct 16;104(42):16438-43 [17940043]
Am J Surg Pathol. 2008 Apr;32(4):600-7 [18277882]
Proc Natl Acad Sci U S A. 2008 Dec 16;105(50):19756-61 [19060217]
Am J Surg Pathol. 2009 Jun;33(6):894-904 [19295406]
Mod Pathol. 2009 Jun;22(6):824-32 [19329941]
Cancer. 2009 Jun 15;115(12):2640-51 [19365862]
Am J Surg Pathol. 2009 Jul;33(7):1065-77 [19390421]
Am J Surg Pathol. 2009 Oct;33(10):1529-39 [19574883]
Am J Surg Pathol. 2010 Apr;34(4):533-40 [20182341]
Am J Surg Pathol. 2010 May;34(5):697-706 [20410807]
Int J Oncol. 2011 Apr;38(4):933-9 [21274508]
Oncol Rep. 2011 Oct;26(4):965-70 [21725617]
Pathol Oncol Res. 2011 Sep;17(3):639-44 [21258884]
Am J Surg Pathol. 2011 Oct;35(10):1463-72 [21921784]
Pediatr Dev Pathol. 2011 Sep-Oct;14(5):353-9 [21417895]
Appl Immunohistochem Mol Morphol. 2012 Jul;20(4):410-2 [22495380]
Hum Pathol. 2012 Nov;43(11):1955-63 [22516245]
J Biomed Sci. 2013;20:6 [23363002]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1097/PAS.0000000000000116
ER -
TY - JOUR
T1 - Genome-wide association study identifies multiple loci associated with bladder cancer risk.
AN - 1499133164; 24163127
AB - Candidate gene and genome-wide association studies (GWAS) have identified 11 independent susceptibility loci associated with bladder cancer risk. To discover additional risk variants, we conducted a new GWAS of 2422 bladder cancer cases and 5751 controls, followed by a meta-analysis with two independently published bladder cancer GWAS, resulting in a combined analysis of 6911 cases and 11 814 controls of European descent. TaqMan genotyping of 13 promising single nucleotide polymorphisms with P < 1 × 10(-5) was pursued in a follow-up set of 801 cases and 1307 controls. Two new loci achieved genome-wide statistical significance: rs10936599 on 3q26.2 (P = 4.53 × 10(-9)) and rs907611 on 11p15.5 (P = 4.11 × 10(-8)). Two notable loci were also identified that approached genome-wide statistical significance: rs6104690 on 20p12.2 (P = 7.13 × 10(-7)) and rs4510656 on 6p22.3 (P = 6.98 × 10(-7)); these require further studies for confirmation. In conclusion, our study has identified new susceptibility alleles for bladder cancer risk that require fine-mapping and laboratory investigation, which could further understanding into the biological underpinnings of bladder carcinogenesis.
JF - Human molecular genetics
AU - Figueroa, Jonine D
AU - Ye, Yuanqing
AU - Siddiq, Afshan
AU - Garcia-Closas, Montserrat
AU - Chatterjee, Nilanjan
AU - Prokunina-Olsson, Ludmila
AU - Cortessis, Victoria K
AU - Kooperberg, Charles
AU - Cussenot, Olivier
AU - Benhamou, Simone
AU - Prescott, Jennifer
AU - Porru, Stefano
AU - Dinney, Colin P
AU - Malats, Núria
AU - Baris, Dalsu
AU - Purdue, Mark
AU - Jacobs, Eric J
AU - Albanes, Demetrius
AU - Wang, Zhaoming
AU - Deng, Xiang
AU - Chung, Charles C
AU - Tang, Wei
AU - Bas Bueno-de-Mesquita, H
AU - Trichopoulos, Dimitrios
AU - Ljungberg, Börje
AU - Clavel-Chapelon, Françoise
AU - Weiderpass, Elisabete
AU - Krogh, Vittorio
AU - Dorronsoro, Miren
AU - Travis, Ruth
AU - Tjønneland, Anne
AU - Brenan, Paul
AU - Chang-Claude, Jenny
AU - Riboli, Elio
AU - Conti, David
AU - Gago-Dominguez, Manuela
AU - Stern, Mariana C
AU - Pike, Malcolm C
AU - Van Den Berg, David
AU - Yuan, Jian-Min
AU - Hohensee, Chancellor
AU - Rodabough, Rebecca
AU - Cancel-Tassin, Geraldine
AU - Roupret, Morgan
AU - Comperat, Eva
AU - Chen, Constance
AU - De Vivo, Immaculata
AU - Giovannucci, Edward
AU - Hunter, David J
AU - Kraft, Peter
AU - Lindstrom, Sara
AU - Carta, Angela
AU - Pavanello, Sofia
AU - Arici, Cecilia
AU - Mastrangelo, Giuseppe
AU - Kamat, Ashish M
AU - Lerner, Seth P
AU - Barton Grossman, H
AU - Lin, Jie
AU - Gu, Jian
AU - Pu, Xia
AU - Hutchinson, Amy
AU - Burdette, Laurie
AU - Wheeler, William
AU - Kogevinas, Manolis
AU - Tardón, Adonina
AU - Serra, Consol
AU - Carrato, Alfredo
AU - García-Closas, Reina
AU - Lloreta, Josep
AU - Schwenn, Molly
AU - Karagas, Margaret R
AU - Johnson, Alison
AU - Schned, Alan
AU - Armenti, Karla R
AU - Hosain, G M
AU - Andriole, Gerald
AU - Grubb, Robert
AU - Black, Amanda
AU - Ryan Diver, W
AU - Gapstur, Susan M
AU - Weinstein, Stephanie J
AU - Virtamo, Jarmo
AU - Haiman, Chris A
AU - Landi, Maria T
AU - Caporaso, Neil
AU - Fraumeni, Joseph F
AU - Vineis, Paolo
AU - Wu, Xifeng
AU - Silverman, Debra T
AU - Chanock, Stephen
AU - Rothman, Nathaniel
AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, USA.
Y1 - 2014/03/01/
PY - 2014
DA - 2014 Mar 01
SP - 1387
EP - 1398
VL - 23
IS - 5
KW - Index Medicus
KW - Genotype
KW - Risk
KW - Polymorphism, Single Nucleotide
KW - Humans
KW - Case-Control Studies
KW - Genetic Predisposition to Disease
KW - Meta-Analysis as Topic
KW - Linkage Disequilibrium
KW - Urinary Bladder Neoplasms -- pathology
KW - Genetic Loci
KW - Urinary Bladder Neoplasms -- genetics
KW - Genome-Wide Association Study
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Human+molecular+genetics&rft.atitle=Genome-wide+association+study+identifies+multiple+loci+associated+with+bladder+cancer+risk.&rft.au=Figueroa%2C+Jonine+D%3BYe%2C+Yuanqing%3BSiddiq%2C+Afshan%3BGarcia-Closas%2C+Montserrat%3BChatterjee%2C+Nilanjan%3BProkunina-Olsson%2C+Ludmila%3BCortessis%2C+Victoria+K%3BKooperberg%2C+Charles%3BCussenot%2C+Olivier%3BBenhamou%2C+Simone%3BPrescott%2C+Jennifer%3BPorru%2C+Stefano%3BDinney%2C+Colin+P%3BMalats%2C+N%C3%BAria%3BBaris%2C+Dalsu%3BPurdue%2C+Mark%3BJacobs%2C+Eric+J%3BAlbanes%2C+Demetrius%3BWang%2C+Zhaoming%3BDeng%2C+Xiang%3BChung%2C+Charles+C%3BTang%2C+Wei%3BBas+Bueno-de-Mesquita%2C+H%3BTrichopoulos%2C+Dimitrios%3BLjungberg%2C+B%C3%B6rje%3BClavel-Chapelon%2C+Fran%C3%A7oise%3BWeiderpass%2C+Elisabete%3BKrogh%2C+Vittorio%3BDorronsoro%2C+Miren%3BTravis%2C+Ruth%3BTj%C3%B8nneland%2C+Anne%3BBrenan%2C+Paul%3BChang-Claude%2C+Jenny%3BRiboli%2C+Elio%3BConti%2C+David%3BGago-Dominguez%2C+Manuela%3BStern%2C+Mariana+C%3BPike%2C+Malcolm+C%3BVan+Den+Berg%2C+David%3BYuan%2C+Jian-Min%3BHohensee%2C+Chancellor%3BRodabough%2C+Rebecca%3BCancel-Tassin%2C+Geraldine%3BRoupret%2C+Morgan%3BComperat%2C+Eva%3BChen%2C+Constance%3BDe+Vivo%2C+Immaculata%3BGiovannucci%2C+Edward%3BHunter%2C+David+J%3BKraft%2C+Peter%3BLindstrom%2C+Sara%3BCarta%2C+Angela%3BPavanello%2C+Sofia%3BArici%2C+Cecilia%3BMastrangelo%2C+Giuseppe%3BKamat%2C+Ashish+M%3BLerner%2C+Seth+P%3BBarton+Grossman%2C+H%3BLin%2C+Jie%3BGu%2C+Jian%3BPu%2C+Xia%3BHutchinson%2C+Amy%3BBurdette%2C+Laurie%3BWheeler%2C+William%3BKogevinas%2C+Manolis%3BTard%C3%B3n%2C+Adonina%3BSerra%2C+Consol%3BCarrato%2C+Alfredo%3BGarc%C3%ADa-Closas%2C+Reina%3BLloreta%2C+Josep%3BSchwenn%2C+Molly%3BKaragas%2C+Margaret+R%3BJohnson%2C+Alison%3BSchned%2C+Alan%3BArmenti%2C+Karla+R%3BHosain%2C+G+M%3BAndriole%2C+Gerald%3BGrubb%2C+Robert%3BBlack%2C+Amanda%3BRyan+Diver%2C+W%3BGapstur%2C+Susan+M%3BWeinstein%2C+Stephanie+J%3BVirtamo%2C+Jarmo%3BHaiman%2C+Chris+A%3BLandi%2C+Maria+T%3BCaporaso%2C+Neil%3BFraumeni%2C+Joseph+F%3BVineis%2C+Paolo%3BWu%2C+Xifeng%3BSilverman%2C+Debra+T%3BChanock%2C+Stephen%3BRothman%2C+Nathaniel&rft.aulast=Figueroa&rft.aufirst=Jonine&rft.date=2014-03-01&rft.volume=23&rft.issue=5&rft.spage=1387&rft.isbn=&rft.btitle=&rft.title=Human+molecular+genetics&rft.issn=1460-2083&rft_id=info:doi/10.1093%2Fhmg%2Fddt519
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-10-15
N1 - Date created - 2014-02-10
N1 - Date revised - 2017-01-13
N1 - SuppNotes - Cited By:
Lancet. 2005 Aug 20-26;366(9486):649-59 [16112301]
Hum Mol Genet. 2011 Nov 1;20(21):4282-9 [21824976]
Genetics. 2004 Aug;167(4):2067-81 [15342541]
Int J Cancer. 1985 Jun 15;35(6):703-6 [4008097]
Nat Genet. 2006 Aug;38(8):904-9 [16862161]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/hmg/ddt519
ER -
TY - JOUR
T1 - Structural basis for HIV-1 neutralization by 2F5-like antibodies m66 and m66.6.
AN - 1499131128; 24335316
AB - Antibodies m66.6 and 2F5 are the only effective human HIV-1-neutralizing antibodies reported thus far to recognize the N-terminal region of the membrane-proximal external region (MPER) of the gp41 subunit of the HIV-1 envelope glycoprotein. Although 2F5 has been extensively characterized, much less is known about antibody m66.6 or antibody m66, a closely related light-chain variant. Here, we report the crystal structure of m66 in complex with its gp41 epitope, along with unbound structures of m66 and m66.6. We used mutational and binding analyses to decipher antibody elements critical for their recognition of gp41 and determined the molecular basis that underlies their neutralization of HIV-1. When bound by m66, the N-terminal region of the gp41 MPER adopts a conformation comprising a helix, followed by an extended loop. Comparison of gp41-bound m66 to unbound m66.6 identified three light-chain residues of m66.6 that were confirmed through mutagenesis to underlie the greater breadth of m66.6-mediated virus neutralization. Recognition of gp41 by m66 also revealed similarities to antibody 2F5 both in the conformation of crucial epitope residues as well as in the angle of antibody approach. Aromatic residues at the tip of the m66.6 heavy-chain third complementarity-determining region, as in the case of 2F5, were determined to be critical for virus neutralization in a manner that correlated with antibody recognition of the MPER in a lipid context. Antibodies m66, m66.6, and 2F5 thus utilize similar mechanistic elements to recognize a common gp41-MPER epitope and to neutralize HIV-1.
JF - Journal of virology
AU - Ofek, Gilad
AU - Zirkle, Brett
AU - Yang, Yongping
AU - Zhu, Zhongyu
AU - McKee, Krisha
AU - Zhang, Baoshan
AU - Chuang, Gwo-Yu
AU - Georgiev, Ivelin S
AU - O'Dell, Sijy
AU - Doria-Rose, Nicole
AU - Mascola, John R
AU - Dimitrov, Dimiter S
AU - Kwong, Peter D
AD - Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Y1 - 2014/03//
PY - 2014
DA - March 2014
SP - 2426
EP - 2441
VL - 88
IS - 5
KW - Antibodies, Neutralizing
KW - 0
KW - Antigen-Antibody Complex
KW - Complementarity Determining Regions
KW - Epitopes
KW - HIV Antibodies
KW - HIV Envelope Protein gp41
KW - Peptides
KW - Index Medicus
KW - Models, Molecular
KW - Humans
KW - Complementarity Determining Regions -- chemistry
KW - HIV Envelope Protein gp41 -- metabolism
KW - Antigen-Antibody Complex -- chemistry
KW - Peptides -- immunology
KW - HIV Envelope Protein gp41 -- immunology
KW - Protein Interaction Domains and Motifs -- immunology
KW - Amino Acid Sequence
KW - Protein Binding -- immunology
KW - Complementarity Determining Regions -- metabolism
KW - Molecular Docking Simulation
KW - Complementarity Determining Regions -- genetics
KW - Neutralization Tests
KW - Molecular Sequence Data
KW - Peptides -- chemistry
KW - Epitopes -- chemistry
KW - Epitopes -- immunology
KW - Mutation
KW - HIV Envelope Protein gp41 -- chemistry
KW - Protein Conformation
KW - HIV-1 -- metabolism
KW - HIV-1 -- immunology
KW - HIV Antibodies -- metabolism
KW - HIV Antibodies -- immunology
KW - Antibodies, Neutralizing -- chemistry
KW - Antibodies, Neutralizing -- immunology
KW - HIV Antibodies -- chemistry
KW - Antibodies, Neutralizing -- metabolism
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1499131128?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Structural+basis+for+HIV-1+neutralization+by+2F5-like+antibodies+m66+and+m66.6.&rft.au=Ofek%2C+Gilad%3BZirkle%2C+Brett%3BYang%2C+Yongping%3BZhu%2C+Zhongyu%3BMcKee%2C+Krisha%3BZhang%2C+Baoshan%3BChuang%2C+Gwo-Yu%3BGeorgiev%2C+Ivelin+S%3BO%27Dell%2C+Sijy%3BDoria-Rose%2C+Nicole%3BMascola%2C+John+R%3BDimitrov%2C+Dimiter+S%3BKwong%2C+Peter+D&rft.aulast=Ofek&rft.aufirst=Gilad&rft.date=2014-03-01&rft.volume=88&rft.issue=5&rft.spage=2426&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=1098-5514&rft_id=info:doi/10.1128%2FJVI.02837-13
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-04-08
N1 - Date created - 2014-02-12
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1128/JVI.02837-13
ER -
TY - JOUR
T1 - Pre-exposure prophylaxis for conception (Prep-C) as a risk reduction strategy in HIV- positive men and HIV-negative women in the UK
AN - 1499081050; 4528511
AB - Couples wishing to have biological children when one partner is HIV positive and the other is HIV negative present clinicians with complex clinical, social and ethical considerations. We established two multidisciplinary pre-conception services for HIV- positive individuals and their partners. We report the first UK use of pre-exposure prophylaxis for conception (PrEP-C) as part of an overall risk reduction strategy. Couples were counselled and written informed consent for PrEP-C was obtained. Patient demographics, HIV and medical histories were recorded. Males underwent baseline semen analysis and seminal HIV viral load testing. Females had full fertility screens. Both partners were screened for sexually transmitted infections. All couples used timed ovulatory intercourse (TOI). Tenofovir±emtricitabine was taken by the female at protocol designated times before±after TOI. Thirty-two male positive/female negative couples used the services. Thirteen couples have used PrEP-C (median age of male 41 years (range 32-56), female 31 (28-43); median CD4 533 (236-1194); all male plasma and seminal HIV viral loads were undetectable). Eleven pregnancies in 10 couples have resulted in 7 live births, 1 ongoing pregnancy and 4 miscarriages (5/40, 6/40, 10/40 and 1 twin 17/40) after a median of 2.5 attempts (range 1-5). PrEP-C was well tolerated with no discontinuations and no HIV transmissions. These data suggest that PrEP-C is a safe and effective option for serodiscordant couples wishing to conceive; a standardised protocol has been developed; data collection via a central database is under way. Reprinted by permission of Routledge, Taylor & Francis Ltd.
JF - AIDS care
AU - Whetham, J
AU - Taylor, S
AU - Charlwood, L
AU - Keith, T
AU - Howell, R
AU - McInnes, C
AU - Payne, E
AU - Home, J
AU - White, D
AU - Gilleece, Y
AD - Brighton and Sussex University Hospitals NHS Trust ; National Institutes of Health, United Kingdom
Y1 - 2014/03//
PY - 2014
DA - Mar 2014
SP - 332
EP - 336
VL - 26
IS - 3
SN - 0954-0121, 0954-0121
KW - Sociology
KW - Gender
KW - Children
KW - HIV
KW - United Kingdom
KW - Sexually transmitted diseases
KW - Design
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1499081050?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS+care&rft.atitle=Pre-exposure+prophylaxis+for+conception+%28Prep-C%29+as+a+risk+reduction+strategy+in+HIV-+positive+men+and+HIV-negative+women+in+the+UK&rft.au=Whetham%2C+J%3BTaylor%2C+S%3BCharlwood%2C+L%3BKeith%2C+T%3BHowell%2C+R%3BMcInnes%2C+C%3BPayne%2C+E%3BHome%2C+J%3BWhite%2C+D%3BGilleece%2C+Y&rft.aulast=Whetham&rft.aufirst=J&rft.date=2014-03-01&rft.volume=26&rft.issue=3&rft.spage=332&rft.isbn=&rft.btitle=&rft.title=AIDS+care&rft.issn=09540121&rft_id=info:doi/10.1080%2F09540121.2013.819406
LA - English
DB - International Bibliography of the Social Sciences (IBSS)
N1 - Date revised - 2014-02-10
N1 - Last updated - 2014-02-18
N1 - SubjectsTermNotLitGenreText - 3458 2991 9429 9416 2153; 5703 3617 6220; 5421 6091; 2212; 11581 3617 6220; 438 462 129 302
DO - http://dx.doi.org/10.1080/09540121.2013.819406
ER -
TY - JOUR
T1 - Differences in testing, stigma, and perceived consequences of stigmatization among heterosexual men and women living with HIV in Bengaluru, India
AN - 1499080718; 4528514
AB - Approximately 2.4 million people in India are living with HIV. Gender inequality affects HIV prevention, detection, and management. The purpose of this paper was to describe gender differences in the experience of living with HIV in Bengaluru, India. A subsample of n = 313 (159 men and 154 women) from a larger cohort was used for these analyses. Participants were recruited through AIDS service organizations. They completed an interviewer-administered survey assessing HIV testing experience, types of stigma, and perceived consequences of stigmatization. The majority of men (67%) reported getting HIV tested because of illness, while women were more likely to be tested after learning their spouse's HIV-positive status (42%). More men (59%) than women (45%, p<0.05) were tested in private care settings. Men reported significantly higher mean levels of internalized stigma (men: M=0.71, SD = 0.63; women: M=0.46, SD = 0.55; p<0.001), whereas the women reported significantly higher scores for enacted stigma (men: M=1.30, SD = 1.69; women: M=2.10, SD = 2.17; p<0.001). These differences remained significant after controlling for potential socio-demographic covariates. Following their diagnosis, more women reported moving out of their homes (men: 16%; women: 26%; p<0.05). More men (89%) than women (66%; p<0.001) reported to have modified their sexual behavior after being diagnosed. These findings suggest that the experience of living with HIV and HIV stigma varies by gender in this population. Suggestions for a gender-based approach to HIV prevention and stigma reduction are provided. Reprinted by permission of Routledge, Taylor & Francis Ltd.
JF - AIDS care
AU - Malavé, S
AU - Ramakrishna, J
AU - Heylen, E
AU - Bharat, S
AU - Ekstrand, M L
AD - University of California, San Francisco ; National Institute of Mental Health and Neuroscience ; Tata Institute of Social Sciences
Y1 - 2014/03//
PY - 2014
DA - Mar 2014
SP - 396
EP - 403
VL - 26
IS - 3
SN - 0954-0121, 0954-0121
KW - Sociology
KW - Prevention
KW - Karnataka
KW - Gender differentiation
KW - HIV
KW - Health services
KW - Stigma
KW - India
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1499080718?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS+care&rft.atitle=Differences+in+testing%2C+stigma%2C+and+perceived+consequences+of+stigmatization+among+heterosexual+men+and+women+living+with+HIV+in+Bengaluru%2C+India&rft.au=Malav%C3%A9%2C+S%3BRamakrishna%2C+J%3BHeylen%2C+E%3BBharat%2C+S%3BEkstrand%2C+M+L&rft.aulast=Malav%C3%A9&rft.aufirst=S&rft.date=2014-03-01&rft.volume=26&rft.issue=3&rft.spage=396&rft.isbn=&rft.btitle=&rft.title=AIDS+care&rft.issn=09540121&rft_id=info:doi/10.1080%2F09540121.2013.819409
LA - English
DB - International Bibliography of the Social Sciences (IBSS)
N1 - Date revised - 2014-02-10
N1 - Last updated - 2014-02-18
N1 - SubjectsTermNotLitGenreText - 5423 3549 2688 2449 10404; 5703 3617 6220; 12258 11762 11859 11856; 10072; 5792 10484; 175 387 30; 197 175 387 30
DO - http://dx.doi.org/10.1080/09540121.2013.819409
ER -
TY - JOUR
T1 - Sphingolipid signaling reduces basal P-glycoprotein activity in renal proximal tubule.
AN - 1492699913; 24385389
AB - P-glycoprotein is an ATP-driven xenobiotic export pump that is highly expressed in barrier and excretory tissues, where it greatly influences drug pharmacokinetics. Recent studies in the blood-brain and spinal cord barriers identified a sphingolipid-based signaling pathway that regulates basal activity of P-glycoprotein. Here we use an established comparative renal model that permits direct measurement of P-glycoprotein activity to determine whether such signaling occurs in another tissue, killifish renal proximal tubule. Isolated killifish tubules exposed to 0.01-1.0 μM sphingosine-1-phosphate (S1P) exhibited a profound decrease in P-glycoprotein transport activity, measured as specific accumulation of a fluorescent cyclosporine A derivative in the tubule lumen. Loss of activity had a rapid onset and was fully reversible when the S1P was removed. Transport mediated by multidrug resistance-associated protein 2 (Mrp2) or a teleost fish organic anion transporter (Oat) was not affected. S1P effects were blocked by a specific S1P receptor 1 (S1PR1) antagonist and mimicked by a S1PR agonist. Sphingosine also reduced P-glycoprotein transport activity and those effects were blocked by an inhibitor of sphingosine kinase and by the S1PR1 antagonist. These results for a comparative renal model suggest that sphingolipid signaling to P-glycoprotein is not just restricted to the blood-brain and blood-spinal cord barriers, but occurs in other excretory and barrier tissues.
JF - The Journal of pharmacology and experimental therapeutics
AU - Miller, David S
AD - Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina; and Mount Desert Island Biological Laboratory, Salsbury Cove, Maine.
Y1 - 2014/03//
PY - 2014
DA - March 2014
SP - 459
EP - 464
VL - 348
IS - 3
KW - Lysophospholipids
KW - 0
KW - P-Glycoprotein
KW - Receptors, Lysosphingolipid
KW - sphingosine 1-phosphate
KW - 26993-30-6
KW - Sphingosine
KW - NGZ37HRE42
KW - Index Medicus
KW - Animals
KW - Receptors, Lysosphingolipid -- agonists
KW - Receptors, Lysosphingolipid -- metabolism
KW - In Vitro Techniques
KW - Fundulidae
KW - Biological Transport
KW - Signal Transduction
KW - Receptors, Lysosphingolipid -- antagonists & inhibitors
KW - Sphingosine -- metabolism
KW - P-Glycoprotein -- metabolism
KW - Kidney Tubules, Proximal -- metabolism
KW - Lysophospholipids -- pharmacology
KW - Lysophospholipids -- metabolism
KW - Sphingosine -- pharmacology
KW - Kidney Tubules, Proximal -- drug effects
KW - Sphingosine -- analogs & derivatives
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.atitle=Sphingolipid+signaling+reduces+basal+P-glycoprotein+activity+in+renal+proximal+tubule.&rft.au=Miller%2C+David+S&rft.aulast=Miller&rft.aufirst=David&rft.date=2014-03-01&rft.volume=348&rft.issue=3&rft.spage=459&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.issn=1521-0103&rft_id=info:doi/10.1124%2Fjpet.113.210641
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-04-02
N1 - Date created - 2014-01-28
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1124/jpet.113.210641
ER -
TY - CPAPER
T1 - Epitope Mapping Of An Anti-Bla g 1 ScFv Used For Cockroach Allergen Quantitation
T2 - 2014 Annual Meeting of the American Academy of Allergy, Asthma and Immunology (AAAAI 2014)
AN - 1518614275; 6283841
JF - 2014 Annual Meeting of the American Academy of Allergy, Asthma and Immunology (AAAAI 2014)
AU - Mueller, Geoffrey
AU - Ankney, John
AU - Pedersen, Lars
AU - Khurana, Taruna
AU - Slater, Jay
AU - Glesner, Jill
AU - Pomes, Anna
AU - London, Robert
Y1 - 2014/02/28/
PY - 2014
DA - 2014 Feb 28
KW - Allergens
KW - Epitope mapping
KW - Quantitation
KW - Fv
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518614275?accountid=14244
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L2 - http://www.aaaai.org/Aaaai/media/MediaLibrary/PDF%20Documents/Announcements/am14-final-prog.pdf
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-23
N1 - Last updated - 2014-04-24
ER -
TY - CPAPER
T1 - Estradiol Has a Negative Impact On The Anaphylactic Response In Mice, Independent From Mast Cell Degranulation
T2 - 2014 Annual Meeting of the American Academy of Allergy, Asthma and Immunology (AAAAI 2014)
AN - 1518613859; 6283715
JF - 2014 Annual Meeting of the American Academy of Allergy, Asthma and Immunology (AAAAI 2014)
AU - Hox, Valerie
AU - Desai, Avanti
AU - Bandara, Geethani
AU - Gilfillan, Alasdair
AU - Beaven, Michael
AU - Olivera, Ana
AU - Metcalfe, Dean
Y1 - 2014/02/28/
PY - 2014
DA - 2014 Feb 28
KW - Anaphylaxis
KW - Degranulation
KW - Mast cells
KW - Mice
KW - Estradiol
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L2 - http://www.aaaai.org/Aaaai/media/MediaLibrary/PDF%20Documents/Announcements/am14-final-prog.pdf
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-23
N1 - Last updated - 2014-04-24
ER -
TY - CPAPER
T1 - Human EMR1, An Eosinophil-Specific Surface Receptor Of Unknown Function, Is Modulated In Vivo and In Vitro
T2 - 2014 Annual Meeting of the American Academy of Allergy, Asthma and Immunology (AAAAI 2014)
AN - 1518612949; 6283723
JF - 2014 Annual Meeting of the American Academy of Allergy, Asthma and Immunology (AAAAI 2014)
AU - Legrand, Fanny
AU - Tomasevic, Nenad
AU - Makiya, Michelle
AU - Bebbington, Christopher
AU - Klion, Amy
Y1 - 2014/02/28/
PY - 2014
DA - 2014 Feb 28
KW - Receptor mechanisms
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L2 - http://www.aaaai.org/Aaaai/media/MediaLibrary/PDF%20Documents/Announcements/am14-final-prog.pdf
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-23
N1 - Last updated - 2014-04-24
ER -
TY - CPAPER
T1 - Outcome Measures Of Challenge Testing In Patients With Physically Induced-Urticaria
T2 - 2014 Annual Meeting of the American Academy of Allergy, Asthma and Immunology (AAAAI 2014)
AN - 1518612717; 6283901
JF - 2014 Annual Meeting of the American Academy of Allergy, Asthma and Immunology (AAAAI 2014)
AU - Metcalfe, Dean
AU - Arceo, Sarah
AU - Young, Michael
AU - Nelson, Celeste
AU - Komarow, Hirsh
Y1 - 2014/02/28/
PY - 2014
DA - 2014 Feb 28
KW - Hypersensitivity
KW - Epidemiology
KW - Lung
KW - Immunology
KW - Asthma
KW - Respiratory diseases
KW - Public health
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L2 - http://www.aaaai.org/Aaaai/media/MediaLibrary/PDF%20Documents/Announcements/am14-final-prog.pdf
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-23
N1 - Last updated - 2014-04-24
ER -
TY - CPAPER
T1 - Gene Expression Profiling Of Food-Induced Anaphylaxis Associated With Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)
T2 - 2014 Annual Meeting of the American Academy of Allergy, Asthma and Immunology (AAAAI 2014)
AN - 1518612445; 6283613
JF - 2014 Annual Meeting of the American Academy of Allergy, Asthma and Immunology (AAAAI 2014)
AU - Munoz-Cano, Rosa
AU - Bartra, Joan
AU - Scheffel, Jorg
AU - Pascal, Mariona
AU - Dema, Barbara
AU - Valero, Antonio
AU - Olivera, Ana
AU - Picado, Cesar
AU - Rivera, Juan
Y1 - 2014/02/28/
PY - 2014
DA - 2014 Feb 28
KW - Gene expression
KW - Anaphylaxis
KW - Food
KW - Profiling
KW - Drugs
KW - Antiinflammatory agents
KW - Nonsteroidal antiinflammatory drugs
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L2 - http://www.aaaai.org/Aaaai/media/MediaLibrary/PDF%20Documents/Announcements/am14-final-prog.pdf
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-23
N1 - Last updated - 2014-04-24
ER -
TY - CPAPER
T1 - Teasing and Bullying Among Adolescents With Food Allergy
T2 - 2014 Annual Meeting of the American Academy of Allergy, Asthma and Immunology (AAAAI 2014)
AN - 1518611622; 6284081
JF - 2014 Annual Meeting of the American Academy of Allergy, Asthma and Immunology (AAAAI 2014)
AU - Lin, Adora
AU - Sharma, Hemant
Y1 - 2014/02/28/
PY - 2014
DA - 2014 Feb 28
KW - Food hypersensitivity
KW - Bullying
KW - Adolescents
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L2 - http://www.aaaai.org/Aaaai/media/MediaLibrary/PDF%20Documents/Announcements/am14-final-prog.pdf
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-23
N1 - Last updated - 2014-04-24
ER -
TY - CPAPER
T1 - Worldwide Impact Of LAD2 Mast Cell Line On Mast Cell Biology Research
T2 - 2014 Annual Meeting of the American Academy of Allergy, Asthma and Immunology (AAAAI 2014)
AN - 1518610944; 6283709
JF - 2014 Annual Meeting of the American Academy of Allergy, Asthma and Immunology (AAAAI 2014)
AU - Kirshenbaum, Arnold
AU - Petrik, Amy
AU - Walsh, Rosemary
AU - Vepa, Sury
AU - Metcalfe, Dean
Y1 - 2014/02/28/
PY - 2014
DA - 2014 Feb 28
KW - Mast cells
KW - Cytology
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L2 - http://www.aaaai.org/Aaaai/media/MediaLibrary/PDF%20Documents/Announcements/am14-final-prog.pdf
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-23
N1 - Last updated - 2014-04-24
ER -
TY - JOUR
T1 - Evaluating the additivity of perfluoroalkyl acids in binary combinations on peroxisome proliferator-activated receptor-α activation.
AN - 1499137621; 24374136
AB - Perfluoroalkyl acids (PFAAs) are found globally in the environment, detected in humans and wildlife, and are typically present as mixtures of PFAA congeners. Mechanistic studies have found that responses to PFAAs are mediated in part by PPARα. Our previous studies showed that individual PFAAs activate PPARα transfected into COS-1 cells. The goal of the current study was to determine if binary combinations of perfluorooctanoic acid (PFOA) and another PFAA act in an additive fashion to activate PPARα in the mouse one-hybrid in vitro model. COS-1 cells were transiently transfected with mouse PPARα luciferase reporter construct and exposed to either vehicle control (0.1% DMSO or water), PPARα agonist (WY14643, 10 μM), PFOA at 1-128μM, perfluorononanoic acid (PFNA) at 1-128 μM, perfluorohexanoic acid (PFHxA) at 8-1024 μM, perfluorooctane sulfonate (PFOS) at 4-384 μM or perfluorohexane sulfonate (PFHxS) at 8-2048 μM to generate sigmoidal concentration-response curves. In addition, cells were exposed to binary combinations of PFOA+either PFNA, PFHxA, PFOS or PFHxS in an 8×8 factorial design. The concentration-response data for individual chemicals were fit to sigmoidal curves and analyzed with nonlinear regression to generate EC₅₀s and Hillslopes, which were used in response-addition and concentration-addition models to calculate predicted responses for mixtures in the same plate. All PFOA+PFAA combinations produced concentration-response curves that were closely aligned with the predicted curves for both response addition and concentration addition at low concentrations. However, at higher concentrations of all chemicals, the observed response curves deviated from the predicted models of additivity. We conclude that binary combinations of PFAAs behave additively at the lower concentration ranges in activating PPARα in this in vitro system. Published by Elsevier Ireland Ltd.
JF - Toxicology
AU - Wolf, Cynthia J
AU - Rider, Cynthia V
AU - Lau, Christopher
AU - Abbott, Barbara D
AD - Developmental Toxicology Branch, Toxicity Assessment Division, National Health and Environmental Effects Research Laboratory, ORD, U.S. EPA, Research Triangle Park, NC 27711, United States. Electronic address: wolf.cynthiaj@epa.gov. ; National Toxicology Program, NIEHS, Research Triangle Park, NC 27709, United States. ; Developmental Toxicology Branch, Toxicity Assessment Division, National Health and Environmental Effects Research Laboratory, ORD, U.S. EPA, Research Triangle Park, NC 27711, United States.
Y1 - 2014/02/28/
PY - 2014
DA - 2014 Feb 28
SP - 43
EP - 54
VL - 316
KW - Alkanesulfonic Acids
KW - 0
KW - Caprylates
KW - Environmental Pollutants
KW - Fluorocarbons
KW - PPAR alpha
KW - Pyrimidines
KW - pirinixic acid
KW - 86C4MRT55A
KW - perfluorooctanoic acid
KW - 947VD76D3L
KW - Index Medicus
KW - Additivity
KW - PFOA
KW - Mixtures
KW - Perfluoroalkyl acids
KW - PPARα
KW - Regression Analysis
KW - Animals
KW - Alkanesulfonic Acids -- administration & dosage
KW - COS Cells
KW - Transfection
KW - Dose-Response Relationship, Drug
KW - Alkanesulfonic Acids -- toxicity
KW - Cercopithecus aethiops
KW - Pyrimidines -- pharmacology
KW - Alkanesulfonic Acids -- chemistry
KW - Mice
KW - Fluorocarbons -- chemistry
KW - Caprylates -- administration & dosage
KW - PPAR alpha -- drug effects
KW - Caprylates -- chemistry
KW - Environmental Pollutants -- toxicity
KW - Fluorocarbons -- administration & dosage
KW - Fluorocarbons -- toxicity
KW - Environmental Pollutants -- chemistry
KW - Caprylates -- toxicity
KW - PPAR alpha -- metabolism
KW - Environmental Pollutants -- administration & dosage
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-04-15
N1 - Date created - 2014-02-11
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.tox.2013.12.002
ER -
TY - JOUR
T1 - A bacterial homolog of a eukaryotic inositol phosphate signaling enzyme mediates cross-kingdom dialog in the mammalian gut.
AN - 1504152424; 24529702
AB - Dietary InsP6 can modulate eukaryotic cell proliferation and has complex nutritive consequences, but its metabolism in the mammalian gastrointestinal tract is poorly understood. Therefore, we performed phylogenetic analyses of the gastrointestinal microbiome in order to search for candidate InsP6 phosphatases. We determined that prominent gut bacteria express homologs of the mammalian InsP6 phosphatase (MINPP) and characterized the enzyme from Bacteroides thetaiotaomicron (BtMinpp). We show that BtMinpp has exceptionally high catalytic activity, which we rationalize on the basis of mutagenesis studies and by determining its crystal structure at 1.9 Å resolution. We demonstrate that BtMinpp is packaged inside outer membrane vesicles (OMVs) protecting the enzyme from degradation by gastrointestinal proteases. Moreover, we uncover an example of cross-kingdom cell-to-cell signaling, showing that the BtMinpp-OMVs interact with intestinal epithelial cells to promote intracellular Ca(2+) signaling. Our characterization of BtMinpp offers several directions for understanding how the microbiome serves human gastrointestinal physiology. Copyright © 2014 The Authors. Published by Elsevier Inc. All rights reserved.
JF - Cell reports
AU - Stentz, Régis
AU - Osborne, Samantha
AU - Horn, Nikki
AU - Li, Arthur W H
AU - Hautefort, Isabelle
AU - Bongaerts, Roy
AU - Rouyer, Marine
AU - Bailey, Paul
AU - Shears, Stephen B
AU - Hemmings, Andrew M
AU - Brearley, Charles A
AU - Carding, Simon R
AD - Gut Health and Food Safety Programme, Institute of Food Research, Norwich NR4 7UA, UK. ; School of Biological Sciences, University of East Anglia, Norwich NR4 7TJ, UK. ; Department of Computational and Systems Biology, John Innes Centre, Norwich NR4 7UH, UK. ; Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA. ; School of Biological Sciences, University of East Anglia, Norwich NR4 7TJ, UK; School of Chemistry, University of East Anglia, Norwich NR4 7TJ, UK. ; School of Biological Sciences, University of East Anglia, Norwich NR4 7TJ, UK. Electronic address: c.brearley@uea.ac.uk. ; Gut Health and Food Safety Programme, Institute of Food Research, Norwich NR4 7UA, UK; Norwich Medical School, University of East Anglia, Norwich NR4 7TJ, UK. Electronic address: simon.carding@ifr.ac.uk.
Y1 - 2014/02/27/
PY - 2014
DA - 2014 Feb 27
SP - 646
EP - 656
VL - 6
IS - 4
KW - Bacterial Proteins
KW - 0
KW - Phosphoric Monoester Hydrolases
KW - EC 3.1.3.2
KW - multiple inositol-polyphosphate phosphatase
KW - EC 3.1.3.62
KW - Index Medicus
KW - Proteolysis
KW - Phylogeny
KW - Humans
KW - Molecular Sequence Data
KW - Intestinal Mucosa -- microbiology
KW - Catalytic Domain
KW - Intestinal Mucosa -- metabolism
KW - HT29 Cells
KW - Amino Acid Sequence
KW - Mutation
KW - Calcium Signaling
KW - Host-Pathogen Interactions
KW - Phosphoric Monoester Hydrolases -- chemistry
KW - Bacteroides -- genetics
KW - Bacterial Proteins -- genetics
KW - Bacterial Proteins -- chemistry
KW - Bacteroides -- enzymology
KW - Bacterial Proteins -- metabolism
KW - Phosphoric Monoester Hydrolases -- genetics
KW - Bacteroides -- chemistry
KW - Phosphoric Monoester Hydrolases -- metabolism
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-11-07
N1 - Date created - 2014-03-03
N1 - Date revised - 2017-01-14
N1 - Genetic sequence - 4FDT; PDB; 4FDU
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.celrep.2014.01.021
ER -
TY - JOUR
T1 - Washing older blood units before transfusion reduces plasma iron and improves outcomes in experimental canine pneumonia.
AN - 1503555845; 24366359
AB - In a randomized controlled blinded trial, 2-year-old purpose-bred beagles (n = 24), with Staphylococcus aureus pneumonia, were exchanged-transfused with either 7- or 42-day-old washed or unwashed canine universal donor blood (80 mL/kg in 4 divided doses). Washing red cells (RBC) before transfusion had a significantly different effect on canine survival, multiple organ injury, plasma iron, and cell-free hemoglobin (CFH) levels depending on the age of stored blood (all, P < .05 for interactions). Washing older units of blood improved survival rates, shock score, lung injury, cardiac performance and liver function, and reduced levels of non-transferrin bound iron and plasma labile iron. In contrast, washing fresh blood worsened all these same clinical parameters and increased CFH levels. Our data indicate that transfusion of fresh blood, which results in less hemolysis, CFH, and iron release, is less toxic than transfusion of older blood in critically ill infected subjects. However, washing older blood prevented elevations in plasma circulating iron and improved survival and multiple organ injury in animals with an established pulmonary infection. Our data suggest that fresh blood should not be washed routinely because, in a setting of established infection, washed RBC are prone to release CFH and result in worsened clinical outcomes.
JF - Blood
AU - Cortés-Puch, Irene
AU - Wang, Dong
AU - Sun, Junfeng
AU - Solomon, Steven B
AU - Remy, Kenneth E
AU - Fernandez, Melinda
AU - Feng, Jing
AU - Kanias, Tamir
AU - Bellavia, Landon
AU - Sinchar, Derek
AU - Perlegas, Andreas
AU - Solomon, Michael A
AU - Kelley, Walter E
AU - Popovsky, Mark A
AU - Gladwin, Mark T
AU - Kim-Shapiro, Daniel B
AU - Klein, Harvey G
AU - Natanson, Charles
AD - Critical Care Medicine Department, Clinical Center, National Institutes of Health, Bethesda, MD;
Y1 - 2014/02/27/
PY - 2014
DA - 2014 Feb 27
SP - 1403
EP - 1411
VL - 123
IS - 9
KW - Iron
KW - E1UOL152H7
KW - Abridged Index Medicus
KW - Index Medicus
KW - Animals
KW - Down-Regulation
KW - Treatment Outcome
KW - Dogs
KW - Disease Models, Animal
KW - Acute Lung Injury -- mortality
KW - Acute Lung Injury -- etiology
KW - Blood Preservation
KW - Blood Specimen Collection -- methods
KW - Erythrocyte Transfusion -- adverse effects
KW - Pneumonia, Staphylococcal -- mortality
KW - Erythrocyte Transfusion -- methods
KW - Pneumonia, Staphylococcal -- therapy
KW - Iron -- isolation & purification
KW - Erythrocytes -- cytology
KW - Iron -- blood
KW - Plasma -- chemistry
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Blood&rft.atitle=Washing+older+blood+units+before+transfusion+reduces+plasma+iron+and+improves+outcomes+in+experimental+canine+pneumonia.&rft.au=Cort%C3%A9s-Puch%2C+Irene%3BWang%2C+Dong%3BSun%2C+Junfeng%3BSolomon%2C+Steven+B%3BRemy%2C+Kenneth+E%3BFernandez%2C+Melinda%3BFeng%2C+Jing%3BKanias%2C+Tamir%3BBellavia%2C+Landon%3BSinchar%2C+Derek%3BPerlegas%2C+Andreas%3BSolomon%2C+Michael+A%3BKelley%2C+Walter+E%3BPopovsky%2C+Mark+A%3BGladwin%2C+Mark+T%3BKim-Shapiro%2C+Daniel+B%3BKlein%2C+Harvey+G%3BNatanson%2C+Charles&rft.aulast=Cort%C3%A9s-Puch&rft.aufirst=Irene&rft.date=2014-02-27&rft.volume=123&rft.issue=9&rft.spage=1403&rft.isbn=&rft.btitle=&rft.title=Blood&rft.issn=1528-0020&rft_id=info:doi/10.1182%2Fblood-2013-11-539353
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-05-06
N1 - Date created - 2014-02-28
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Vox Sang. 2004 Jul;87(1):19-26 [15260818]
Transfus Med. 2002 Jun;12(3):173-9 [12071873]
N Engl J Med. 2005 Mar 10;352(10):1011-23 [15758012]
J Extra Corpor Technol. 2005 Mar;37(1):58-9 [15804159]
Vox Sang. 2006 Jan;90(1):40-4 [16359354]
Vox Sang. 2006 Jul;91(1):13-9 [16756596]
Transfusion. 2006 Nov;46(11):2014-27 [17076859]
Vox Sang. 2007 Feb;92(2):130-5 [17298575]
Transfusion. 2007 Feb;47(2):248-50 [17302770]
Transfus Med. 2007 Apr;17(2):89-95 [17430464]
Am J Physiol Heart Circ Physiol. 2007 Oct;293(4):H2487-500 [17644570]
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Clin Chem Lab Med. 2010 May;48(5):677-83 [20158444]
Blood. 2010 May 27;115(21):4284-92 [20299509]
Transfus Apher Sci. 2010 Aug;43(1):107-16 [20655807]
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Transfusion. 2012 Jun;52(6):1203-12 [22257314]
J Trauma Acute Care Surg. 2012 Aug;73(2 Suppl 1):S128-33 [22847082]
Intensive Care Med. 2012 Dec;38(12):2063-71 [23111805]
Transfusion. 2012 Jan;52(1):34-8 [21682733]
Crit Care Med. 2013 Mar;41(3):784-90 [23314583]
Blood. 2013 Feb 28;121(9):1663-72 [23255558]
Transfusion. 2013 May;53(5):1001-9 [22897672]
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Comment In:
Blood. 2014 Feb 27;123(9):1287-9 [24578494]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1182/blood-2013-11-539353
ER -
TY - JOUR
T1 - Characterizing the genetic basis of methylome diversity in histologically normal human lung tissue.
AN - 1503551301; 24572595
AB - The genetic regulation of the human epigenome is not fully appreciated. Here we describe the effects of genetic variants on the DNA methylome in human lung based on methylation-quantitative trait loci (meQTL) analyses. We report 34,304 cis- and 585 trans-meQTLs, a genetic-epigenetic interaction of surprising magnitude, including a regulatory hotspot. These findings are replicated in both breast and kidney tissues and show distinct patterns: cis-meQTLs mostly localize to CpG sites outside of genes, promoters and CpG islands (CGIs), while trans-meQTLs are over-represented in promoter CGIs. meQTL SNPs are enriched in CTCF-binding sites, DNaseI hypersensitivity regions and histone marks. Importantly, four of the five established lung cancer risk loci in European ancestry are cis-meQTLs and, in aggregate, cis-meQTLs are enriched for lung cancer risk in a genome-wide analysis of 11,587 subjects. Thus, inherited genetic variation may affect lung carcinogenesis by regulating the human methylome.
JF - Nature communications
AU - Shi, Jianxin
AU - Marconett, Crystal N
AU - Duan, Jubao
AU - Hyland, Paula L
AU - Li, Peng
AU - Wang, Zhaoming
AU - Wheeler, William
AU - Zhou, Beiyun
AU - Campan, Mihaela
AU - Lee, Diane S
AU - Huang, Jing
AU - Zhou, Weiyin
AU - Triche, Tim
AU - Amundadottir, Laufey
AU - Warner, Andrew
AU - Hutchinson, Amy
AU - Chen, Po-Han
AU - Chung, Brian S I
AU - Pesatori, Angela C
AU - Consonni, Dario
AU - Bertazzi, Pier Alberto
AU - Bergen, Andrew W
AU - Freedman, Mathew
AU - Siegmund, Kimberly D
AU - Berman, Benjamin P
AU - Borok, Zea
AU - Chatterjee, Nilanjan
AU - Tucker, Margaret A
AU - Caporaso, Neil E
AU - Chanock, Stephen J
AU - Laird-Offringa, Ite A
AU - Landi, Maria Teresa
AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Bethesda, Maryland 20892, USA. ; 1] Department of Surgery, USC/Norris Comprehensive Cancer Center, Keck School of Medicine, Los Angeles, California 90089, USA [2] Department of Biochemistry and Molecular Biology, USC/Norris Comprehensive Cancer Center, Keck School of Medicine, Los Angeles, California 90089, USA. ; Center for Psychiatric Genetics, Department of Psychiatry and Behavioral Sciences, North Shore University Health System Research Institute, University of Chicago Pritzker School of Medicine, Evanston, Illinois 60201, USA. ; Information Management Services Inc., Rockville, Maryland 20852, USA. ; Will Rogers Institute Pulmonary Research Center, Division of Pulmonary, Critical Care and Sleep Medicine, USC Keck School of Medicine, Los Angeles, California 90089, USA. ; Laboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, NIH, DHHS, Bethesda, Maryland 20892, USA. ; Bioinformatics Division, Department of Preventive Medicine, University of Southern California, Los Angeles, California 90089, USA. ; Pathology/Histotechnology Laboratory, Laboratory Animal Sciences Program, Frederick National Laboratory for Cancer Research, Frederick, Maryland 21702, USA. ; Unit of Epidemiology, IRCCS Fondazione Ca' Granda Ospedale Maggiore Policlinico, Department of Clinical Sciences and Community Health, University of Milan, Milan 20122, Italy. ; Molecular Genetics Program, Center for Health Sciences, SRI, Menlo Park, California 94025, USA. ; 1] Program in Medical and Population Genetics, The Broad Institute, Cambridge, Massachusetts 02142, USA [2] Department of Medical Oncology, The Center for Functional Cancer Epigenetics, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA. ; 1] Bioinformatics Division, Department of Preventive Medicine, University of Southern California, Los Angeles, California 90089, USA [2] USC Epigenome Center and USC/Norris Comprehensive Cancer Center, Los Angeles, California 90089, USA. ; 1] Department of Biochemistry and Molecular Biology, USC/Norris Comprehensive Cancer Center, Keck School of Medicine, Los Angeles, California 90089, USA [2] Will Rogers Institute Pulmonary Research Center, Division of Pulmonary, Critical Care and Sleep Medicine, USC Keck School of Medicine, Los Angeles, California 90089, USA.
Y1 - 2014/02/27/
PY - 2014
DA - 2014 Feb 27
SP - 3365
VL - 5
KW - Index Medicus
KW - Polymorphism, Single Nucleotide
KW - Kidney -- metabolism
KW - Humans
KW - European Continental Ancestry Group -- genetics
KW - Epistasis, Genetic
KW - Lung Neoplasms -- ethnology
KW - Genome-Wide Association Study
KW - Genotype
KW - Genetic Predisposition to Disease -- ethnology
KW - Genetic Predisposition to Disease -- genetics
KW - Risk Factors
KW - CpG Islands -- genetics
KW - Lung Neoplasms -- genetics
KW - Promoter Regions, Genetic -- genetics
KW - Breast -- metabolism
KW - Genetic Variation
KW - DNA Methylation
KW - Quantitative Trait Loci -- genetics
KW - Lung -- metabolism
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1503551301?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+communications&rft.atitle=Characterizing+the+genetic+basis+of+methylome+diversity+in+histologically+normal+human+lung+tissue.&rft.au=Shi%2C+Jianxin%3BMarconett%2C+Crystal+N%3BDuan%2C+Jubao%3BHyland%2C+Paula+L%3BLi%2C+Peng%3BWang%2C+Zhaoming%3BWheeler%2C+William%3BZhou%2C+Beiyun%3BCampan%2C+Mihaela%3BLee%2C+Diane+S%3BHuang%2C+Jing%3BZhou%2C+Weiyin%3BTriche%2C+Tim%3BAmundadottir%2C+Laufey%3BWarner%2C+Andrew%3BHutchinson%2C+Amy%3BChen%2C+Po-Han%3BChung%2C+Brian+S+I%3BPesatori%2C+Angela+C%3BConsonni%2C+Dario%3BBertazzi%2C+Pier+Alberto%3BBergen%2C+Andrew+W%3BFreedman%2C+Mathew%3BSiegmund%2C+Kimberly+D%3BBerman%2C+Benjamin+P%3BBorok%2C+Zea%3BChatterjee%2C+Nilanjan%3BTucker%2C+Margaret+A%3BCaporaso%2C+Neil+E%3BChanock%2C+Stephen+J%3BLaird-Offringa%2C+Ite+A%3BLandi%2C+Maria+Teresa&rft.aulast=Shi&rft.aufirst=Jianxin&rft.date=2014-02-27&rft.volume=5&rft.issue=&rft.spage=3365&rft.isbn=&rft.btitle=&rft.title=Nature+communications&rft.issn=2041-1723&rft_id=info:doi/10.1038%2Fncomms4365
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-12-03
N1 - Date created - 2014-02-27
N1 - Date revised - 2017-01-14
N1 - Genetic sequence - PHS000093; dbGaP; GSE52401
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1038/ncomms4365
ER -
TY - JOUR
T1 - The immunological and clinical effects of mutated ras peptide vaccine in combination with IL-2, GM-CSF, or both in patients with solid tumors.
AN - 1504452341; 24565030
AB - Mutant Ras oncogenes produce proteins that are unique to cancer cells and represent attractive targets for vaccine therapy. We have shown previously that vaccinating cancer patients with mutant ras peptides is feasible and capable of inducing a specific immune response against the relevant mutant proteins. Here, we tested the mutant ras peptide vaccine administered in combination with low dose interleukin-2 (IL-2) or/and granulocyte-macrophage colony-stimulating factor (GM-CSF) in order to enhance the vaccine immune response.
5000 μg of the corresponding mutant ras peptide was given subcutaneously (SQ) along with IL-2 (Arm A), GM-CSF (Arm B) or both (Arm C). IL-2 was given SQ at 6.0 million IU/m²/day starting at day 5, 5 days/week for 2 weeks. GM-CSF was given SQ in a dose of 100 μg/day one day prior to each ras peptide vaccination for 4 days. Vaccines were repeated every 5 weeks on arm A and C, and every 4 weeks on arm B, for a maximum of 15 cycles or until disease progression. We treated 53 advanced cancer patients (38 with colorectal, 11 with pancreatic, 1 with common bile duct and 3 with lung) on 3 different arms (16 on arm A, 18 on arm B, and 19 on arm C). The median progression free survival (PFS) and overall survival (OS) was 3.6 and 16.9 months, respectively, for all patients evaluable for clinical response (n = 48). There was no difference in PFS or OS between the three arms (P = 0.73 and 0.99, respectively). Most adverse events were grade 1-2 toxicities and resolved spontaneously. The vaccine induced an immune response to the relevant ras peptide in a total of 20 out of 37 evaluable patients (54%) by ELISPOT, proliferative assay, or both. While 92.3% of patients on arm B had a positive immune response, only 31% of patients on arm A and 36% of patients on arm C had positive immune responses (P = 0.003, Fisher's exact test).
The reported data showed that IL-2 might have a negative effect on the specific immune response induced by the relevant mutant ras vaccine in patients with advanced cancer. This observation deserves further investigations. NCI97C0141.
JF - Journal of translational medicine
AU - Rahma, Osama E
AU - Hamilton, J Michael
AU - Wojtowicz, Malgorzata
AU - Dakheel, Omar
AU - Bernstein, Sarah
AU - Liewehr, David J
AU - Steinberg, Seth M
AU - Khleif, Samir N
AD - Cancer Vaccine Branch, CCR, NCI, 10 Center Drive, Bethesda, MD 20892, USA. skhleif@gru.edu.
Y1 - 2014/02/24/
PY - 2014
DA - 2014 Feb 24
SP - 55
VL - 12
KW - Cancer Vaccines
KW - 0
KW - Interleukin-2
KW - Vaccines, Subunit
KW - Granulocyte-Macrophage Colony-Stimulating Factor
KW - 83869-56-1
KW - ras Proteins
KW - EC 3.6.5.2
KW - Index Medicus
KW - Immunity -- immunology
KW - Humans
KW - Enzyme-Linked Immunospot Assay
KW - Adult
KW - Treatment Outcome
KW - Molecular Sequence Data
KW - Aged
KW - Middle Aged
KW - Amino Acid Sequence
KW - T-Lymphocytes, Regulatory -- immunology
KW - ras Proteins -- genetics
KW - Neoplasms -- drug therapy
KW - Cancer Vaccines -- adverse effects
KW - Vaccines, Subunit -- therapeutic use
KW - Vaccines, Subunit -- chemistry
KW - Interleukin-2 -- therapeutic use
KW - Cancer Vaccines -- therapeutic use
KW - Neoplasms -- prevention & control
KW - Granulocyte-Macrophage Colony-Stimulating Factor -- therapeutic use
KW - Vaccines, Subunit -- adverse effects
KW - Neoplasms -- immunology
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1504452341?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+translational+medicine&rft.atitle=The+immunological+and+clinical+effects+of+mutated+ras+peptide+vaccine+in+combination+with+IL-2%2C+GM-CSF%2C+or+both+in+patients+with+solid+tumors.&rft.au=Rahma%2C+Osama+E%3BHamilton%2C+J+Michael%3BWojtowicz%2C+Malgorzata%3BDakheel%2C+Omar%3BBernstein%2C+Sarah%3BLiewehr%2C+David+J%3BSteinberg%2C+Seth+M%3BKhleif%2C+Samir+N&rft.aulast=Rahma&rft.aufirst=Osama&rft.date=2014-02-24&rft.volume=12&rft.issue=&rft.spage=55&rft.isbn=&rft.btitle=&rft.title=Journal+of+translational+medicine&rft.issn=1479-5876&rft_id=info:doi/10.1186%2F1479-5876-12-55
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-09-05
N1 - Date created - 2014-03-04
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Clin Cancer Res. 2009 Feb 15;15(4):1443-51 [19228745]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1186/1479-5876-12-55
ER -
TY - JOUR
T1 - Association between Maternal Serum Perfluoroalkyl Substances during Pregnancy and Maternal and Cord Thyroid Hormones: Taiwan Maternal and Infant Cohort Study
AN - 1534851235; 20047042
AB - Background: Perfluoroalkyl substances (PFASs) are synthetic compounds that are widely used in industry and are often detectable in humans. In pregnant rats and their pups, PFASs can interfere with thyroid hormone homeostasis. In humans, maternal thyroid hormones supply the fetus throughout pregnancy, and thyroid hormones play a critical role in fetal growth and neurodevelopment. Objectives: We investigated the association between maternal PFAS exposure and thyroid hormone status in pregnant women and neonates. Methods: In a study of environmental exposure and health in Taiwan, we measured serum concentrations of nine PFASs and four thyroid hormones for 285 pregnant women in their third trimester, and also measured cord serum thyroid hormones for 116 neonates. Associations between maternal PFASs and maternal and cord thyroid hormones were examined in multiple linear regression models. Results: Perfluorohexanesulfonic acid concentrations were positively associated with maternal thyroid-stimulating hormone (TSH) levels. Pregnant women with higher levels of perfluorononanoic acid (PFNA), perfluoroundecanoic acid (PFUnDA), and perfluorododecanoic acid (PFDoDA) had lower free thyroxine (T4) and total T4 levels. For example, we estimated that maternal free T4 levels decreased 0.019 ng/dL (95% CI: -0.028, -0.009) with each nanogram per milliliter increase in maternal PFNA. Finally, maternal PFNA, PFUnDA, and PFDoDA levels were associated with lower cord total triiodothyronine (T3) and total T4 levels, and maternal perfluorodecanoic acid (PFDeA) was associated with lower cord total T3. Conclusions: Our results suggest that exposure to some PFASs during pregnancy may interfere with thyroid hormone homeostasis in pregnant women and fetuses. Citation: Wang Y, Rogan WJ, Chen PC, Lien GW, Chen HY, Tseng YC, Longnecker MP, Wang SL. 2014. Association between maternal serum perfluoroalkyl substances during pregnancy and maternal and cord thyroid hormones: Taiwan Maternal and Infant Cohort Study. Environ Health Perspect 122:529-534; http://dx.doi.org/10.1289/ehp.1306925
JF - Environmental Health Perspectives
AU - Wang, Yan
AU - Rogan, Walter J
AU - Chen, Pau-Chung
AU - Lien, Guang-Wen
AU - Chen, Hsiao-Yen
AU - Tseng, Ying-Chih
AU - Longnecker, Matthew P
AU - Wang, Shu-Li
AD - Epidemiology Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA
Y1 - 2014/02/21/
PY - 2014
DA - 2014 Feb 21
SP - 529
EP - 534
PB - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States
VL - 122
IS - 5
SN - 0091-6765, 0091-6765
KW - Environment Abstracts; Health & Safety Science Abstracts
KW - Rats
KW - Taiwan
KW - Thyroid
KW - Neonates
KW - Hormones
KW - Fetuses
KW - Pregnancy
KW - Infants
KW - H 6000:Natural Disasters/Civil Defense/Emergency Management
KW - ENA 02:Toxicology & Environmental Safety
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534851235?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Health+Perspectives&rft.atitle=Association+between+Maternal+Serum+Perfluoroalkyl+Substances+during+Pregnancy+and+Maternal+and+Cord+Thyroid+Hormones%3A+Taiwan+Maternal+and+Infant+Cohort+Study&rft.au=Wang%2C+Yan%3BRogan%2C+Walter+J%3BChen%2C+Pau-Chung%3BLien%2C+Guang-Wen%3BChen%2C+Hsiao-Yen%3BTseng%2C+Ying-Chih%3BLongnecker%2C+Matthew+P%3BWang%2C+Shu-Li&rft.aulast=Wang&rft.aufirst=Yan&rft.date=2014-02-21&rft.volume=122&rft.issue=5&rft.spage=529&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1306925
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-01
N1 - Last updated - 2015-05-13
N1 - SubjectsTermNotLitGenreText - Rats; Thyroid; Neonates; Hormones; Fetuses; Infants; Pregnancy; Taiwan
DO - http://dx.doi.org/10.1289/ehp.1306925
ER -
TY - JOUR
T1 - Introduction to thematic minireview series: Development of human therapeutics based on induced pluripotent stem cell (iPSC) technology.
AN - 1501835497; 24362035
AB - With the advent of human induced pluripotent stem cell (hiPSC) technology, it is now possible to derive patient-specific cell lines that are of great potential in both basic research and the development of new therapeutics for human diseases. Not only do hiPSCs offer unprecedented opportunities to study cellular differentiation and model human diseases, but the differentiated cell types obtained from iPSCs may become therapeutics themselves. These cells can also be used in the screening of therapeutics and in toxicology assays for potential liabilities of therapeutic agents. The remarkable achievement of transcription factor reprogramming to generate iPSCs was recognized by the award of the Nobel Prize in Medicine to Shinya Yamanaka in 2012, just 6 years after the first publication of reprogramming methods to generate hiPSCs (Takahashi, K., Tanabe, K., Ohnuki, M., Narita, M., Ichisaka, T., Tomoda, K., and Yamanaka, S. (2007) Cell 131, 861-872). This minireview series highlights both the promises and challenges of using iPSC technology for disease modeling, drug screening, and the development of stem cell therapeutics.
JF - The Journal of biological chemistry
AU - Rao, Mahendra
AU - Gottesfeld, Joel M
AD - From the Center for Regenerative Medicine, National Institutes of Health, Bethesda, Maryland 20892 and.
Y1 - 2014/02/21/
PY - 2014
DA - 2014 Feb 21
SP - 4553
EP - 4554
VL - 289
IS - 8
KW - Index Medicus
KW - Genomic Instability
KW - Immunogenicity
KW - Gene Correction
KW - Stem Cells
KW - Regenerative Medicine
KW - Toxicology
KW - Induced Pluripotent Stem Cells
KW - Humans
KW - Drug Evaluation, Preclinical
KW - Induced Pluripotent Stem Cells -- cytology
KW - Stem Cell Transplantation
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-04-22
N1 - Date created - 2014-02-24
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
J Biol Chem. 2014 Feb 21;289(8):4585-93 [24362021]
J Biol Chem. 2014 Feb 21;289(8):4555-61 [24362027]
J Biol Chem. 2014 Feb 21;289(8):4578-84 [24362040]
J Biol Chem. 2014 Feb 21;289(8):4562-70 [24362033]
J Biol Chem. 2014 Feb 21;289(8):4571-7 [24362036]
J Biol Chem. 2014 Feb 21;289(8):4594-9 [24362028]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1074/jbc.R113.543652
ER -
TY - JOUR
T1 - International Myeloma Working Group consensus statement for the management, treatment, and supportive care of patients with myeloma not eligible for standard autologous stem-cell transplantation.
AN - 1499148888; 24419113
AB - To provide an update on recent advances in the management of patients with multiple myeloma who are not eligible for autologous stem-cell transplantation.
A comprehensive review of the literature on diagnostic criteria is provided, and treatment options and management of adverse events are summarized. Patients with symptomatic disease and organ damage (ie, hypercalcemia, renal failure, anemia, or bone lesions) require immediate treatment. The International Staging System and chromosomal abnormalities identify high- and standard-risk patients. Proteasome inhibitors, immunomodulatory drugs, corticosteroids, and alkylating agents are the most active agents. The presence of concomitant diseases, frailty, or disability should be assessed and, if present, treated with reduced-dose approaches. Bone disease, renal damage, hematologic toxicities, infections, thromboembolism, and peripheral neuropathy are the most frequent disabling events requiring prompt and active supportive care.
These recommendations will help clinicians ensure the most appropriate care for patients with myeloma in everyday clinical practice.
JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology
AU - Palumbo, Antonio
AU - Rajkumar, S Vincent
AU - San Miguel, Jesus F
AU - Larocca, Alessandra
AU - Niesvizky, Ruben
AU - Morgan, Gareth
AU - Landgren, Ola
AU - Hajek, Roman
AU - Einsele, Hermann
AU - Anderson, Kenneth C
AU - Dimopoulos, Meletios A
AU - Richardson, Paul G
AU - Cavo, Michele
AU - Spencer, Andrew
AU - Stewart, A Keith
AU - Shimizu, Kazuyuki
AU - Lonial, Sagar
AU - Sonneveld, Pieter
AU - Durie, Brian G M
AU - Moreau, Philippe
AU - Orlowski, Robert Z
AD - Antonio Palumbo and Alessandra Larocca, University of Torino, Torino; Michele Cavo, Seràgnoli Institute of Hematology, Bologna University School of Medicine, Bologna, Italy; S. Vincent Rajkumar, Mayo Clinic, Rochester, MN; Jesus F. San Miguel, University Hospital of Salamanca, Salamanca, Spain; Ruben Niesvizky, Weill Cornell Medical College, New York, NY; Gareth Morgan, Royal Marsden Hospital, London, United Kingdom; Ola Landgren, National Cancer Institute, Bethesda, MD; Roman Hajek, University of Ostrava School of Medicine and University Hospital Ostrava, Ostrava, Czech Republic; Hermann Einsele, University of Wurzburg, Wurzburg, Germany; Kenneth C. Anderson and Paul G. Richardson, Dana-Farber Cancer Institute, Boston, MA; Meletios A. Dimopoulos, University of Athens School of Medicine, Athens, Greece; Andrew Spencer, Alfred Hospital, Melbourne, Victoria, Australia; A. Keith Stewart, Mayo Clinic, Scottsdale, AZ; Kazuyuki Shimizu, Aichi Gakuin Hospital, Nagoya, Japan; Sagar Lonial, Emory University, Atlanta, GA; Pieter Sonneveld, Erasmus Medical Centre, Rotterdam, the Netherlands; Brian G.M. Durie, Cedars-Sinai Comprehensive Cancer Center, Los Angeles, CA; Philippe Moreau, University Hospital, Nantes, France; and Robert Z. Orlowski, MD Anderson Cancer Center, Houston, TX.
Y1 - 2014/02/20/
PY - 2014
DA - 2014 Feb 20
SP - 587
EP - 600
VL - 32
IS - 6
KW - Index Medicus
KW - Humans
KW - Prognosis
KW - Hematopoietic Stem Cell Transplantation
KW - Palliative Care
KW - Multiple Myeloma -- diagnosis
KW - Multiple Myeloma -- therapy
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1499148888?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.atitle=International+Myeloma+Working+Group+consensus+statement+for+the+management%2C+treatment%2C+and+supportive+care+of+patients+with+myeloma+not+eligible+for+standard+autologous+stem-cell+transplantation.&rft.au=Palumbo%2C+Antonio%3BRajkumar%2C+S+Vincent%3BSan+Miguel%2C+Jesus+F%3BLarocca%2C+Alessandra%3BNiesvizky%2C+Ruben%3BMorgan%2C+Gareth%3BLandgren%2C+Ola%3BHajek%2C+Roman%3BEinsele%2C+Hermann%3BAnderson%2C+Kenneth+C%3BDimopoulos%2C+Meletios+A%3BRichardson%2C+Paul+G%3BCavo%2C+Michele%3BSpencer%2C+Andrew%3BStewart%2C+A+Keith%3BShimizu%2C+Kazuyuki%3BLonial%2C+Sagar%3BSonneveld%2C+Pieter%3BDurie%2C+Brian+G+M%3BMoreau%2C+Philippe%3BOrlowski%2C+Robert+Z&rft.aulast=Palumbo&rft.aufirst=Antonio&rft.date=2014-02-20&rft.volume=32&rft.issue=6&rft.spage=587&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.issn=1527-7755&rft_id=info:doi/10.1200%2FJCO.2013.48.7934
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-04-14
N1 - Date created - 2014-02-17
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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Blood. 2012 Jan 5;119(1):7-15 [22021371]
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Leukemia. 2012 Jan;26(1):73-85 [22024721]
Blood. 2012 Jan 26;119(4):933-9; quiz 1093 [21835953]
Chest. 2012 Feb;141(2 Suppl):e419S-94S [22315268]
Clin Lymphoma Myeloma Leuk. 2012 Feb;12(1):5-11 [22178143]
Blood. 2012 Mar 29;119(13):3003-15 [22271445]
Leukemia. 2012 Apr;26(4):595-608 [22193964]
N Engl J Med. 2012 May 10;366(19):1759-69 [22571200]
Leuk Lymphoma. 2012 Jul;53(7):1318-20 [22211836]
Haematologica. 2012 Aug;97(8):1272-7 [22371180]
Blood. 2012 Sep 27;120(13):2581-8 [22889759]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1200/JCO.2013.48.7934
ER -
TY - JOUR
T1 - Nomogram to predict cycle-one serious drug-related toxicity in phase I oncology trials.
AN - 1499146793; 24419130
AB - All patients in phase I trials do not have equivalent susceptibility to serious drug-related toxicity (SDRT). Our goal was to develop a nomogram to predict the risk of cycle-one SDRT to better select appropriate patients for phase I trials.
The prospectively maintained database of patients with solid tumor enrolled onto Cancer Therapeutics Evaluation Program-sponsored phase I trials activated between 2000 and 2010 was used. SDRT was defined as a grade ≥ 4 hematologic or grade ≥ 3 nonhematologic toxicity attributed, at least possibly, to study drug(s). Logistic regression was used to test the association of candidate factors to cycle-one SDRT. A final model, or nomogram, was chosen based on both clinical and statistical significance and validated internally using a bootstrapping technique and externally in an independent data set. Data from 3,104 patients enrolled onto 127 trials were analyzed to build the nomogram. In a model with multiple covariates, Eastern Cooperative Oncology Group performance status, WBC count, creatinine clearance, albumin, AST, number of study drugs, biologic study drug (yes v no), and dose (relative to maximum administered) were significant predictors of cycle-one SDRT. All significant factors except dose were included in the final nomogram. The model was validated both internally (bootstrap-adjusted concordance index, 0.60) and externally (concordance index, 0.64).
This nomogram can be used to accurately predict a patient's risk for SDRT at the time of enrollment. Excluding patients at high risk for SDRT should improve the safety and efficiency of phase I trials.
JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology
AU - Hyman, David M
AU - Eaton, Anne A
AU - Gounder, Mrinal M
AU - Smith, Gary L
AU - Pamer, Erika G
AU - Hensley, Martee L
AU - Spriggs, David R
AU - Ivy, Percy
AU - Iasonos, Alexia
AD - David M. Hyman, Anne A. Eaton, Mrinal M. Gounder, Erika G. Pamer, Martee L. Hensley, David R. Spriggs, and Alexia Iasonos, Memorial Sloan-Kettering Cancer Center; David M. Hyman, Mrinal M. Gounder, Martee L. Hensley, David R. Spriggs, and Alexia Iasonos, Weill Cornell Medical College, New York, NY; and Gary L. Smith and Percy Ivy, National Cancer Institute, Bethesda, MD.
Y1 - 2014/02/20/
PY - 2014
DA - 2014 Feb 20
SP - 519
EP - 526
VL - 32
IS - 6
KW - Antineoplastic Agents
KW - 0
KW - Index Medicus
KW - Young Adult
KW - Prospective Studies
KW - Aged, 80 and over
KW - Risk Factors
KW - Humans
KW - Cohort Studies
KW - Adult
KW - Treatment Outcome
KW - Prognosis
KW - Databases, Factual
KW - Aged
KW - Middle Aged
KW - Adolescent
KW - Clinical Trials, Phase I as Topic -- methods
KW - Clinical Trials, Phase I as Topic -- statistics & numerical data
KW - Antineoplastic Agents -- administration & dosage
KW - Nomograms
KW - Antineoplastic Agents -- adverse effects
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.atitle=Nomogram+to+predict+cycle-one+serious+drug-related+toxicity+in+phase+I+oncology+trials.&rft.au=Hyman%2C+David+M%3BEaton%2C+Anne+A%3BGounder%2C+Mrinal+M%3BSmith%2C+Gary+L%3BPamer%2C+Erika+G%3BHensley%2C+Martee+L%3BSpriggs%2C+David+R%3BIvy%2C+Percy%3BIasonos%2C+Alexia&rft.aulast=Hyman&rft.aufirst=David&rft.date=2014-02-20&rft.volume=32&rft.issue=6&rft.spage=519&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.issn=1527-7755&rft_id=info:doi/10.1200%2FJCO.2013.49.8808
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-04-14
N1 - Date created - 2014-02-17
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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Cancer. 2012 Mar 1;118(5):1422-8 [21823111]
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Comment In:
J Clin Oncol. 2014 Oct 1;32(28):3200 [25071106]
J Clin Oncol. 2014 Feb 20;32(6):489-90 [24419111]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1200/JCO.2013.49.8808
ER -
TY - JOUR
T1 - Microbial release from seeded beach sediments during wave conditions
AN - 1656033858; 2015-012657
AB - Beach sands can sustain indigenous and introduced populations of enterococci. The objective of this study was to evaluate wave action in promoting the release of introduced bacteria. To accomplish this objective this study developed a method to assess attachment and identified conditions under which introduced bacteria are integrated into the sand. A new "shearing assay" showed that attachment of the introduced spike mimicked that of the natural sand when the spike was allowed to integrate into the sand for 24 h at room temperature at a sand moisture content of 20%. Experiments in a wave flume showed that waves were capable of releasing about 60% of the total bacteria added. This suggests that for the range of wave conditions evaluated (height: 1.9-10.5 cm, period:1-2.7 s), waves were incapable of releasing all of the bacteria. Further study is needed to evaluate bacteria attachment mechanisms. Abstract Copyright (2014) Elsevier, B.V.
JF - Marine Pollution Bulletin
AU - Phillips, Matthew C
AU - Feng, Zhixuan
AU - Vogel, Laura J
AU - Reniers, Ad J H M
AU - Haus, Brian K
AU - Enns, Amber A
AU - Zhang, Yifan
AU - Hernandez, David B
AU - Solo-Gabriele, Helena M
Y1 - 2014/02/15/
PY - 2014
DA - 2014 Feb 15
SP - 114
EP - 122
PB - Elsevier, Oxford
VL - 79
IS - 1-2
SN - 0025-326X, 0025-326X
KW - sand
KW - experimental studies
KW - clastic sediments
KW - waves
KW - statistical analysis
KW - dye tracers
KW - pollution
KW - flume studies
KW - laboratory studies
KW - beaches
KW - Enterococcus
KW - bacteria
KW - sediments
KW - pore water
KW - microorganisms
KW - 22:Environmental geology
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1656033858?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ageorefmodule&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Marine+Pollution+Bulletin&rft.atitle=Microbial+release+from+seeded+beach+sediments+during+wave+conditions&rft.au=Phillips%2C+Matthew+C%3BFeng%2C+Zhixuan%3BVogel%2C+Laura+J%3BReniers%2C+Ad+J+H+M%3BHaus%2C+Brian+K%3BEnns%2C+Amber+A%3BZhang%2C+Yifan%3BHernandez%2C+David+B%3BSolo-Gabriele%2C+Helena+M&rft.aulast=Phillips&rft.aufirst=Matthew&rft.date=2014-02-15&rft.volume=79&rft.issue=1-2&rft.spage=114&rft.isbn=&rft.btitle=&rft.title=Marine+Pollution+Bulletin&rft.issn=0025326X&rft_id=info:doi/10.1016%2Fj.marpolbul.2013.12.029
L2 - http://www.sciencedirect.com/science/journal/0025326X
LA - English
DB - GeoRef
N1 - Copyright - GeoRef, Copyright 2015, American Geosciences Institute. Reference includes data from CAPCAS, Elsevier Scientific Publishers, Amsterdam, Netherlands
N1 - Date revised - 2015-01-01
N1 - Number of references - 58
N1 - Document feature - illus.
N1 - Last updated - 2015-02-19
N1 - CODEN - MPNBAZ
N1 - SubjectsTermNotLitGenreText - bacteria; beaches; clastic sediments; dye tracers; Enterococcus; experimental studies; flume studies; laboratory studies; microorganisms; pollution; pore water; sand; sediments; statistical analysis; waves
DO - http://dx.doi.org/10.1016/j.marpolbul.2013.12.029
ER -
TY - JOUR
T1 - HTS navigator: freely accessible cheminformatics software for analyzing high-throughput screening data
AN - 1534819235; 19360551
AB - Summary: We report on the development of the high-throughput screening (HTS) Navigator software to analyze and visualize the results of HTS of chemical libraries. The HTS Navigator processes output files from different plate readers' formats, computes the overall HTS matrix, automatically detects hits and has different types of baseline navigation and correction features. The software incorporates advanced cheminformatics capabilities such as chemical structure storage and visualization, fast similarity search and chemical neighborhood analysis for retrieved hits. The software is freely available for academic laboratories.
JF - Bioinformatics
AU - Fourches, Denis
AU - Sassano, Maria F
AU - Roth, Bryan L
AU - Tropsha, Alexander
AD - super(1)Division of Chemical Biology and Medicinal Chemistry, UNC Eshelman School of Pharmacy, University of North Carolina at Chapel Hill and super(2)Department of Pharmacology and the NIMH Psychoactive Drug Screening Program, School of Medicine, University of North Carolina Chapel Hill School of Medicine, Chapel Hill, NC 27599, USA
Y1 - 2014/02/15/
PY - 2014
DA - 2014 Feb 15
SP - 588
EP - 589
PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL - 30
IS - 4
SN - 1367-4803, 1367-4803
KW - Biochemistry Abstracts 2: Nucleic Acids; Biotechnology and Bioengineering Abstracts
KW - Computer programs
KW - software
KW - Data processing
KW - Informatics
KW - high-throughput screening
KW - Bioinformatics
KW - Internet
KW - N 14810:Methods
KW - W 30960:Bioinformatics & Computer Applications
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Bioinformatics&rft.atitle=HTS+navigator%3A+freely+accessible+cheminformatics+software+for+analyzing+high-throughput+screening+data&rft.au=Fourches%2C+Denis%3BSassano%2C+Maria+F%3BRoth%2C+Bryan+L%3BTropsha%2C+Alexander&rft.aulast=Fourches&rft.aufirst=Denis&rft.date=2014-02-15&rft.volume=30&rft.issue=4&rft.spage=588&rft.isbn=&rft.btitle=&rft.title=Bioinformatics&rft.issn=13674803&rft_id=info:doi/10.1093%2Fbioinformatics%2Fbtt718
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-06-01
N1 - Last updated - 2016-05-13
N1 - SubjectsTermNotLitGenreText - Computer programs; software; Data processing; Informatics; high-throughput screening; Bioinformatics; Internet
DO - http://dx.doi.org/10.1093/bioinformatics/btt718
ER -
TY - JOUR
T1 - EGFRvIII mCAR-modified T-cell therapy cures mice with established intracerebral glioma and generates host immunity against tumor-antigen loss.
AN - 1500701886; 24352643
AB - Chimeric antigen receptor (CAR) transduced T cells represent a promising immune therapy that has been shown to successfully treat cancers in mice and humans. However, CARs targeting antigens expressed in both tumors and normal tissues have led to significant toxicity. Preclinical studies have been limited by the use of xenograft models that do not adequately recapitulate the immune system of a clinically relevant host. A constitutively activated mutant of the naturally occurring epidermal growth factor receptor (EGFRvIII) is antigenically identical in both human and mouse glioma, but is also completely absent from any normal tissues.
We developed a third-generation, EGFRvIII-specific murine CAR (mCAR), and performed tests to determine its efficacy in a fully immunocompetent mouse model of malignant glioma. At elevated doses, infusion with EGFRvIII mCAR T cells led to cures in all mice with brain tumors. In addition, antitumor efficacy was found to be dependent on lymphodepletive host conditioning. Selective blockade with EGFRvIII soluble peptide significantly abrogated the activity of EGFRvIII mCAR T cells in vitro and in vivo, and may offer a novel strategy to enhance the safety profile for CAR-based therapy. Finally, mCAR-treated, cured mice were resistant to rechallenge with EGFRvIII(NEG) tumors, suggesting generation of host immunity against additional tumor antigens.
All together, these data support that third-generation, EGFRvIII-specific mCARs are effective against gliomas in the brain and highlight the importance of syngeneic, immunocompetent models in the preclinical evaluation of tumor immunotherapies. ©2013 AACR
JF - Clinical cancer research : an official journal of the American Association for Cancer Research
AU - Sampson, John H
AU - Choi, Bryan D
AU - Sanchez-Perez, Luis
AU - Suryadevara, Carter M
AU - Snyder, David J
AU - Flores, Catherine T
AU - Schmittling, Robert J
AU - Nair, Smita K
AU - Reap, Elizabeth A
AU - Norberg, Pamela K
AU - Herndon, James E
AU - Kuan, Chien-Tsun
AU - Morgan, Richard A
AU - Rosenberg, Steven A
AU - Johnson, Laura A
AD - Authors' Affiliations: Duke Brain Tumor Immunotherapy Program, Division of Neurosurgery, Department of Surgery; Department of Pathology; The Preston Robert Tisch Brain Tumor Center at Duke, Duke University Medical Center; Department of Biostatistics and Bioinformatics, Duke University, Durham, North Carolina; and Surgery Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland.
Y1 - 2014/02/15/
PY - 2014
DA - 2014 Feb 15
SP - 972
EP - 984
VL - 20
IS - 4
SN - 1078-0432, 1078-0432
KW - Receptors, Antigen, T-Cell
KW - 0
KW - Single-Chain Antibodies
KW - epidermal growth factor receptor VIII
KW - Receptor, Epidermal Growth Factor
KW - EC 2.7.10.1
KW - Index Medicus
KW - Neoplasm Transplantation
KW - Animals
KW - T-Lymphocytes -- transplantation
KW - Humans
KW - Mice
KW - Cell Line, Tumor
KW - T-Lymphocytes -- immunology
KW - Single-Chain Antibodies -- metabolism
KW - Brain Neoplasms -- therapy
KW - Receptor, Epidermal Growth Factor -- metabolism
KW - Adoptive Transfer
KW - Brain Neoplasms -- immunology
KW - Receptors, Antigen, T-Cell -- metabolism
KW - Receptor, Epidermal Growth Factor -- immunology
KW - Brain Neoplasms -- metabolism
KW - Astrocytoma -- metabolism
KW - Astrocytoma -- immunology
KW - Astrocytoma -- therapy
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1500701886?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+cancer+research+%3A+an+official+journal+of+the+American+Association+for+Cancer+Research&rft.atitle=EGFRvIII+mCAR-modified+T-cell+therapy+cures+mice+with+established+intracerebral+glioma+and+generates+host+immunity+against+tumor-antigen+loss.&rft.au=Sampson%2C+John+H%3BChoi%2C+Bryan+D%3BSanchez-Perez%2C+Luis%3BSuryadevara%2C+Carter+M%3BSnyder%2C+David+J%3BFlores%2C+Catherine+T%3BSchmittling%2C+Robert+J%3BNair%2C+Smita+K%3BReap%2C+Elizabeth+A%3BNorberg%2C+Pamela+K%3BHerndon%2C+James+E%3BKuan%2C+Chien-Tsun%3BMorgan%2C+Richard+A%3BRosenberg%2C+Steven+A%3BJohnson%2C+Laura+A&rft.aulast=Sampson&rft.aufirst=John&rft.date=2014-02-15&rft.volume=20&rft.issue=4&rft.spage=972&rft.isbn=&rft.btitle=&rft.title=Clinical+cancer+research+%3A+an+official+journal+of+the+American+Association+for+Cancer+Research&rft.issn=10780432&rft_id=info:doi/10.1158%2F1078-0432.CCR-13-0709
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-10-14
N1 - Date created - 2014-02-18
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
J Neuroimmunol. 2000 Feb 1;103(1):16-25 [10674985]
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Cancer. 1996 Apr 15;77(8):1551-5 [8608542]
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Blood. 2010 Nov 11;116(19):3875-86 [20631379]
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Blood. 2010 Nov 18;116(20):4099-102 [20668228]
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J Clin Oncol. 2011 Mar 1;29(7):917-24 [21282551]
Mol Ther. 2011 Mar;19(3):620-6 [21157437]
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Blood. 2012 Mar 22;119(12):2709-20 [22160384]
Mol Ther. 2012 May;20(5):882-4 [22549804]
Hum Gene Ther. 2012 Oct;23(10):1043-53 [22780919]
Clin Vaccine Immunol. 2013 Mar;20(3):319-27 [23283640]
N Engl J Med. 2013 Apr 18;368(16):1509-18 [23527958]
Oncogene. 2013 May 23;32(21):2670-81 [22797070]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1158/1078-0432.CCR-13-0709
ER -
TY - JOUR
T1 - (R,R')-4'-methoxy-1-naphthylfenoterol targets GPR55-mediated ligand internalization and impairs cancer cell motility.
AN - 1494310629; 24355564
AB - (R,R')-4'-Methoxy-1-naphthylfenoterol (MNF) promotes growth inhibition and apoptosis of human HepG2 hepatocarcinoma cells via cannabinoid receptor (CBR) activation. The synthetic CB1R inverse agonist, AM251, has been shown to block the anti-mitogenic effect of MNF in these cells; however, AM251 is also an agonist of the recently deorphanized, lipid-sensing receptor, GPR55, whose upregulation contributes to carcinogenesis. Here, we investigated the role of MNF in GPR55 signaling in human HepG2 and PANC-1 cancer cell lines in culture by focusing first on internalization of the fluorescent ligand Tocrifluor 1117 (T1117). Initial results indicated that cell pretreatment with GPR55 agonists, including the atypical cannabinoid O-1602 and l-α-lysophosphatidylinositol, dose-dependently reduced the rate of cellular T1117 uptake, a process that was sensitive to MNF inhibition. GPR55 internalization and signaling mediated by O-1602 was blocked by MNF in GPR55-expressing HEK293 cells. Pretreatment of HepG2 and PANC-1 cells with MNF significantly abrogated the induction of ERK1/2 phosphorylation in response to AM251 and O-1602. Moreover, MNF exerted a coordinated negative regulation of AM251 and O-1602 inducible processes, including changes in cellular morphology and cell migration using scratch wound healing assay. This study shows for the first time that MNF impairs GPR55-mediated signaling and, therefore, may have therapeutic potential in the management of cancer.
Published by Elsevier Inc.
JF - Biochemical pharmacology
AU - Paul, Rajib K
AU - Wnorowski, Artur
AU - Gonzalez-Mariscal, Isabel
AU - Nayak, Surendra K
AU - Pajak, Karolina
AU - Moaddel, Ruin
AU - Indig, Fred E
AU - Bernier, Michel
AU - Wainer, Irving W
AD - Laboratory of Clinical Investigation, National Institute on Aging, National Institutes of Health (NIH), Baltimore, MD 21224, USA. Electronic address: paulrk@mail.nih.gov. ; Laboratory of Medicinal Chemistry and Neuroengineering, Department of Chemistry, Medical University of Lublin, 20-093 Lublin, Poland. Electronic address: artur.wnorowski@gmail.com. ; Laboratory of Clinical Investigation, National Institute on Aging, National Institutes of Health (NIH), Baltimore, MD 21224, USA. Electronic address: isabel.gonzalezmariscal@nih.gov. ; SRI International (S.K.N.), Harrisonburg, VA 22802, USA. Electronic address: surendra.nayak@sri.com. ; Laboratory of Medicinal Chemistry and Neuroengineering, Department of Chemistry, Medical University of Lublin, 20-093 Lublin, Poland. Electronic address: karolina.pajak@umlub.pl. ; Laboratory of Clinical Investigation, National Institute on Aging, National Institutes of Health (NIH), Baltimore, MD 21224, USA. Electronic address: moaddelru@grc.nia.nih.gov. ; Laboratory of Clinical Investigation, National Institute on Aging, National Institutes of Health (NIH), Baltimore, MD 21224, USA. Electronic address: indigfr@grc.nia.nih.gov. ; Laboratory of Clinical Investigation, National Institute on Aging, National Institutes of Health (NIH), Baltimore, MD 21224, USA. Electronic address: bernierm@mail.nih.gov. ; Laboratory of Clinical Investigation, National Institute on Aging, National Institutes of Health (NIH), Baltimore, MD 21224, USA. Electronic address: wainerir@grc.nia.nih.gov.
Y1 - 2014/02/15/
PY - 2014
DA - 2014 Feb 15
SP - 547
EP - 561
VL - 87
IS - 4
KW - GPR55 protein, human
KW - 0
KW - Ligands
KW - Piperidines
KW - Pyrazoles
KW - Receptor, Cannabinoid, CB1
KW - Receptors, G-Protein-Coupled
KW - Fenoterol
KW - 22M9P70OQ9
KW - AM 251
KW - 3I4FA44MAI
KW - Index Medicus
KW - Ligand internalization
KW - GPR55
KW - G-protein coupled receptor
KW - Cellular morphology
KW - Cell motility
KW - Pyrazoles -- metabolism
KW - Pyrazoles -- administration & dosage
KW - Receptor, Cannabinoid, CB1 -- agonists
KW - Pyrazoles -- chemistry
KW - Receptor, Cannabinoid, CB1 -- physiology
KW - Piperidines -- chemistry
KW - Hep G2 Cells
KW - Humans
KW - HEK293 Cells
KW - Piperidines -- administration & dosage
KW - Piperidines -- metabolism
KW - Drug Inverse Agonism
KW - Neoplasms -- drug therapy
KW - Receptors, G-Protein-Coupled -- antagonists & inhibitors
KW - Neoplasms -- pathology
KW - Fenoterol -- administration & dosage
KW - Cell Movement -- physiology
KW - Receptors, G-Protein-Coupled -- metabolism
KW - Fenoterol -- analogs & derivatives
KW - Endocytosis -- drug effects
KW - Cell Movement -- drug effects
KW - Molecular Targeted Therapy -- methods
KW - Endocytosis -- physiology
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1494310629?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+pharmacology&rft.atitle=%28R%2CR%27%29-4%27-methoxy-1-naphthylfenoterol+targets+GPR55-mediated+ligand+internalization+and+impairs+cancer+cell+motility.&rft.au=Paul%2C+Rajib+K%3BWnorowski%2C+Artur%3BGonzalez-Mariscal%2C+Isabel%3BNayak%2C+Surendra+K%3BPajak%2C+Karolina%3BMoaddel%2C+Ruin%3BIndig%2C+Fred+E%3BBernier%2C+Michel%3BWainer%2C+Irving+W&rft.aulast=Paul&rft.aufirst=Rajib&rft.date=2014-02-15&rft.volume=87&rft.issue=4&rft.spage=547&rft.isbn=&rft.btitle=&rft.title=Biochemical+pharmacology&rft.issn=1873-2968&rft_id=info:doi/10.1016%2Fj.bcp.2013.11.020
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-03-27
N1 - Date created - 2014-02-03
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Br J Pharmacol. 2010 Feb;159(4):787-96 [20136833]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.bcp.2013.11.020
ER -
TY - JOUR
T1 - Case-case comparison of smoking and alcohol risk associations with Epstein-Barr virus-positive gastric cancer.
AN - 1466374975; 23904115
AB - Helicobacter pylori is the primary cause of gastric cancer. However, monoclonal Epstein-Barr virus (EBV) nucleic acid is also present in up to 10% of these tumors worldwide. EBV prevalence is increased with male sex, nonantral localization and surgically disrupted anatomy. To further examine associations between EBV and gastric cancer, we organized an international consortium of 11 studies with tumor EBV status assessed by in situ hybridization. We pooled individual-level data on 2,648 gastric cancer patients, including 184 (7%) with EBV-positive cancers; all studies had information on cigarette use (64% smokers) and nine had data on alcohol (57% drinkers). We compared patients with EBV-positive and EBV-negative tumors to evaluate smoking and alcohol interactions with EBV status. To account for within-population clustering, multilevel logistic regression models were used to estimate interaction odds ratios (OR) adjusted for distributions of sex (72% male), age (mean 59 years), tumor histology (56% Lauren intestinal-type), anatomic subsite (61% noncardia) and year of diagnosis (1983-2012). In unadjusted analyses, the OR of EBV positivity with smoking was 2.2 [95% confidence interval (CI) 1.6-3.2]. The OR was attenuated to 1.5 (95% CI 1.01-2.3) by adjustment for the possible confounders. There was no significant interaction of EBV status with alcohol drinking (crude OR 1.4; adjusted OR 1.0). Our data indicate the smoking association with gastric cancer is stronger for EBV-positive than EBV-negative tumors. Conversely, the null association with alcohol does not vary by EBV status. Distinct epidemiologic characteristics of EBV-positive cancer further implicate the virus as a cofactor in gastric carcinogenesis. © 2013 UICC.
JF - International journal of cancer
AU - Camargo, M Constanza
AU - Koriyama, Chihaya
AU - Matsuo, Keitaro
AU - Kim, Woo-Ho
AU - Herrera-Goepfert, Roberto
AU - Liao, Linda M
AU - Eurgast-EPIC Group
AU - Yu, Jun
AU - Carrasquilla, Gabriel
AU - Sung, Joseph J Y
AU - Alvarado-Cabrero, Isabel
AU - Lissowska, Jolanta
AU - Meneses-Gonzalez, Fernando
AU - Yatabe, Yashushi
AU - Ding, Ti
AU - Hu, Nan
AU - Taylor, Philip R
AU - Morgan, Douglas R
AU - Gulley, Margaret L
AU - Torres, Javier
AU - Akiba, Suminori
AU - Rabkin, Charles S
AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, USA. ; Eurgast-EPIC Group
Y1 - 2014/02/15/
PY - 2014
DA - 2014 Feb 15
SP - 948
EP - 953
VL - 134
IS - 4
KW - Index Medicus
KW - gastric cancer
KW - smoking
KW - alcohol
KW - EBV
KW - pooled-analysis
KW - Odds Ratio
KW - Neoplasm Staging
KW - Humans
KW - Prognosis
KW - Aged
KW - Aged, 80 and over
KW - Risk Factors
KW - Adult
KW - Case-Control Studies
KW - Follow-Up Studies
KW - Middle Aged
KW - Female
KW - Male
KW - Herpesvirus 4, Human -- pathogenicity
KW - Adenocarcinoma -- etiology
KW - Alcohol Drinking -- adverse effects
KW - Smoking -- adverse effects
KW - Epstein-Barr Virus Infections -- virology
KW - Stomach Neoplasms -- etiology
KW - Epstein-Barr Virus Infections -- complications
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-02-20
N1 - Date created - 2013-12-09
N1 - Date revised - 2017-01-13
N1 - SuppNotes - Cited By:
Br J Cancer. 2011 Jun 28;105(1):38-43 [21654677]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1002/ijc.28402
ER -
TY - JOUR
T1 - ROS and RNS induced apoptosis through p53 and iNOS mediated pathway by a dibasic hydroxamic acid molecule in leukemia cells.
AN - 1490773199; 24269727
AB - Anticancer drugs induce apoptosis to cancer cells and also exhibit undesired toxicity to normal cells. Therefore development of novel agents triggering apoptosis and have low toxicity towards normal cells is most important. Hydroxamic acids suppress tumour cell growth through apoptosis but the underlying mechanism is poorly understood. Herein, we describe the apoptotic potential of a dibasic hydroxamic acid derivative, viz., oxayl bis (N-phenyl) hydroxamic acid (OBPHA), which induces apoptosis through generation of both ROS and NO in doxorubicin resistant T-lymphoblastic leukemia, CEM/ADR5000 cells. Present study discloses that OBPHA selectively kills cancerous cells irrespective of their drug resistant phenotype. We also determined the crystal structure of OBPHA to understand the structural requirements for apoptosis; the study reveals that the presence of substituted hydroxamic acid groups (-CO-NH-OH) favours the generation of NO possibly through auto degeneration. Along with the induction of caspase 3 mediated intrinsic apoptosis; OBPHA also activates p53 dependent signalling cascade and downregulates HDAC3 expression in a time dependent manner possibly due to increased ROS and NO production and simultaneous decrease in cellular GSH level. Thus ROS and NO mediated downstream signalling are essential for the anticancer effect of OBPHA. Therefore OBPHA, having a structurally relevant pharmacophore provides important insight into the development of new ROS and RNS generating chemicals inducing p53 dependent apoptosis.
Copyright © 2013 Elsevier B.V. All rights reserved.
JF - European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences
AU - Banerjee, Kaushik
AU - Ganguly, Avishek
AU - Chakraborty, Paramita
AU - Sarkar, Avijit
AU - Singh, Suryabhan
AU - Chatterjee, Mitali
AU - Bhattacharya, Subrato
AU - Choudhuri, Soumitra Kumar
AD - Department of In Vitro Carcinogenesis and Cellular Chemotherapy, Chittaranjan National Cancer Institute, Kolkata, India. ; Department of Pharmacology, Institute of Post Graduate Medical Education and Research, Kolkata, India. ; Department of Chemistry, Banaras Hindu University, Varanasi, India. ; Department of In Vitro Carcinogenesis and Cellular Chemotherapy, Chittaranjan National Cancer Institute, Kolkata, India. Electronic address: soumitra01@yahoo.com.
Y1 - 2014/02/14/
PY - 2014
DA - 2014 Feb 14
SP - 146
EP - 164
VL - 52
KW - Antineoplastic Agents
KW - 0
KW - Benzeneacetamides
KW - Hydroxamic Acids
KW - Oxalates
KW - Reactive Nitrogen Species
KW - Reactive Oxygen Species
KW - Tumor Suppressor Protein p53
KW - oxalyl bis(N-phenyl)hydroxamic acid
KW - Nitric Oxide
KW - 31C4KY9ESH
KW - NOS2 protein, human
KW - EC 1.14.13.39
KW - Nitric Oxide Synthase Type II
KW - Caspase 3
KW - EC 3.4.22.-
KW - Glutathione
KW - GAN16C9B8O
KW - Index Medicus
KW - Reactive nitrogen species
KW - HDAC3
KW - p53
KW - Apoptosis
KW - Reactive oxygen species
KW - iNOS
KW - Glutathione -- metabolism
KW - Humans
KW - Nitric Oxide -- metabolism
KW - Cell Line, Tumor
KW - Leukemia -- drug therapy
KW - Leukocytes, Mononuclear -- physiology
KW - Membrane Potential, Mitochondrial -- drug effects
KW - Cell Survival -- drug effects
KW - Cells, Cultured
KW - Leukemia -- metabolism
KW - Apoptosis -- drug effects
KW - Nitric Oxide Synthase Type II -- metabolism
KW - Leukocytes, Mononuclear -- drug effects
KW - Caspase 3 -- metabolism
KW - Reactive Oxygen Species -- metabolism
KW - Benzeneacetamides -- pharmacology
KW - Oxalates -- pharmacology
KW - Reactive Nitrogen Species -- metabolism
KW - Tumor Suppressor Protein p53 -- metabolism
KW - Hydroxamic Acids -- pharmacology
KW - Antineoplastic Agents -- pharmacology
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-09-08
N1 - Date created - 2014-01-13
N1 - Date revised - 2017-01-13
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.ejps.2013.11.009
ER -
TY - CPAPER
T1 - Susceptibility to Lung Disease: Integrated Genetic and Genomic Approaches
T2 - 2014 Annual Meeting of the American Association for the Advancement of Science (AAAS 2014)
AN - 1510100048; 6280205
JF - 2014 Annual Meeting of the American Association for the Advancement of Science (AAAS 2014)
AU - Kleeberger, Steven
Y1 - 2014/02/13/
PY - 2014
DA - 2014 Feb 13
KW - Lung diseases
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510100048?accountid=14244
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L2 - https://aaas.confex.com/aaas/2014/webprogram/start.html
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-03-24
N1 - Last updated - 2014-03-26
ER -
TY - CPAPER
T1 - Convergence Technologies on the Horizon
T2 - 2014 Annual Meeting of the American Association for the Advancement of Science (AAAS 2014)
AN - 1510100046; 6279971
JF - 2014 Annual Meeting of the American Association for the Advancement of Science (AAAS 2014)
AU - Seto, Belinda
Y1 - 2014/02/13/
PY - 2014
DA - 2014 Feb 13
KW - Technology
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510100046?accountid=14244
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L2 - https://aaas.confex.com/aaas/2014/webprogram/start.html
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-03-24
N1 - Last updated - 2014-03-26
ER -
TY - CPAPER
T1 - Autoimmune Diseases: From Basic Mechanism to Clinical Therapeutics
T2 - 2014 Annual Meeting of the American Association for the Advancement of Science (AAAS 2014)
AN - 1510095593; 6280212
JF - 2014 Annual Meeting of the American Association for the Advancement of Science (AAAS 2014)
AU - Kaplan, Mariana
Y1 - 2014/02/13/
PY - 2014
DA - 2014 Feb 13
KW - Autoimmune diseases
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L2 - https://aaas.confex.com/aaas/2014/webprogram/start.html
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-03-24
N1 - Last updated - 2014-03-26
ER -
TY - CPAPER
T1 - Medical, Occupational, Engineering, and Safety Aspects in Biodefense Research
T2 - 2014 Annual Meeting of the American Association for the Advancement of Science (AAAS 2014)
AN - 1510095448; 6280153
JF - 2014 Annual Meeting of the American Association for the Advancement of Science (AAAS 2014)
AU - Takafuji, Ernest
Y1 - 2014/02/13/
PY - 2014
DA - 2014 Feb 13
KW - Safety engineering
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-03-24
N1 - Last updated - 2014-03-26
ER -
TY - CPAPER
T1 - Emergence of Protozoal Diseases Impacting Arctic Communities
T2 - 2014 Annual Meeting of the American Association for the Advancement of Science (AAAS 2014)
AN - 1510094989; 6279802
JF - 2014 Annual Meeting of the American Association for the Advancement of Science (AAAS 2014)
AU - Grigg, Mike
Y1 - 2014/02/13/
PY - 2014
DA - 2014 Feb 13
KW - Arctic
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-03-24
N1 - Last updated - 2014-03-26
ER -
TY - CPAPER
T1 - Understanding Gene-Environmental Interactions in the Etiology of Addictions
T2 - 2014 Annual Meeting of the American Association for the Advancement of Science (AAAS 2014)
AN - 1510091795; 6279757
JF - 2014 Annual Meeting of the American Association for the Advancement of Science (AAAS 2014)
AU - Compton, Wilson
Y1 - 2014/02/13/
PY - 2014
DA - 2014 Feb 13
KW - Etiology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Association+for+the+Advancement+of+Science+%28AAAS+2014%29&rft.atitle=Understanding+Gene-Environmental+Interactions+in+the+Etiology+of+Addictions&rft.au=Compton%2C+Wilson&rft.aulast=Compton&rft.aufirst=Wilson&rft.date=2014-02-13&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Association+for+the+Advancement+of+Science+%28AAAS+2014%29&rft.issn=&rft_id=info:doi/
L2 - https://aaas.confex.com/aaas/2014/webprogram/start.html
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-03-24
N1 - Last updated - 2014-03-26
ER -
TY - JOUR
T1 - Molecular control of δ-opioid receptor signalling.
AN - 1499147634; 24413399
AB - Opioids represent widely prescribed and abused medications, although their signal transduction mechanisms are not well understood. Here we present the 1.8 Å high-resolution crystal structure of the human δ-opioid receptor (δ-OR), revealing the presence and fundamental role of a sodium ion in mediating allosteric control of receptor functional selectivity and constitutive activity. The distinctive δ-OR sodium ion site architecture is centrally located in a polar interaction network in the seven-transmembrane bundle core, with the sodium ion stabilizing a reduced agonist affinity state, and thereby modulating signal transduction. Site-directed mutagenesis and functional studies reveal that changing the allosteric sodium site residue Asn 131 to an alanine or a valine augments constitutive β-arrestin-mediated signalling. Asp95Ala, Asn310Ala and Asn314Ala mutations transform classical δ-opioid antagonists such as naltrindole into potent β-arrestin-biased agonists. The data establish the molecular basis for allosteric sodium ion control in opioid signalling, revealing that sodium-coordinating residues act as 'efficacy switches' at a prototypic G-protein-coupled receptor.
JF - Nature
AU - Fenalti, Gustavo
AU - Giguere, Patrick M
AU - Katritch, Vsevolod
AU - Huang, Xi-Ping
AU - Thompson, Aaron A
AU - Cherezov, Vadim
AU - Roth, Bryan L
AU - Stevens, Raymond C
AD - 1] Department of Integrative Structural and Computational Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, California 92037, USA [2]. ; 1] National Institute of Mental Health Psychoactive Drug Screening Program and Department of Pharmacology and Division of Chemical Biology and Medicinal Chemistry, University of North Carolina Chapel Hill Medical School, Chapel Hill, North Carolina 27599, USA [2]. ; Department of Integrative Structural and Computational Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, California 92037, USA. ; National Institute of Mental Health Psychoactive Drug Screening Program and Department of Pharmacology and Division of Chemical Biology and Medicinal Chemistry, University of North Carolina Chapel Hill Medical School, Chapel Hill, North Carolina 27599, USA.
Y1 - 2014/02/13/
PY - 2014
DA - 2014 Feb 13
SP - 191
EP - 196
VL - 506
IS - 7487
KW - Arrestins
KW - 0
KW - Ligands
KW - Narcotic Antagonists
KW - Receptors, Opioid, delta
KW - beta-Arrestins
KW - Naltrexone
KW - 5S6W795CQM
KW - Asparagine
KW - 7006-34-0
KW - Sodium
KW - 9NEZ333N27
KW - naltrindole
KW - G167Z38QA4
KW - Index Medicus
KW - Allosteric Site -- genetics
KW - Allosteric Regulation -- drug effects
KW - Allosteric Site -- drug effects
KW - Models, Molecular
KW - Humans
KW - Naltrexone -- analogs & derivatives
KW - Asparagine -- metabolism
KW - Naltrexone -- chemistry
KW - Structure-Activity Relationship
KW - Sodium -- pharmacology
KW - Mutagenesis, Site-Directed
KW - Allosteric Regulation -- genetics
KW - Narcotic Antagonists -- chemistry
KW - Asparagine -- genetics
KW - Naltrexone -- pharmacology
KW - Naltrexone -- metabolism
KW - Narcotic Antagonists -- metabolism
KW - Crystallography, X-Ray
KW - Narcotic Antagonists -- pharmacology
KW - Arrestins -- metabolism
KW - Sodium -- metabolism
KW - Receptors, Opioid, delta -- chemistry
KW - Receptors, Opioid, delta -- antagonists & inhibitors
KW - Signal Transduction -- drug effects
KW - Receptors, Opioid, delta -- metabolism
KW - Receptors, Opioid, delta -- agonists
KW - Receptors, Opioid, delta -- genetics
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-02-19
N1 - Date created - 2014-02-13
N1 - Date revised - 2017-01-14
N1 - Genetic sequence - 4N6H; PDB
N1 - SuppNotes - Cited By:
Br J Pharmacol. 2000 Jul;130(5):987-96 [10882382]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1038/nature12944
ER -
TY - JOUR
T1 - DLC1 induces expression of E-cadherin in prostate cancer cells through Rho pathway and suppresses invasion.
AN - 1499131728; 23376848
AB - E-cadherin is a cell-cell adhesion molecule that acts as a suppressor of cancer cell invasion and its expression is downregulated in many advanced, poorly differentiated, human cancers. In this study, we found that the expression of DLC1 (deleted in liver cancer 1) tumor-suppressor gene in metastatic prostate carcinoma (PCA) cells increased the expression of E-cadherin and resulted in an elevated rate of cell-cell aggregation as measured by aggregation assay. DLC1-mediated increase in E-cadherin expression was not dependent on α-catenin, a DLC1-binding protein associated with E-cadherin, and/or cellular density. The increase of E-cadherin expression occurred at mRNA level and relied on DLC1 RhoGAP function, leading to suppression of high level of RhoA-GTP and RhoC-GTP activity in metastatic PCA cells. Application of Rho/ROCK inhibitors produced the same effect as introduction of DLC1. Knocking down of RhoA produced a moderate increase in E-cadherin whereas knocking down of RhoC resulted in a significant increase of E-cadherin. Downregulation of E-cadherin caused by constitutively active RhoA(V14) and RhoC(V14) could not be reversed by expression of DLC1 in DLC1-negative cell line. DLC1-mediated suppression of metastatic PCA cells invasion was comparable with the one associated with ectopic E-cadherin expression, or caused by suppression of Rho pathway either by Rho/ROCK inhibitors, or by shRNA repression. This study demonstrates that DLC1 expression positively regulates E-cadherin and suppresses highly metastatic PCA cell invasion by modulating Rho pathway, which appears as a feasible therapeutic target in cancers with high activity of RhoGTPases.
JF - Oncogene
AU - Tripathi, V
AU - Popescu, N C
AU - Zimonjic, D B
AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Y1 - 2014/02/06/
PY - 2014
DA - 2014 Feb 06
SP - 724
EP - 733
VL - 33
IS - 6
KW - Cadherins
KW - 0
KW - DLC1 protein, human
KW - GTPase-Activating Proteins
KW - Tumor Suppressor Proteins
KW - rho GTPase-activating protein
KW - rho-Associated Kinases
KW - EC 2.7.11.1
KW - Index Medicus
KW - Neoplasm Invasiveness
KW - Gene Knockdown Techniques
KW - Cell Differentiation -- physiology
KW - Transfection
KW - Humans
KW - Cell Line, Tumor
KW - Cell Aggregation -- physiology
KW - Male
KW - Prostatic Neoplasms -- metabolism
KW - Prostatic Neoplasms -- pathology
KW - GTPase-Activating Proteins -- genetics
KW - rho-Associated Kinases -- metabolism
KW - GTPase-Activating Proteins -- metabolism
KW - Tumor Suppressor Proteins -- metabolism
KW - GTPase-Activating Proteins -- physiology
KW - Tumor Suppressor Proteins -- genetics
KW - Prostatic Neoplasms -- genetics
KW - rho-Associated Kinases -- genetics
KW - Cadherins -- biosynthesis
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-06-26
N1 - Date created - 2014-02-06
N1 - Date revised - 2017-01-13
N1 - Last updated - 2017-01-18
DO - http://dx.doi.org/10.1038/onc.2013.7
ER -
TY - JOUR
T1 - Aprataxin resolves adenylated RNA-DNA junctions to maintain genome integrity.
AN - 1499121868; 24362567
AB - Faithful maintenance and propagation of eukaryotic genomes is ensured by three-step DNA ligation reactions used by ATP-dependent DNA ligases. Paradoxically, when DNA ligases encounter nicked DNA structures with abnormal DNA termini, DNA ligase catalytic activity can generate and/or exacerbate DNA damage through abortive ligation that produces chemically adducted, toxic 5'-adenylated (5'-AMP) DNA lesions. Aprataxin (APTX) reverses DNA adenylation but the context for deadenylation repair is unclear. Here we examine the importance of APTX to RNase-H2-dependent excision repair (RER) of a lesion that is very frequently introduced into DNA, a ribonucleotide. We show that ligases generate adenylated 5' ends containing a ribose characteristic of RNase H2 incision. APTX efficiently repairs adenylated RNA-DNA, and acting in an RNA-DNA damage response (RDDR), promotes cellular survival and prevents S-phase checkpoint activation in budding yeast undergoing RER. Structure-function studies of human APTX-RNA-DNA-AMP-Zn complexes define a mechanism for detecting and reversing adenylation at RNA-DNA junctions. This involves A-form RNA binding, proper protein folding and conformational changes, all of which are affected by heritable APTX mutations in ataxia with oculomotor apraxia 1. Together, these results indicate that accumulation of adenylated RNA-DNA may contribute to neurological disease.
JF - Nature
AU - Tumbale, Percy
AU - Williams, Jessica S
AU - Schellenberg, Matthew J
AU - Kunkel, Thomas A
AU - Williams, R Scott
AD - 1] Laboratory of Structural Biology, National Institute of Environmental Health Sciences, NIH, DHHS, Research Triangle Park, North Carolina 27709, USA [2]. ; 1] Laboratory of Structural Biology, National Institute of Environmental Health Sciences, NIH, DHHS, Research Triangle Park, North Carolina 27709, USA [2] Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, NIH, DHHS, Research Triangle Park, North Carolina 27709, USA [3]. ; 1] Laboratory of Structural Biology, National Institute of Environmental Health Sciences, NIH, DHHS, Research Triangle Park, North Carolina 27709, USA [2] Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, NIH, DHHS, Research Triangle Park, North Carolina 27709, USA. ; Laboratory of Structural Biology, National Institute of Environmental Health Sciences, NIH, DHHS, Research Triangle Park, North Carolina 27709, USA.
Y1 - 2014/02/06/
PY - 2014
DA - 2014 Feb 06
SP - 111
EP - 115
VL - 506
IS - 7486
KW - APTX protein, human
KW - 0
KW - DNA-Binding Proteins
KW - Nuclear Proteins
KW - Schizosaccharomyces pombe Proteins
KW - Adenosine Monophosphate
KW - 415SHH325A
KW - RNA
KW - 63231-63-0
KW - DNA
KW - 9007-49-2
KW - Exodeoxyribonucleases
KW - EC 3.1.-
KW - Hnt3 protein, S pombe
KW - ribonuclease HII
KW - EC 3.1.26.-
KW - Ribonuclease H
KW - EC 3.1.26.4
KW - Zinc
KW - J41CSQ7QDS
KW - Index Medicus
KW - Humans
KW - Exodeoxyribonucleases -- metabolism
KW - Apraxias -- genetics
KW - Nucleic Acid Conformation
KW - Ribonuclease H -- metabolism
KW - Cell Survival
KW - S Phase Cell Cycle Checkpoints
KW - Saccharomyces cerevisiae -- genetics
KW - Saccharomyces cerevisiae -- metabolism
KW - Protein Conformation
KW - DNA Repair
KW - Models, Molecular
KW - Schizosaccharomyces -- metabolism
KW - Zinc -- metabolism
KW - Structure-Activity Relationship
KW - Ataxia Telangiectasia -- genetics
KW - Adenosine Monophosphate -- metabolism
KW - Schizosaccharomyces pombe Proteins -- metabolism
KW - Hypoalbuminemia -- genetics
KW - Protein Folding
KW - Mutation -- genetics
KW - Cerebellar Ataxia -- congenital
KW - Schizosaccharomyces pombe Proteins -- chemistry
KW - Exodeoxyribonucleases -- chemistry
KW - Saccharomyces cerevisiae -- cytology
KW - Nuclear Proteins -- genetics
KW - DNA-Binding Proteins -- chemistry
KW - RNA -- metabolism
KW - DNA -- metabolism
KW - Genome, Human -- genetics
KW - DNA-Binding Proteins -- genetics
KW - DNA -- chemistry
KW - RNA -- chemistry
KW - Nuclear Proteins -- chemistry
KW - Nuclear Proteins -- metabolism
KW - DNA-Binding Proteins -- metabolism
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-02-18
N1 - Date created - 2014-02-06
N1 - Date revised - 2017-01-14
N1 - Genetic sequence - 4NDI; PDB; 4NDH; 4NDG; 4NDF
N1 - SuppNotes - Cited By:
DNA Repair (Amst). 2009 Jun 4;8(6):760-6 [19303373]
J Biol Chem. 2008 Dec 5;283(49):33994-4001 [18836178]
Acta Crystallogr D Biol Crystallogr. 2010 Feb;66(Pt 2):213-21 [20124702]
Proc Natl Acad Sci U S A. 2010 Mar 16;107(11):4949-54 [20194773]
Nucleic Acids Res. 2010 Apr;38(6):e85 [20008099]
Acta Crystallogr D Biol Crystallogr. 2010 Apr;66(Pt 4):486-501 [20383002]
DNA Repair (Amst). 2010 Jun 4;9(6):690-9 [20399152]
Biochemistry. 2010 Jul 27;49(29):6165-76 [20518483]
Nat Chem Biol. 2010 Oct;6(10):774-81 [20729855]
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Nat Struct Mol Biol. 2011 Nov;18(11):1189-95 [21984210]
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Cell. 2012 May 25;149(5):1008-22 [22579044]
Nature. 2012 Jul 12;487(7406):196-201 [22785315]
Mol Cell. 2012 Sep 28;47(6):980-6 [22864116]
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Cell. 2002 Nov 15;111(4):495-505 [12437923]
Cell. 2003 Feb 7;112(3):391-401 [12581528]
Neurology. 2003 Mar 11;60(5):868-70 [12629250]
Mol Cell Biol. 2003 Apr;23(7):2309-15 [12640116]
J Biol Chem. 1997 Sep 5;272(36):22591-9 [9278414]
Science. 1997 Oct 10;278(5336):286-90 [9323207]
Nature. 2004 Nov 25;432(7016):473-8 [15565146]
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J Biol Chem. 2007 Mar 30;282(13):9469-74 [17276982]
Annu Rev Biochem. 2008;77:313-38 [18518823]
Hum Mol Genet. 2009 Nov 1;18(21):4102-17 [19643912]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1038/nature12824
ER -
TY - CPAPER
T1 - Sustainable and Climate Resilient Healthcare Facilities: an update on federal efforts
T2 - 94th American Meteorological Society Annual Meeting (AMS 2014)
AN - 1518611807; 6282169
JF - 94th American Meteorological Society Annual Meeting (AMS 2014)
AU - Balbus, John
Y1 - 2014/02/02/
PY - 2014
DA - 2014 Feb 02
KW - Health care
KW - Climate
KW - Sustainable development
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=94th+American+Meteorological+Society+Annual+Meeting+%28AMS+2014%29&rft.atitle=Sustainable+and+Climate+Resilient+Healthcare+Facilities%3A+an+update+on+federal+efforts&rft.au=Balbus%2C+John&rft.aulast=Balbus&rft.aufirst=John&rft.date=2014-02-02&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=94th+American+Meteorological+Society+Annual+Meeting+%28AMS+2014%29&rft.issn=&rft_id=info:doi/
L2 - https://ams.confex.com/ams/94Annual/webprogram/meeting.html
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-23
N1 - Last updated - 2014-04-24
ER -
TY - JOUR
T1 - Building the Strategic National Stockpile Through the NIAID Radiation Nuclear Countermeasures Program
AN - 1842512251; 19002850
AB - The possibility of a public health radiological or nuclear emergency in the United States remains a concern. Media attention focused on lost radioactive sources and international nuclear threats, as well as the potential for accidents in nuclear power facilities (e.g., Windscale, Three Mile Island, Chernobyl, and Fukushima) highlight the need to address this critical national security issue. To date, no drugs have been licensed to mitigate/treat the acute and longaterm radiation injuries that would result in the event of largeascale, radiation, or nuclear public health emergency. However, recent evaluation of several candidate radiation medical countermeasures (MCMs) has provided initial proofaofaconcept of efficacy. The goal of the Radiation Nuclear Countermeasures Program (RNCP) of the National Institute of Allergy and Infectious Diseases (National Institutes of Health) is to help ensure the government stockpiling of safe and efficacious MCMs to treat radiation injuries, including, but not limited to, hematopoietic, gastrointestinal, pulmonary, cutaneous, renal, cardiovascular, and central nervous systems. In addition to supporting research in these areas, the RNCP continues to fund research and development of decorporation agents targeting internal radionuclide contamination, and biodosimetry platforms (e.g., biomarkers and devices) to assess the levels of an individual's radiation exposure, capabilities that would be critical in a mass casualty scenario. New areas of research within the program include a focus on special populations, especially pediatric and geriatric civilians, as well as combination studies, in which drugs are tested within the context of expected medical care management (e.g., antibiotics and growth factors). Moving forward, challenges facing the RNCP, as well as the entire radiation research field, include further advancement and qualification of animal models, dose conversion from animal models to humans, biomarker identification, and formulation development. This paper provides a review of recent work and collaborations supported by the RNCP.
JF - Drug Development Research
AU - Rios, Carmen I
AU - Cassatt, David R
AU - DiCarlo, Andrea L
AU - Macchiarini, Francesca
AU - Ramakrishnan, Narayani
AU - Norman, MaiaKim
AU - Maidment, Bert W
AD - Radiation Nuclear Countermeasures Program, Division of Allergy, Immunology and Transplantation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, 20892, USA.
Y1 - 2014/02//
PY - 2014
DA - February 2014
SP - 23
EP - 28
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 75
IS - 1
SN - 0272-4391, 0272-4391
KW - Toxicology Abstracts
KW - radiation
KW - nuclear
KW - medical countermeasures
KW - dosimetry
KW - animal models
KW - mitigators
KW - treatment
KW - Central nervous system
KW - Injuries
KW - Contamination
KW - Pediatrics
KW - Animal models
KW - Antibiotics
KW - Drug development
KW - biomarkers
KW - Public health
KW - Hypersensitivity
KW - Accidents
KW - Islands
KW - Infectious diseases
KW - Radiation
KW - Reviews
KW - Radioisotopes
KW - Kidney
KW - Geriatrics
KW - Drugs
KW - X 24390:Radioactive Materials
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1842512251?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Drug+Development+Research&rft.atitle=Building+the+Strategic+National+Stockpile+Through+the+NIAID+Radiation+Nuclear+Countermeasures+Program&rft.au=Rios%2C+Carmen+I%3BCassatt%2C+David+R%3BDiCarlo%2C+Andrea+L%3BMacchiarini%2C+Francesca%3BRamakrishnan%2C+Narayani%3BNorman%2C+MaiaKim%3BMaidment%2C+Bert+W&rft.aulast=Rios&rft.aufirst=Carmen&rft.date=2014-02-01&rft.volume=75&rft.issue=1&rft.spage=23&rft.isbn=&rft.btitle=&rft.title=Drug+Development+Research&rft.issn=02724391&rft_id=info:doi/10.1002%2Fddr.21163
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2016-11-01
N1 - Last updated - 2016-12-22
N1 - SubjectsTermNotLitGenreText - Central nervous system; Contamination; Injuries; Pediatrics; Animal models; Drug development; Antibiotics; biomarkers; Public health; Accidents; Hypersensitivity; Islands; Radiation; Infectious diseases; Reviews; Geriatrics; Kidney; Radioisotopes; Drugs
DO - http://dx.doi.org/10.1002/ddr.21163
ER -
TY - JOUR
T1 - Punishment insensitivity and impaired reinforcement learning in preschoolers
AN - 1748688877
AB - Background Youth and adults with psychopathic traits display disrupted reinforcement learning. Advances in measurement now enable examination of this association in preschoolers. The current study examines relations between reinforcement learning in preschoolers and parent ratings of reduced responsiveness to socialization, conceptualized as a developmental vulnerability to psychopathic traits. Methods One hundred and fifty-seven preschoolers (mean age 4.7 ± 0.8 years) participated in a substudy that was embedded within a larger project. Children completed the ‘Stars-in-Jars’ task, which involved learning to select rewarded jars and avoid punished jars. Maternal report of responsiveness to socialization was assessed with the Punishment Insensitivity and Low Concern for Others scales of the Multidimensional Assessment of Preschool Disruptive Behavior (MAP-DB). Results Punishment Insensitivity, but not Low Concern for Others, was significantly associated with reinforcement learning in multivariate models that accounted for age and sex. Specifically, higher Punishment Insensitivity was associated with significantly lower overall performance and more errors on punished trials (‘passive avoidance’). Conclusions Impairments in reinforcement learning manifest in preschoolers who are high in maternal ratings of Punishment Insensitivity. If replicated, these findings may help to pinpoint the neurodevelopmental antecedents of psychopathic tendencies and suggest novel intervention targets beginning in early childhood.
JF - Journal of Child Psychology and Psychiatry and Allied Disciplines
AU - Briggs-Gowan, Margaret J
AU - Nichols, Sara R
AU - Voss, Joel
AU - Zobel, Elvira
AU - Carter, Alice S
AU - McCarthy, Kimberly J
AU - Pine, Daniel S
AU - Blair, James
AU - Wakschlag, Lauren S
AD - Department of Psychiatry, University of Connecticut Health Center, Farmington, CT, USA. ; Department of Medical Social Sciences, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA. ; Department of Psychology, University of Massachusetts-Boston, Boston, MA, USA. ; The National Institute of Mental Health, Division of Intramural Research Programs, Rockville, MD, USA. ; Department of Psychiatry, University of Connecticut Health Center, Farmington, CT, USA.
Y1 - 2014/02//
PY - 2014
DA - Feb 2014
SP - 154
EP - 161
CY - Cambridge
PB - Blackwell Publishing Ltd.
VL - 55
IS - 2
SN - 0021-9630
KW - Psychology
KW - Assessment
KW - Vulnerability
KW - Young people
KW - Avoidance
KW - Childhood
KW - Children
KW - Disruptive behaviour
KW - Early intervention programmes
KW - Learning
KW - Measurement
KW - Passive avoidance
KW - Preschool children
KW - Psychopathy
KW - Punishment
KW - Reinforcement
KW - Responsiveness
KW - Socialization
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1748688877?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Child+Psychology+and+Psychiatry+and+Allied+Disciplines&rft.atitle=Punishment+insensitivity+and+impaired+reinforcement+learning+in+preschoolers&rft.au=Briggs-Gowan%2C+Margaret+J%3BNichols%2C+Sara+R%3BVoss%2C+Joel%3BZobel%2C+Elvira%3BCarter%2C+Alice+S%3BMcCarthy%2C+Kimberly+J%3BPine%2C+Daniel+S%3BBlair%2C+James%3BWakschlag%2C+Lauren+S&rft.aulast=Briggs-Gowan&rft.aufirst=Margaret&rft.date=2014-02-01&rft.volume=55&rft.issue=2&rft.spage=154&rft.isbn=&rft.btitle=&rft.title=Journal+of+Child+Psychology+and+Psychiatry+and+Allied+Disciplines&rft.issn=00219630&rft_id=info:doi/10.1111%2Fjcpp.12132
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Date revised - 2014-10-14
N1 - Last updated - 2016-05-12
DO - http://dx.doi.org/10.1111/jcpp.12132
ER -
TY - JOUR
T1 - Genome-wide Transcriptional Sequencing Identifies Novel Mutations in Metabolic Genes in Human Hepatocellular Carcinoma
AN - 1717493134; PQ0002002377
AB - We report on next-generation transcriptome sequencing results of three human hepatocellular carcinoma tumor/tumor-adjacent pairs. This analysis robustly examined ~12,000 genes for both expression differences and molecular alterations. We observed 4,513 and 1,182 genes demonstrating 2-fold or greater increase or decrease in expression relative to their normal, respectively. Network analysis of expression data identified the Aurora B signaling, FOXM1 transcription factor network and Wnt signaling pathways pairs being altered in HCC. We validated as differential gene expression findings in a large data set containing of 434 liver normal/tumor sample pairs. In addition to known driver mutations in TP53 and CTNNB1, our mutation analysis identified non-synonymous mutations in genes implicated in metabolic diseases, i.e. diabetes and obesity: IRS1, HMGCS1, ATP8B1, PRMT6 and CLU, suggesting a common molecular etiology for HCC of alternative pathogenic origin.
JF - Cancer Genomics & Proteomics
AU - Meerzaman, Daoud M
AU - Yan, Chunhua
AU - Chen, Qing-Rong
AU - Edmonson, Michael N
AU - Schaefer, Carl F
AU - Clifford, Robert J
AU - Dunn, Barbara K
AU - Dong, Li
AU - Finney, Richard P
AU - Cultraro, Constance M
AD - Center for Bioinformatics and Information Technology, National Cancer Institute, Rockville, MD, U.S.A., meerzamd@mail.nih.gov
Y1 - 2014/02//
PY - 2014
DA - February 2014
SP - 1
EP - 12
PB - International Institute of Anticancer Research, 1st km Kapandritiou-Kalamou Road Kapandriti Attiki 19014 Greece
VL - 11
IS - 1
SN - 1109-6535, 1109-6535
KW - Biochemistry Abstracts 2: Nucleic Acids; Biotechnology and Bioengineering Abstracts; Genetics Abstracts; Oncogenes & Growth Factors Abstracts
KW - Hepatocellular carcinoma (HCC)
KW - RNA-seq
KW - gene expression
KW - mutation RNA-seq
KW - mutation
KW - Obesity
KW - aurora B protein
KW - Etiology
KW - Wnt protein
KW - Data processing
KW - Metabolic disorders
KW - Tumors
KW - p53 protein
KW - Diabetes mellitus
KW - Gene expression
KW - Transcription factors
KW - proteomics
KW - Mutation
KW - Hepatocellular carcinoma
KW - Signal transduction
KW - B 26660:Miscellaneous Oncogenes & Growth Factors
KW - G 07880:Human Genetics
KW - N 14835:Protein-Nucleic Acids Association
KW - W 30960:Bioinformatics & Computer Applications
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1717493134?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Genomics+%26+Proteomics&rft.atitle=Genome-wide+Transcriptional+Sequencing+Identifies+Novel+Mutations+in+Metabolic+Genes+in+Human+Hepatocellular+Carcinoma&rft.au=Meerzaman%2C+Daoud+M%3BYan%2C+Chunhua%3BChen%2C+Qing-Rong%3BEdmonson%2C+Michael+N%3BSchaefer%2C+Carl+F%3BClifford%2C+Robert+J%3BDunn%2C+Barbara+K%3BDong%2C+Li%3BFinney%2C+Richard+P%3BCultraro%2C+Constance+M&rft.aulast=Meerzaman&rft.aufirst=Daoud&rft.date=2014-02-01&rft.volume=11&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Cancer+Genomics+%26+Proteomics&rft.issn=11096535&rft_id=info:doi/
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-09-01
N1 - Last updated - 2016-02-18
N1 - SubjectsTermNotLitGenreText - Obesity; Etiology; aurora B protein; Data processing; Wnt protein; Metabolic disorders; Tumors; p53 protein; Gene expression; Diabetes mellitus; Transcription factors; proteomics; Mutation; Signal transduction; Hepatocellular carcinoma
ER -
TY - JOUR
T1 - Lung Segmentation in Chest Radiographs Using Anatomical Atlases With Nonrigid Registration
AN - 1676352613; PQ0001418089
AB - The National Library of Medicine (NLM) is developing a digital chest X-ray (CXR) screening system for deployment in resource constrained communities and developing countries worldwide with a focus on early detection of tuberculosis. A critical component in the computer-aided diagnosis of digital CXRs is the automatic detection of the lung regions. In this paper, we present a nonrigid registration-driven robust lung segmentation method using image retrieval-based patient specific adaptive lung models that detects lung boundaries, surpassing state-of-the-art performance. The method consists of three main stages: 1) a content-based image retrieval approach for identifying training images (with masks) most similar to the patient CXR using a partial Radon transform and Bhattacharyya shape similarity measure, 2) creating the initial patient-specific anatomical model of lung shape using SIFT-flow for deformable registration of training masks to the patient CXR, and 3) extracting refined lung boundaries using a graph cuts optimization approach with a customized energy function. Our average accuracy of 95.4% on the public JSRT database is the highest among published results. A similar degree of accuracy of 94.1% and 91.7% on two new CXR datasets from Montgomery County, MD, USA, and India, respectively, demonstrates the robustness of our lung segmentation approach.
JF - IEEE Transactions on Medical Imaging
AU - Candemir, Sema
AU - Jaeger, Stefan
AU - Palaniappan, Kannappan
AU - Musco, Jonathan P
AU - Singh, Rahul K
AU - Xue, Zhiyun
AU - Karargyris, Alexandros
AU - Antani, Sameer
AU - Thoma, George
AU - McDonald, Clement J
AD - Lister Hill National Center for Biomedical Communications U. S. National Library of Medicine, National Institutes of Health, Bethesda, MD, USA
Y1 - 2014/02//
PY - 2014
DA - Feb 2014
SP - 577
EP - 590
PB - Institute of Electrical and Electronics Engineers, Inc., 345 E. 47th St. NY NY 10017-2394 United States
VL - 33
IS - 2
SN - 0278-0062, 0278-0062
KW - Biotechnology and Bioengineering Abstracts
KW - Mycobacterium
KW - Image processing
KW - Chest
KW - Radon
KW - Models
KW - Databases
KW - Atlases
KW - Lung
KW - Energy
KW - Ionizing radiation
KW - Boundaries
KW - Segmentation
KW - Tuberculosis
KW - Radiography
KW - Developing countries
KW - W 30910:Imaging
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1676352613?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=IEEE+Transactions+on+Medical+Imaging&rft.atitle=Lung+Segmentation+in+Chest+Radiographs+Using+Anatomical+Atlases+With+Nonrigid+Registration&rft.au=Candemir%2C+Sema%3BJaeger%2C+Stefan%3BPalaniappan%2C+Kannappan%3BMusco%2C+Jonathan+P%3BSingh%2C+Rahul+K%3BXue%2C+Zhiyun%3BKarargyris%2C+Alexandros%3BAntani%2C+Sameer%3BThoma%2C+George%3BMcDonald%2C+Clement+J&rft.aulast=Candemir&rft.aufirst=Sema&rft.date=2014-02-01&rft.volume=33&rft.issue=2&rft.spage=577&rft.isbn=&rft.btitle=&rft.title=IEEE+Transactions+on+Medical+Imaging&rft.issn=02780062&rft_id=info:doi/10.1109%2FTMI.2013.2290491
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-04-01
N1 - Last updated - 2015-11-16
N1 - SubjectsTermNotLitGenreText - Image processing; Chest; Radon; Models; Databases; Atlases; Lung; Ionizing radiation; Energy; Segmentation; Boundaries; Tuberculosis; Radiography; Developing countries; Mycobacterium
DO - http://dx.doi.org/10.1109/TMI.2013.2290491
ER -
TY - JOUR
T1 - TRIM5[alpha] Variations Influence Transduction Efficiency With Lentiviral Vectors in Both Human and Rhesus CD34+ Cells In Vitro and In Vivo
AN - 1673387559; PQ0001387667
AB - Human immunodeficiency virus type 1 (HIV-1) vectors can transduce human hematopoietic stem cells (HSC), but transduction efficiency varies among individuals. The innate immune factor tripartite motif-containing protein 5[alpha] (TRIM5[alpha]) plays an important role for restriction of retroviral infection. In this study, we examined whether TRIM5[alpha] could account for variations in transduction efficiency using both an established rhesus gene therapy model and human CD34+ cell culture. Evaluation of TRIM5[alpha] genotypes (Mamu-1, -2, -3, -4, -5, and TrimCyp) in 16 rhesus macaques that were transplanted with transduced CD34+ cells showed a significant correlation between TRIM5[alpha] Mamu-4 and high gene marking in both lymphocytes and granulocytes 6 months after transplantation. Since significant human TRIM5[alpha] coding polymorphisms were not known, we evaluated TRIM5[alpha] expression levels in human CD34+ cells from 14 donors. Three days after HIV-1 vector transduction, measured transduction efficiency varied significantly among donors and was negatively correlated with TRIM5[alpha] expression levels. In summary, transduction efficiency in both rhesus and human CD34+ cells was influenced by TRIM5[alpha] variations (genotypes and expression levels). Our findings are important for both understanding and mitigating the variability of transduction efficiency for rhesus and human CD34+ cells.
JF - Molecular Therapy
AU - Evans, Molly E
AU - Kumkhaek, Chutima
AU - Hsieh, Matthew M
AU - Donahue, Robert E
AU - Tisdale, John F
AU - Uchida, Naoya
AD - Molecular and Clinical Hematology Branch, National Heart Lung and Blood Institutes/National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA, uchidan@nhlbi.nih.gov
Y1 - 2014/02//
PY - 2014
DA - Feb 2014
SP - 348
EP - 358
PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom
VL - 22
IS - 2
SN - 1525-0016, 1525-0016
KW - Virology & AIDS Abstracts; Biotechnology and Bioengineering Abstracts
KW - Donors
KW - Gene therapy
KW - Gene polymorphism
KW - CD34 antigen
KW - Cell culture
KW - Lymphocytes
KW - Infection
KW - Expression vectors
KW - Leukocytes (granulocytic)
KW - Stem cells
KW - Human immunodeficiency virus 1
KW - Macaca mulatta
KW - W 30905:Medical Applications
KW - V 22360:AIDS and HIV
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1673387559?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+Therapy&rft.atitle=TRIM5%5Balpha%5D+Variations+Influence+Transduction+Efficiency+With+Lentiviral+Vectors+in+Both+Human+and+Rhesus+CD34%2B+Cells+In+Vitro+and+In+Vivo&rft.au=Evans%2C+Molly+E%3BKumkhaek%2C+Chutima%3BHsieh%2C+Matthew+M%3BDonahue%2C+Robert+E%3BTisdale%2C+John+F%3BUchida%2C+Naoya&rft.aulast=Evans&rft.aufirst=Molly&rft.date=2014-02-01&rft.volume=22&rft.issue=2&rft.spage=348&rft.isbn=&rft.btitle=&rft.title=Molecular+Therapy&rft.issn=15250016&rft_id=info:doi/10.1038%2Fmt.2013.256
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-04-01
N1 - Last updated - 2015-11-16
N1 - SubjectsTermNotLitGenreText - Expression vectors; Leukocytes (granulocytic); Donors; Stem cells; Gene therapy; Gene polymorphism; Cell culture; CD34 antigen; Lymphocytes; Infection; Human immunodeficiency virus 1; Macaca mulatta
DO - http://dx.doi.org/10.1038/mt.2013.256
ER -
TY - JOUR
T1 - Chromosome Segregation in Vibrio cholerae
AN - 1664193779; PQ0001238389
AB - The study of chromosome segregation is currently one of the most exciting research frontiers in cell biology. In this review, we discuss our current knowledge of the chromosome segregation process in Vibrio cholerae, based primarily on findings from fluorescence microscopy experiments. This bacterium is of special interest because of its eukaryotic feature of having a divided genome, a feature shared with 10% of known bacteria. We also discuss how the segregation mechanisms of V. cholerae compare with those in other bacteria, and highlight some of the remaining questions regarding the process of bacterial chromosome segregation. copyright 2015 S. Karger AG, Basel
JF - Journal of Molecular Microbiology and Biotechnology
AU - Ramachandran, Revathy
AU - Jha, Jyoti
AU - Chattoraj, Dhruba K
AD - Laboratory of Biochemistry and Molecular Biology, Center for Cancer Research, NCI, National Institutes of Health, Bethesda, Md., USA
Y1 - 2014/02//
PY - 2014
DA - February 2014
SP - 360
EP - 370
PB - S. Karger AG, P.O. Box Basel CH-4009 Switzerland
VL - 24
IS - 5-6
SN - 1464-1801, 1464-1801
KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Microbiology Abstracts B: Bacteriology; Genetics Abstracts; Biotechnology and Bioengineering Abstracts
KW - Bacterial mitosis
KW - Divided genomes
KW - Coordination of replication and segregation
KW - Par-independent polar segregation
KW - Genomes
KW - Vibrio cholerae
KW - Chromosomes
KW - Microbiology
KW - Cytology
KW - Biotechnology
KW - Fluorescence microscopy
KW - J 02310:Genetics & Taxonomy
KW - Q1 08205:Genetics and evolution
KW - Q5 08524:Public health, medicines, dangerous organisms
KW - G 07770:Bacteria
KW - W 30900:Methods
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1664193779?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Molecular+Microbiology+and+Biotechnology&rft.atitle=Chromosome+Segregation+in+Vibrio+cholerae&rft.au=Ramachandran%2C+Revathy%3BJha%2C+Jyoti%3BChattoraj%2C+Dhruba+K&rft.aulast=Ramachandran&rft.aufirst=Revathy&rft.date=2014-02-01&rft.volume=24&rft.issue=5-6&rft.spage=360&rft.isbn=&rft.btitle=&rft.title=Journal+of+Molecular+Microbiology+and+Biotechnology&rft.issn=14641801&rft_id=info:doi/10.1159%2F000368853
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-03-01
N1 - Last updated - 2016-12-22
N1 - SubjectsTermNotLitGenreText - Genomes; Chromosomes; Microbiology; Cytology; Biotechnology; Fluorescence microscopy; Vibrio cholerae
DO - http://dx.doi.org/10.1159/000368853
ER -
TY - JOUR
T1 - Race and health profiles in the United States: an examination of the social gradient through the 2009 CHIS adult survey
AN - 1660388274; PQ0001118513
AB - The objective of this study is to examine the role of the social gradient on multiple health outcomes and behaviors. It was predicted that higher levels of SES, measured by educational attainment and family income, would be associated with positive health behaviors and health status. The study also examined the differential effects of the social gradient in health among different racial/ethnic groups. The study contributes to the literature by illustrating unique patterns and trends of the social gradient across various racial/ethnic populations in a nationally representative sample. Future studies should further explore temporal trends to track the impact of the social gradient for different racial and ethnic populations in tandem with indices of national income inequalities.
JF - Public Health
AU - Nguyen, A B
AU - Moser, R
AU - Chou, W-Y
AD - The National Cancer Institute (NCI), Division of Cancer Control and Population Sciences (DCCPS), 9609 Medical Center Dr., Rm 3E638, Rockville, MD 20850-9761, USA, Anh.Nguyen3@nih.gov
PY - 2014
SP - 1076
EP - 1086
PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom
VL - 128
IS - 12
SN - 0033-3506, 0033-3506
KW - Health & Safety Science Abstracts
KW - Health disparities
KW - SES
KW - Race
KW - Ethnicity
KW - Social gradient
KW - USA
KW - Socioeconomics
KW - Ethnic groups
KW - Income
KW - H 12000:Epidemiology and Public Health
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660388274?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Public+Health&rft.atitle=Race+and+health+profiles+in+the+United+States%3A+an+examination+of+the+social+gradient+through+the+2009+CHIS+adult+survey&rft.au=Nguyen%2C+A+B%3BMoser%2C+R%3BChou%2C+W-Y&rft.aulast=Nguyen&rft.aufirst=A&rft.date=2014-02-01&rft.volume=128&rft.issue=12&rft.spage=1076&rft.isbn=&rft.btitle=&rft.title=Public+Health&rft.issn=00333506&rft_id=info:doi/10.1016%2Fj.puhe.2014.10.003
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-03-01
N1 - Last updated - 2015-12-23
N1 - SubjectsTermNotLitGenreText - Socioeconomics; Ethnic groups; Income; USA
DO - http://dx.doi.org/10.1016/j.puhe.2014.10.003
ER -
TY - JOUR
T1 - Coinfection with Plasmodium falciparum and Schistosoma haematobium: Additional Evidence of the Protective Effect of Schistosomiasis on Malaria in Senegalese Children
AN - 1647023865; 21172740
AB - Parasitic infections are associated with high morbidity and mortality in developing countries. Several studies focused on the influence of helminth infections on malaria but the nature of the biological interaction is under debate. Our objective was to undertake a study to explore the influence of the measure of excreted egg load caused by Schistosoma haematobium on Plasmodium falciparum parasite densities. Ten measures of malaria parasite density and two measures of schistosomiasis egg urinary excretion over a 2-year follow-up period on 178 Senegalese children were considered. A linear mixed-effect model was developed to take data dependence into account. This work showed that children with a light S. haematobium infection (1-9 eggs/mL of urine) presented lower P. falciparum parasite densities than children not infected by S. haematobium (P < 0.04). Possible changes caused by parasite coinfections should be considered in the anti-helminth treatment of children and in malaria vaccination development.
JF - American Journal of Tropical Medicine and Hygiene
AU - Lemaitre, Magali
AU - Watier, Laurence
AU - Briand, Valerie
AU - Garcia, Andre
AU - LeHesran, Jean Yves
AU - Cot, Michel
AD - Institut de Recherche pour le Developpement (UMR216), Universite Paris Descartes, Sorbonne Paris Cite, Faculte de Pharmacie, Paris, France; Faculte de pharmacie, Universite Paris Descartes, Paris, France; Inserm, U657, Paris, F-7501 5, France; Institut Pasteur, PhEMI, Paris, F-75015, France; Univ. Versailles Saint Quentin, Faculte de Medecine Paris Ile de France Ouest, EA 4499, F-78035, France; Fogarty International Center, National Institutes of Health, Bethesda, MD 20892, maglemaitre@gmail.com
Y1 - 2014/02//
PY - 2014
DA - February 2014
SP - 329
EP - 334
PB - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States
VL - 90
IS - 2
SN - 0002-9637, 0002-9637
KW - Microbiology Abstracts B: Bacteriology; Microbiology Abstracts C: Algology, Mycology & Protozoology; ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality
KW - Parasites
KW - Human diseases
KW - Schistosoma haematobium
KW - Malaria
KW - Infection
KW - Eggs
KW - Morbidity
KW - Models
KW - Public health
KW - Mortality
KW - Data processing
KW - Schistosomiasis
KW - Plasmodium falciparum
KW - Children
KW - Vaccination
KW - Light effects
KW - Urine
KW - Excretion
KW - Hygiene
KW - Developing countries
KW - Mortality causes
KW - K 03400:Human Diseases
KW - Q1 08484:Species interactions: parasites and diseases
KW - Q5 08502:Methods and instruments
KW - J 02350:Immunology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.atitle=Coinfection+with+Plasmodium+falciparum+and+Schistosoma+haematobium%3A+Additional+Evidence+of+the+Protective+Effect+of+Schistosomiasis+on+Malaria+in+Senegalese+Children&rft.au=Lemaitre%2C+Magali%3BWatier%2C+Laurence%3BBriand%2C+Valerie%3BGarcia%2C+Andre%3BLeHesran%2C+Jean+Yves%3BCot%2C+Michel&rft.aulast=Lemaitre&rft.aufirst=Magali&rft.date=2014-02-01&rft.volume=90&rft.issue=2&rft.spage=329&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.12-0431
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-01-01
N1 - Last updated - 2016-02-04
N1 - SubjectsTermNotLitGenreText - Parasites; Human diseases; Urine; Schistosomiasis; Excretion; Malaria; Hygiene; Mortality causes; Public health; Mortality; Data processing; Children; Infection; Vaccination; Morbidity; Eggs; Models; Light effects; Developing countries; Schistosoma haematobium; Plasmodium falciparum
DO - http://dx.doi.org/10.4269/ajtmh.12-0431
ER -
TY - JOUR
T1 - Calcified Neurocysticercus, Perilesional Edema, and Histologic Inflammation
AN - 1647022849; 21172738
AB - Here, we present the second report of the histopathology of a Taenia solium calcification giving rise to perilesional edema. This has important implications, because if perilesional edema lesions are inflammatory in character, immunosuppressive or anti-inflammatory medications, not just antiepileptic drugs alone, may be useful to prevent or treat recurring episodes in such patients.
JF - American Journal of Tropical Medicine and Hygiene
AU - Nash, Theodore E
AU - Bartelt, Luther A
AU - Korpe, Poonum S
AU - Lopes, Beatriz
AU - Houpt, Eric R
AD - National Institute of Allergy and Infectious Diseases, Bethesda, Maryland; Division of Infectious Diseases and International Health, University of Virginia; Department of Pathology, University of Virginia, Charlottesville, Virginia, erh6k@virginia.edu
Y1 - 2014/02//
PY - 2014
DA - February 2014
SP - 318
EP - 321
PB - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States
VL - 90
IS - 2
SN - 0002-9637, 0002-9637
KW - Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts B: Bacteriology
KW - Calcification
KW - Edema
KW - Taenia solium
KW - Antiepileptic agents
KW - Inflammation
KW - K 03400:Human Diseases
KW - J 02400:Human Diseases
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647022849?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.atitle=Calcified+Neurocysticercus%2C+Perilesional+Edema%2C+and+Histologic+Inflammation&rft.au=Nash%2C+Theodore+E%3BBartelt%2C+Luther+A%3BKorpe%2C+Poonum+S%3BLopes%2C+Beatriz%3BHoupt%2C+Eric+R&rft.aulast=Nash&rft.aufirst=Theodore&rft.date=2014-02-01&rft.volume=90&rft.issue=2&rft.spage=318&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.13-0589
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-01-01
N1 - Last updated - 2016-02-18
N1 - SubjectsTermNotLitGenreText - Calcification; Edema; Antiepileptic agents; Inflammation; Taenia solium
DO - http://dx.doi.org/10.4269/ajtmh.13-0589
ER -
TY - JOUR
T1 - Platelet hyperactivity, neurobehavioral symptoms and depression among Indian women chronically exposed to low level of arsenic
AN - 1647011667; 21321481
AB - The prevalence of neurobehavioral symptoms (NBS) and depression has been investigated in premenopausal rural women of West Bengal, India enrolled from arsenic (As) endemic (groundwater As 11-50 mu g/L; n =342) and control areas (As level less than or equal to 10 mu g/L; n =312). The subjective symptoms questionnaire and Beck's 21-point depression inventory-II were used for the detection of NBS and depression, respectively. Platelet P-selectin expression was measured by flow cytometry, plasma neurotransmitter activity with high performance liquid chromatography and groundwater As level by atomic absorption spectroscopy. The As level in groundwater was 2.72 plus or minus 1.18 mu g/L in control and 28.3 plus or minus 13.51 mu g/L in endemic areas (p 0.05) from that of controls. Moreover, women from endemic areas had 2.3-times more P-selectin-expressing platelets in their circulation (p <0.001). After controlling the potential confounders, chronic low level As (11-50 mu g/L) exposure showed a positive association with the prevalence of neurobehavioral symptoms and depression among Indian women in their child-bearing age.
JF - Neurotoxicology
AU - Mukherjee, Bidisha
AU - Bindhani, Banani
AU - Saha, Hirak
AU - Sinha, Dona
AU - Ray, Manas Ranjan
AD - Department of Experimental Hematology Unit, Chittaranjan National Cancer Institute, Kolkata-700 026, India
PY - 2014
SP - 159
EP - 167
PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands
VL - 45
SN - 0161-813X, 0161-813X
KW - Environment Abstracts; CSA Neurosciences Abstracts; Toxicology Abstracts
KW - Arsenic
KW - Water
KW - Neurobehavioral symptoms
KW - Depression
KW - Indian women
KW - High-performance liquid chromatography
KW - Age
KW - Anxiety
KW - P-selectin
KW - India, West Bengal
KW - Extremities
KW - Flow cytometry
KW - Memory
KW - Dopamine
KW - Ground water
KW - Neurotransmitters
KW - Epinephrine
KW - Inventories
KW - Atomic absorption spectroscopy
KW - Fatigue
KW - ISW, India, West Bengal
KW - Taste
KW - Serotonin
KW - Liquid chromatography
KW - Neurotoxicity
KW - Platelets
KW - Females
KW - Burning
KW - Groundwater
KW - Olfaction
KW - Rural areas
KW - N3 11028:Neuropharmacology & toxicology
KW - X 24360:Metals
KW - ENA 02:Toxicology & Environmental Safety
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647011667?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurotoxicology&rft.atitle=Platelet+hyperactivity%2C+neurobehavioral+symptoms+and+depression+among+Indian+women+chronically+exposed+to+low+level+of+arsenic&rft.au=Mukherjee%2C+Bidisha%3BBindhani%2C+Banani%3BSaha%2C+Hirak%3BSinha%2C+Dona%3BRay%2C+Manas+Ranjan&rft.aulast=Mukherjee&rft.aufirst=Bidisha&rft.date=2014-02-01&rft.volume=45&rft.issue=&rft.spage=159&rft.isbn=&rft.btitle=&rft.title=Neurotoxicology&rft.issn=0161813X&rft_id=info:doi/10.1016%2Fj.neuro.2014.10.011
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-01-01
N1 - Last updated - 2016-01-21
N1 - SubjectsTermNotLitGenreText - High-performance liquid chromatography; Inventories; Atomic absorption spectroscopy; Arsenic; Fatigue; Depression; Anxiety; P-selectin; Taste; Serotonin; Flow cytometry; Memory; Dopamine; Platelets; Ground water; Burning; Neurotransmitters; Epinephrine; Olfaction; Extremities; Age; Liquid chromatography; Neurotoxicity; Females; Groundwater; Rural areas; ISW, India, West Bengal; India, West Bengal
DO - http://dx.doi.org/10.1016/j.neuro.2014.10.011
ER -
TY - JOUR
T1 - N super(6)-methyladenosine modification destabilizes developmental regulators in embryonic stem cells
AN - 1566842939; 20108949
AB - N super(6)-methyladenosine (m super(6)A) has been identified as the most abundant internal modification of messenger RNA in eukaryotes. m super(6)A modification is involved in cell fate determination in yeast and embryo development in plants. Its mammalian function remains unknown but thousands of mammalian mRNAs and long non-coding RNAs (lncRNAs) show m super(6)A modification and m super(6)A demethylases are required for mammalian energy homeostasis and fertility. We identify two proteins, the putative m super(6)A MTase, methyltransferase-like 3 (Mettl3; ref. ), and a related but uncharacterized protein Mettl14, that function synergistically to control m super(6)A formation in mammalian cells. Knockdown of Mettl3 and Mettl14 in mouse embryonic stem cells (mESCs) led to similar phenotypes, characterized by lack of m super(6)A RNA methylation and lost self-renewal capability. A large number of transcripts, including many encoding developmental regulators, exhibit m super(6)A methylation inversely correlated with mRNA stability and gene expression. The human antigen R (HuR) and microRNA pathways were linked to these effects. This gene regulatory mechanism operating in mESCs through m super(6)A methylation is required to keep mESCs at their ground state and may be relevant to thousands of mRNAs and lncRNAs in various cell types.
JF - Nature Cell Biology
AU - Wang, Yang
AU - Li, Yue
AU - Toth, Julia I
AU - Petroski, Matthew D
AU - Zhang, Zhaolei
AU - Zhao, Jing Crystal
AD - Tumor Initiation and Maintenance Program, NCI-designated Cancer Center, Sanford Burnham Medical Research Institute, La Jolla, California 92037, USA
Y1 - 2014/02//
PY - 2014
DA - Feb 2014
SP - 191
EP - 198
PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL - 16
IS - 2
SN - 1465-7392, 1465-7392
KW - Genetics Abstracts; Biotechnology and Bioengineering Abstracts
KW - mRNA stability
KW - Fertility
KW - miRNA
KW - non-coding RNA
KW - mRNA
KW - Gene expression
KW - HuR protein
KW - Stem cells
KW - Mammalian cells
KW - Energy balance
KW - Embryo cells
KW - DNA methylation
KW - Cell fate
KW - W 30940:Products
KW - G 07800:Plants and Algae
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1566842939?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+Cell+Biology&rft.atitle=N+super%286%29-methyladenosine+modification+destabilizes+developmental+regulators+in+embryonic+stem+cells&rft.au=Wang%2C+Yang%3BLi%2C+Yue%3BToth%2C+Julia+I%3BPetroski%2C+Matthew+D%3BZhang%2C+Zhaolei%3BZhao%2C+Jing+Crystal&rft.aulast=Wang&rft.aufirst=Yang&rft.date=2014-02-01&rft.volume=16&rft.issue=2&rft.spage=191&rft.isbn=&rft.btitle=&rft.title=Nature+Cell+Biology&rft.issn=14657392&rft_id=info:doi/10.1038%2Fncb2902
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-09-01
N1 - Last updated - 2014-10-30
N1 - SubjectsTermNotLitGenreText - Fertility; mRNA stability; miRNA; non-coding RNA; mRNA; Gene expression; Stem cells; HuR protein; Embryo cells; Energy balance; Mammalian cells; DNA methylation; Cell fate
DO - http://dx.doi.org/10.1038/ncb2902
ER -
TY - JOUR
T1 - Re: The sonopartogram: a novel method for recording the progress of labor by ultrasound. W. A. Hassan, T. Eggeboe, M. Ferguson, A. Gillett, J. Studd, D. Pasupathy and C. C. Lees. Ultrasound Obstet Gynecol 2014; 43: 189-194
AN - 1560106699; 19433860
AB - Linked Comment: Ultrasound Obstet Gynecol 2014; 43: 189-194
JF - Ultrasound in Obstetrics and Gynecology
AU - Yeo, L
AD - Perinatology Research Branch, NICHD/NIH/DHHS, Bethesda, MD, and Detroit, MI, USA.
Y1 - 2014/02//
PY - 2014
DA - Feb 2014
SP - 137
EP - 138
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 43
IS - 2
SN - 0960-7692, 0960-7692
KW - Biotechnology and Bioengineering Abstracts
KW - Gynecology
KW - Ultrasound
KW - Obstetrics
KW - W 30910:Imaging
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Ultrasound+in+Obstetrics+and+Gynecology&rft.atitle=Re%3A+The+sonopartogram%3A+a+novel+method+for+recording+the+progress+of+labor+by+ultrasound.+W.+A.+Hassan%2C+T.+Eggeboe%2C+M.+Ferguson%2C+A.+Gillett%2C+J.+Studd%2C+D.+Pasupathy+and+C.+C.+Lees.+Ultrasound+Obstet+Gynecol+2014%3B+43%3A+189-194&rft.au=Yeo%2C+L&rft.aulast=Yeo&rft.aufirst=L&rft.date=2014-02-01&rft.volume=43&rft.issue=2&rft.spage=137&rft.isbn=&rft.btitle=&rft.title=Ultrasound+in+Obstetrics+and+Gynecology&rft.issn=09607692&rft_id=info:doi/10.1002%2Fuog.13300
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-09-01
N1 - Last updated - 2014-09-05
N1 - SubjectsTermNotLitGenreText - Gynecology; Obstetrics; Ultrasound
DO - http://dx.doi.org/10.1002/uog.13300
ER -
TY - JOUR
T1 - Imaging of lipids in rat heart by MALDI-MS with silver nanoparticles
AN - 1551080608; 20113106
AB - Lipids are a major component of heart tissue and perform several important functions such as energy storage, signaling, and as building blocks of biological membranes. The heart lipidome is quite diverse consisting of glycerophospholipids such as phosphatidylcholines (PCs), phosphatidylethanolamines (PEs), phosphatidylinositols (Pis), phosphatidylglycerols (PGs), cardiolipins (CLs), and glycerolipids, mainly triacylglycerols (TAGs). In this study, mass spectrometry imaging (MSI) enabled by matrix implantation of ionized silver nanoparticles (AgNP) was used to map several classes of lipids in heart tissue. The use of AgNP matrix implantation was motivated by our previous work showing that implantation doses of only 10 super(l4)/cm super(2) of 2 nm gold nanoparticulates into the first 10 nm of the near surface of the tissue enabled detection of most brain lipids (including neutral lipid species such as cerebrosides) more efficiently than traditional organic MALDI matrices. Herein, a similar implantation of 500 eV AgNP super(-) across the entire heart tissue section results in a quick, reproducible, solvent-free, uniform matrix concentration of 6 nm AgNP residing near the tissue surface. MALDI-MSI analysis of either positive or negative ions produce high-quality images of several heart lipid species. In negative ion mode, 24 lipid species [16 PEs, 4 PIs, 1 PG, 1 CL, 2 sphingomyelins (SMs)] were imaged. Positive ion images were also obtained from 29 lipid species (10 PCs, 5 PEs, 5 SMs, 9 TAGs) with the TAG species being heavily concentrated in vascular regions of the heart.
JF - Analytical and Bioanalytical Chemistry
AU - Jackson, Shelley N
AU - Baldwin, Kathrine
AU - Muller, Ludovic
AU - Womack, Virginia M
AU - Schultz, J Albert
AU - Balaban, Carey
AU - Woods, Amina S
AD - Structural Biology Unit, NIDA IRP, NIH, 333 Cassell Drive, Room 1120, Baltimore, MD 21224, USA, awoods@intra.nida.nih.gov
PY - 2014
SP - 1377
EP - 1386
PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL - 406
IS - 5
SN - 1618-2642, 1618-2642
KW - Aqualine Abstracts; Water Resources Abstracts
KW - MALDI
KW - Mass spectrometry imaging
KW - Lipids
KW - Silver nanoparticles
KW - Mass Spectrometry
KW - Ions
KW - Buildings
KW - Storage
KW - Gold
KW - Biological Membranes
KW - Silver
KW - AQ 00001:Water Resources and Supplies
KW - SW 0540:Properties of water
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aaqualine&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Analytical+and+Bioanalytical+Chemistry&rft.atitle=Imaging+of+lipids+in+rat+heart+by+MALDI-MS+with+silver+nanoparticles&rft.au=Jackson%2C+Shelley+N%3BBaldwin%2C+Kathrine%3BMuller%2C+Ludovic%3BWomack%2C+Virginia+M%3BSchultz%2C+J+Albert%3BBalaban%2C+Carey%3BWoods%2C+Amina+S&rft.aulast=Jackson&rft.aufirst=Shelley&rft.date=2014-02-01&rft.volume=406&rft.issue=5&rft.spage=1377&rft.isbn=&rft.btitle=&rft.title=Analytical+and+Bioanalytical+Chemistry&rft.issn=16182642&rft_id=info:doi/10.1007%2Fs0026-013-7525-6
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-12-01
N1 - Number of references - 39
N1 - Last updated - 2016-01-21
N1 - SubjectsTermNotLitGenreText - Storage; Ions; Mass Spectrometry; Lipids; Gold; Biological Membranes; Buildings; Silver
DO - http://dx.doi.org/10.1007/s0026-013-7525-6
ER -
TY - JOUR
T1 - Impact of body size and physical activity during adolescence and adult life on overall and cause-specific mortality in a large cohort study from Iran
AN - 1534846874; 19441623
AB - We conducted this study to examine life-course body size and physical activity in relation to total and cause-specific mortality, which has not previously been studied in the low and middle-income countries in Asia. The Golestan Cohort Study is a population-based cohort in northeastern Iran in which 50,045 people above the age of 40 have been followed since 2004. Participants were shown a validated pictogram to assess body size at ages 15, 30, and the time of recruitment. Information on occupational physical activity at these ages was also collected. Subjects were followed up annually, and cause of death was determined. Cox regression models were adjusted for age at cohort start, smoking, socioeconomic status, ethnicity, place of residence, education, and opium use. Models for body size were also adjusted for physical activity at the same age, and vice versa. During a total of 252,740 person-years of follow-up (mean follow-up duration 5.1 plus or minus 1.3 years) through December 2011, 2,529 of the cohort participants died. Larger body sizes at ages 15 or 30 in both sexes were associated with increased overall mortality. Cancer mortality was more strongly associated with adolescent obesity, and cardiovascular mortality with early adulthood body size. Weight gain between these ages was associated with cardiovascular mortality. Obese adolescents who lost weight still had increased mortality from all medical causes in both sexes. Physical activity during adolescence and early adulthood had no association with mortality, but at cohort baseline higher levels of activity were associated with reduced mortality. Mortality in this Middle-Eastern population was associated with obesity both during adolescence and early adult life.
JF - European Journal of Epidemiology
AU - Etemadi, Arash
AU - Abnet, Christian C
AU - Kamangar, Farin
AU - Islami, Farhad
AU - Khademi, Hooman
AU - Pourshams, Akram
AU - Poustchi, Hossein
AU - Bagheri, Mohammad
AU - Sohrabpour, Amir Ali
AU - Aliasgar, Ali
AU - Khoshnia, Masoud
AU - Wacholder, Sholom
AU - Matthews, Charles C
AU - Pharoah, Paul D
AU - Brennan, Paul
AU - Boffetta, Paolo
AU - Malekzadeh, Reza
AU - Dawsey, Sanford M
AD - Digestive Oncology Research Center, Digestive Disease Research Institute, Tehran University of Medical Sciences, Tehran, Iran, arash.etemadi@nih.gov
Y1 - 2014/02//
PY - 2014
DA - Feb 2014
SP - 95
EP - 109
PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL - 29
IS - 2
SN - 0393-2990, 0393-2990
KW - Physical Education Index
KW - Anthropometry
KW - Obesity
KW - Death
KW - Weight
KW - Adolescence
KW - Cardiorespiratory
KW - Exercise
KW - Adults
KW - Sex
KW - PE 030:Exercise, Health & Physical Fitness
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534846874?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aphysicaleducation&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+Journal+of+Epidemiology&rft.atitle=Impact+of+body+size+and+physical+activity+during+adolescence+and+adult+life+on+overall+and+cause-specific+mortality+in+a+large+cohort+study+from+Iran&rft.au=Etemadi%2C+Arash%3BAbnet%2C+Christian+C%3BKamangar%2C+Farin%3BIslami%2C+Farhad%3BKhademi%2C+Hooman%3BPourshams%2C+Akram%3BPoustchi%2C+Hossein%3BBagheri%2C+Mohammad%3BSohrabpour%2C+Amir+Ali%3BAliasgar%2C+Ali%3BKhoshnia%2C+Masoud%3BWacholder%2C+Sholom%3BMatthews%2C+Charles+C%3BPharoah%2C+Paul+D%3BBrennan%2C+Paul%3BBoffetta%2C+Paolo%3BMalekzadeh%2C+Reza%3BDawsey%2C+Sanford+M&rft.aulast=Etemadi&rft.aufirst=Arash&rft.date=2014-02-01&rft.volume=29&rft.issue=2&rft.spage=95&rft.isbn=&rft.btitle=&rft.title=European+Journal+of+Epidemiology&rft.issn=03932990&rft_id=info:doi/10.1007%2Fs10654-014-9883-6
LA - English
DB - Physical Education Index
N1 - Date revised - 2014-06-01
N1 - Number of references - 48
N1 - Last updated - 2015-10-28
N1 - SubjectsTermNotLitGenreText - Anthropometry; Obesity; Death; Weight; Adolescence; Cardiorespiratory; Adults; Exercise; Sex
DO - http://dx.doi.org/10.1007/s10654-014-9883-6
ER -
TY - JOUR
T1 - RADIATION-EXPOSED POPULATIONS: WHO, WHY, AND HOW TO STUDY
AN - 1524411550; 19642280
AB - Everyone is exposed to natural and man-made ionizing radiation that can originate from sources in the environment and in medical and occupational settings. Our present understanding of radiation- related health risks derives primarily from multidisciplinary health risk (epidemiologic) studies that provide the key information on radiation-associated health outcomes, quantify radiation-related disease risks, and enhance understanding of mechanisms of radiation-related disease pathogenesis. Such information is central to quantifying risks in relation to benefits; addressing public concerns, including societal and clinical needs in relation to radiation exposure; and providing the database needed for establishing recommendations for radiation protection. This paper describes a wide range of populations exposed to radiation and the motivation and key methodological criteria that drive the rationale and priority of studying such populations. Also, discussed are alternative methods for evaluating radiation-related health risks in these populations, with a major focus on epidemiologic approaches. This paper concludes with a short summary of major high-lights from radiation epidemiologic research and important unanswered questions.
JF - Health Physics
AU - Simon, Steven L
AU - Linet, Martha S
AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, 9609 Medical Center Dr., Bethesda, MD 20892-9778, ssimon@mail.nih.gov
Y1 - 2014/02//
PY - 2014
DA - Feb 2014
SP - 182
EP - 195
PB - Williams & Wilkins, 351 W. Camden St. Baltimore MD 21201 United States
VL - 106
IS - 2
SN - 0017-9078, 0017-9078
KW - Risk Abstracts; Health & Safety Science Abstracts
KW - epidemiology
KW - exposure, occupational
KW - medical radiation
KW - National Council on Radiation Protection and Measurements
KW - Health risks
KW - Radiation
KW - Ionizing radiation
KW - Priorities
KW - Public concern
KW - R2 23060:Medical and environmental health
KW - H 1000:Occupational Safety and Health
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1524411550?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Health+Physics&rft.atitle=RADIATION-EXPOSED+POPULATIONS%3A+WHO%2C+WHY%2C+AND+HOW+TO+STUDY&rft.au=Simon%2C+Steven+L%3BLinet%2C+Martha+S&rft.aulast=Simon&rft.aufirst=Steven&rft.date=2014-02-01&rft.volume=106&rft.issue=2&rft.spage=182&rft.isbn=&rft.btitle=&rft.title=Health+Physics&rft.issn=00179078&rft_id=info:doi/10.1097%2FHP.0000000000000006
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-05-01
N1 - Last updated - 2015-05-27
N1 - SubjectsTermNotLitGenreText - Health risks; Radiation; Ionizing radiation; Priorities; Public concern
DO - http://dx.doi.org/10.1097/HP.0000000000000006
ER -
TY - JOUR
T1 - INCREASED OCCUPATIONAL RADIATION DOSES: NUCLEAR FUEL CYCLE
AN - 1520378502; 19642289
AB - The increased occupational doses resulting from the Chernobyl nuclear reactor accident that occurred in Ukraine in April 1986, the reactor accident of Fukushima that took place in Japan in March 2011, and the early operations of the Mayak Production Association in Russia in the 1940s and 1950s are presented and discussed. For comparison purposes, the occupational doses due to the other two major reactor accidents (Windscale in the United Kingdom in 1957 and Three Mile Island in the United States in 1979) and to the main plutonium-producing facility in the United States (Hanford Works) are also covered but in less detail. Both for the Chernobyl nuclear reactor accident and the routine operations at Mayak, the considerable efforts made to reconstruct individual doses from external irradiation to a large number of workers revealed that the recorded doses had been overestimated by a factor of about two.
JF - Health Physics
AU - Bouville, Andre
AU - Kryuchkovt, Victor
AD - Federal Medical Biological Agency, Burnasyan Federal Medical Biophysical Center, 46 Zhivopisnaya Street, 123182, Moscow, Russia, andre.bouville@nih.gov
Y1 - 2014/02//
PY - 2014
DA - Feb 2014
SP - 259
EP - 271
PB - Williams & Wilkins, 351 W. Camden St. Baltimore MD 21201 United States
VL - 106
IS - 2
SN - 0017-9078, 0017-9078
KW - Pollution Abstracts; Health & Safety Science Abstracts
KW - National Council on Radiation Protection and Measurements
KW - accidents, nuclear
KW - Chernobyl
KW - occupational safety
KW - USA
KW - Ukraine, Chernobyl
KW - Accidents
KW - Nuclear reactors
KW - Radiation
KW - Irradiation
KW - USA, Washington, Hanford
KW - Ukraine
KW - Nuclear fuels
KW - Russia
KW - H 1000:Occupational Safety and Health
KW - P 6000:TOXICOLOGY AND HEALTH
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1520378502?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Apollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Health+Physics&rft.atitle=INCREASED+OCCUPATIONAL+RADIATION+DOSES%3A+NUCLEAR+FUEL+CYCLE&rft.au=Bouville%2C+Andre%3BKryuchkovt%2C+Victor&rft.aulast=Bouville&rft.aufirst=Andre&rft.date=2014-02-01&rft.volume=106&rft.issue=2&rft.spage=259&rft.isbn=&rft.btitle=&rft.title=Health+Physics&rft.issn=00179078&rft_id=info:doi/10.1097%2FHP.0000000000000066
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-01
N1 - Last updated - 2015-05-27
N1 - SubjectsTermNotLitGenreText - Accidents; Nuclear reactors; Radiation; Irradiation; Nuclear fuels; Ukraine, Chernobyl; USA; Ukraine; USA, Washington, Hanford; Russia
DO - http://dx.doi.org/10.1097/HP.0000000000000066
ER -
TY - JOUR
T1 - NUCLEAR REACTOR ACCIDENTS: EXPOSURES AND HEALTH EFFECTS AMONG MEMBERS OF THE PUBLIC
AN - 1520364341; 19642295
AB - THE FIRST notable nuclear reactor accident occurred in 1957 at the Windscale Plant in Britain. Radioactive super(131)I was released from the reactor building into the surrounding area, but a 50 y follow-up of the highest-exposed group-workers involved in cleanup-found no exposure-related effects on cancer or mortality rates (McGeoghegan et al. 2010).
JF - Health Physics
AU - Hatch, Maureen
AD - Radiation Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD 20892, hatchm@mail.nih.gov
Y1 - 2014/02//
PY - 2014
DA - Feb 2014
SP - 307
EP - 308
PB - Williams & Wilkins, 351 W. Camden St. Baltimore MD 21201 United States
VL - 106
IS - 2
SN - 0017-9078, 0017-9078
KW - Health & Safety Science Abstracts; Pollution Abstracts
KW - British Isles
KW - Mortality
KW - Accidents
KW - Nuclear reactors
KW - H 8000:Radiation Safety/Electrical Safety
KW - P 6000:TOXICOLOGY AND HEALTH
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1520364341?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Apollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Health+Physics&rft.atitle=NUCLEAR+REACTOR+ACCIDENTS%3A+EXPOSURES+AND+HEALTH+EFFECTS+AMONG+MEMBERS+OF+THE+PUBLIC&rft.au=Hatch%2C+Maureen&rft.aulast=Hatch&rft.aufirst=Maureen&rft.date=2014-02-01&rft.volume=106&rft.issue=2&rft.spage=307&rft.isbn=&rft.btitle=&rft.title=Health+Physics&rft.issn=00179078&rft_id=info:doi/10.1097%2FHP.0000000000000014
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-01
N1 - Last updated - 2015-05-27
N1 - SubjectsTermNotLitGenreText - Mortality; Accidents; Nuclear reactors; British Isles
DO - http://dx.doi.org/10.1097/HP.0000000000000014
ER -
TY - JOUR
T1 - Funding Strategies for Population Researchers: Perspectives from the National Institutes of Health
AN - 1520340973; 201419305
AB - The purpose of this article is to briefly describe the application and funding process at the National Institutes of Health (NIH). We target our discussion to demographic and population science at the Eunice Kennedy Shriver National Institute of Child Health & Human Development (NICHD), but the general strategies are applicable to social and behavioral scientists for all NIH funding opportunities. Adapted from the source document.
JF - Population Research and Policy Review
AU - Bures, Regina
AU - Clark, Rebecca
AU - King, Rosalind
AU - Newcomer, Susan
AD - Population Dynamics Branch (PDB), NICHD, 6100 Executive Boulevard, Bethesda, MD, 20892-7510, USA regina.bures@nih.gov
Y1 - 2014/02//
PY - 2014
DA - February 2014
SP - 1
EP - 11
PB - Springer, Dordrecht The Netherlands
VL - 33
IS - 1
SN - 0167-5923, 0167-5923
KW - Social Scientists
KW - Health
KW - Children
KW - article
KW - 1837: demography and human biology; demography (population studies)
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1520340973?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Asocabs&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Population+Research+and+Policy+Review&rft.atitle=Funding+Strategies+for+Population+Researchers%3A+Perspectives+from+the+National+Institutes+of+Health&rft.au=Bures%2C+Regina%3BClark%2C+Rebecca%3BKing%2C+Rosalind%3BNewcomer%2C+Susan&rft.aulast=Bures&rft.aufirst=Regina&rft.date=2014-02-01&rft.volume=33&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Population+Research+and+Policy+Review&rft.issn=01675923&rft_id=info:doi/10.1007%2Fs11113-013-9306-5
LA - English
DB - Sociological Abstracts
N1 - Date revised - 2014-05-01
N1 - Last updated - 2016-09-28
N1 - CODEN - PRPRE8
N1 - SubjectsTermNotLitGenreText - Health; Social Scientists; Children
DO - http://dx.doi.org/10.1007/s11113-013-9306-5
ER -
TY - JOUR
T1 - Profile of male forensic psychiatric inpatients in South India
AN - 1520312790; 201410503
AB - Aim: The study explored the socio-demographic, clinical and legal profile of forensic psychiatric inpatients in an attempt to improve the existing mental health services for prisoners within the prison and in psychiatric hospitals. Methodology: A chart review of 135 forensic psychiatric inpatients admitted between January 2005 and December 2009 was done. A structured data-extraction tool was used for data collection and a descriptive approach for analyses. Results: Subjects were referred either directly from prison (62.2%) or from court (37.8%) for diagnosis, treatment or certification. References to the Mental Health Act 1987, charges and inclusion of first investigation report and behavioural observation report was lacking in most. The majority of prisoners (85.7%) were under trial, murder being the most common charge. Psychiatric diagnosis was made in 90.3%, the most common being psychosis. Substance use (nicotine, alcohol, cannabis) and high-risk behaviours were also common. Conclusion: There is a need to streamline the procedure of referral and to sensitize the referral authorities about the Mental Health Act and mental illnesses, and the need to enclose first investigation reports and behavioural observation reports. De-addiction services and facilities need to be established within prison premises so that the inmates get the benefit of treatment at the earliest opportunity. [Reprinted by permission of Sage Publications Ltd., copyright holder.]
JF - International Journal of Social Psychiatry
AU - Kumar, Dayachandra
AU - Viswanath, Biju
AU - Sebestian, Ami
AU - Holla, Bharath
AU - Konduru, Reddema
AU - Chandrashekar, Chanapatna Rajannachar
AU - Math, Suresh Bada
AD - Department of Psychiatric Nursing, National Institute of Mental Health and Neurosciences (NIMHANS), Bangalore, India
Y1 - 2014/02//
PY - 2014
DA - February 2014
SP - 55
EP - 62
PB - Sage Publications, London UK
VL - 60
IS - 1
SN - 0020-7640, 0020-7640
KW - Forensic psychiatry prison legal
KW - Prisons
KW - Diagnosis
KW - Psychiatric hospitals
KW - Referrals
KW - Mental health
KW - Prisoners
KW - article
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1520312790?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Social+Psychiatry&rft.atitle=Profile+of+male+forensic+psychiatric+inpatients+in+South+India&rft.au=Kumar%2C+Dayachandra%3BViswanath%2C+Biju%3BSebestian%2C+Ami%3BHolla%2C+Bharath%3BKonduru%2C+Reddema%3BChandrashekar%2C+Chanapatna+Rajannachar%3BMath%2C+Suresh+Bada&rft.aulast=Kumar&rft.aufirst=Dayachandra&rft.date=2014-02-01&rft.volume=60&rft.issue=1&rft.spage=55&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Social+Psychiatry&rft.issn=00207640&rft_id=info:doi/10.1177%2F0020764012461334
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Date revised - 2014-05-01
N1 - Number of references - 16
N1 - Last updated - 2016-09-27
N1 - CODEN - IJSPAG
N1 - SubjectsTermNotLitGenreText - Psychiatric hospitals; Prisoners; Prisons; Diagnosis; Mental health; Referrals
DO - http://dx.doi.org/10.1177/0020764012461334
ER -
TY - JOUR
T1 - Global DNA methylation and one-carbon metabolism gene polymorphisms and the risk of breast cancer in the Sister Study
AN - 1512323016; 19325022
AB - Summary Our finding that LINE-1 undermethylation was present in blood collected from women before clinical detection of their tumor provides evidence from a prospective study that lower global methylation is associated with increased risk of breast cancer. Summary Our finding that LINE-1 undermethylation was present in blood collected from women before clinical detection of their tumor provides evidence from a prospective study that lower global methylation is associated with increased risk of breast cancer.
JF - Carcinogenesis
AU - DeRoo, Lisa A
AU - Bolick, Sophia CE
AU - Xu, Zongli
AU - Umbach, David M
AU - Shore, David
AU - Weinberg, Clarice R
AU - Sandler, Dale P
AU - Taylor, Jack A
AD - super(1)Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA,, taylor@niehs.nih.gov
Y1 - 2014/02//
PY - 2014
DA - Feb 2014
SP - 333
EP - 338
PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL - 35
IS - 2
SN - 0143-3334, 0143-3334
KW - Toxicology Abstracts; Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids
KW - Blood
KW - Gene polymorphism
KW - Carcinogenesis
KW - DNA methylation
KW - Breast cancer
KW - Tumors
KW - Metabolism
KW - G 07880:Human Genetics
KW - N 14820:DNA Metabolism & Structure
KW - X 24300:Methods
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Global+DNA+methylation+and+one-carbon+metabolism+gene+polymorphisms+and+the+risk+of+breast+cancer+in+the+Sister+Study&rft.au=DeRoo%2C+Lisa+A%3BBolick%2C+Sophia+CE%3BXu%2C+Zongli%3BUmbach%2C+David+M%3BShore%2C+David%3BWeinberg%2C+Clarice+R%3BSandler%2C+Dale+P%3BTaylor%2C+Jack+A&rft.aulast=DeRoo&rft.aufirst=Lisa&rft.date=2014-02-01&rft.volume=35&rft.issue=2&rft.spage=333&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/10.1093%2Fcarcin%2Fbgt342
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-01
N1 - Last updated - 2014-10-30
N1 - SubjectsTermNotLitGenreText - Blood; Gene polymorphism; Carcinogenesis; DNA methylation; Breast cancer; Tumors; Metabolism
DO - http://dx.doi.org/10.1093/carcin/bgt342
ER -
TY - JOUR
T1 - The Role of Hemocytes in Anopheles gambiae Antiplasmodial Immunity
AN - 1512322459; 19422958
AB - Hemocytes synthesize key components of the mosquito complement-like system, but their role in the activation of antiplasmodial responses has not been established. The effect of activating Toll signaling in hemocytes on Plasmodium survival was investigated by transferring hemocytes or cell-free hemolymph from donor mosquitoes in which the suppressor cactus was silenced. These transfers greatly enhanced antiplasmodial immunity, indicating that hemocytes are active players in the activation of the complement-like system, through an effector/effectors regulated by the Toll pathway. A comparative analysis of hemocyte populations between susceptible G3 and the refractory L3-5 Anopheles gambiae mosquito strains did not reveal significant differences under basal conditions or in response to Plasmodium berghei infection. The response of susceptible mosquitoes to different Plasmodium species revealed similar kinetics following infection with P. berghei,P. yoelii or P. falciparum, but the strength of the priming response was stronger in less compatible mosquito-parasite pairs. The Toll, Imd,STAT or JNK signaling cascades were not essential for the production of the hemocyte differentiation factor (HDF) in response to P. berghei infection, but disruption of Toll, STAT or JNK abolished hemocyte differentiation in response to HDF. We conclude that hemocytes are key mediators of A. gambiae antiplasmodial responses. copyright 2013 S. Karger AG, Basel
JF - Journal of Innate Immunity
AU - Ramirez, Jose Luis
AU - Garver, Lindsey S
AU - Brayner, Fbio Andr
AU - Alves, Luiz Carlos
AU - Rodrigues, Janneth
AU - Molina-Cruz, Alvaro
AU - Barillas-Mury, Carolina
AD - Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Md., USA
Y1 - 2014/02//
PY - 2014
DA - February 2014
SP - 119
EP - 128
PB - S. Karger AG, P.O. Box Basel CH-4009 Switzerland
VL - 6
IS - 2
SN - 1662-811X, 1662-811X
KW - ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Microbiology Abstracts C: Algology, Mycology & Protozoology; Immunology Abstracts
KW - Hemocyte differentiation
KW - Plasmodium
KW - Malaria
KW - Immune priming
KW - Cell survival
KW - Hemolymph
KW - c-Jun amino-terminal kinase
KW - Pest control
KW - Immunity
KW - Infection
KW - Strains
KW - Anopheles gambiae
KW - Plasmodium berghei
KW - Differentiation
KW - Suppressors
KW - Kinetics
KW - Hemocytes
KW - Antiprotozoal agents
KW - Aquatic insects
KW - Signal transduction
KW - K 03340:Effects of Physical & Chemical Factors
KW - F 06945:Insect Immunity
KW - Q1 08485:Species interactions: pests and control
KW - Q5 08524:Public health, medicines, dangerous organisms
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Innate+Immunity&rft.atitle=The+Role+of+Hemocytes+in+Anopheles+gambiae+Antiplasmodial+Immunity&rft.au=Ramirez%2C+Jose+Luis%3BGarver%2C+Lindsey+S%3BBrayner%2C+Fbio+Andr%3BAlves%2C+Luiz+Carlos%3BRodrigues%2C+Janneth%3BMolina-Cruz%2C+Alvaro%3BBarillas-Mury%2C+Carolina&rft.aulast=Ramirez&rft.aufirst=Jose&rft.date=2014-02-01&rft.volume=6&rft.issue=2&rft.spage=119&rft.isbn=&rft.btitle=&rft.title=Journal+of+Innate+Immunity&rft.issn=1662811X&rft_id=info:doi/10.1159%2F000353765
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-01
N1 - Last updated - 2016-09-14
N1 - SubjectsTermNotLitGenreText - Suppressors; Pest control; Immunity; Strains; Aquatic insects; Cell survival; Hemolymph; Differentiation; c-Jun amino-terminal kinase; Kinetics; Hemocytes; Antiprotozoal agents; Infection; Signal transduction; Anopheles gambiae; Plasmodium berghei
DO - http://dx.doi.org/10.1159/000353765
ER -
TY - JOUR
T1 - Print News Coverage of School-Based Human Papillomavirus Vaccine Mandates
AN - 1512193567; 201404606
AB - In 2007, legislation was proposed in 24 states and the District of Columbia for school-based human papillomavirus (HPV) vaccine mandates, and mandates were enacted in Texas, Virginia, and the District of Columbia. Media coverage of these events was extensive, and media messages both reflected and contributed to controversy surrounding these legislative activities. Messages communicated through the media are an important influence on adolescent and parent understanding of school-based vaccine mandates. We conducted structured text analysis of newspaper coverage, including quantitative analysis of 169 articles published in mandate jurisdictions from 2005 to 2009, and qualitative analysis of 63 articles from 2007. Our structured analysis identified topics, key stakeholders and sources, tone, and the presence of conflict. Qualitative thematic analysis identified key messages and issues. Media coverage was often incomplete, providing little context about cervical cancer or screening. Skepticism and autonomy concerns were common. Messages reflected conflict and distrust of government activities, which could negatively impact this and other youth-focused public health initiatives. If school health professionals are aware of the potential issues raised in media coverage of school-based health mandates, they will be more able to convey appropriate health education messages and promote informed decision-making by parents and students. Adapted from the source document.
JF - Journal of School Health
AU - Casciotti, Dana M
AU - Smith, Katherine C
AU - Andon, Lindsay
AU - Vernick, Jon
AU - Tsui, Amy
AU - Klassen, Ann C
AD - Program Analyst, National Library of Medicine, National Institutes of Health, 8600 Rockville Pike, Bethesda, MD 20894 danacasciotti@yahoo.com
Y1 - 2014/02//
PY - 2014
DA - February 2014
SP - 71
EP - 81
PB - Wiley-Blackwell, UK
VL - 84
IS - 2
SN - 0022-4391, 0022-4391
KW - Coverage
KW - Quantitative analysis
KW - School based
KW - Vaccines
KW - Parents
KW - Human papillomaviruses
KW - article
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+School+Health&rft.atitle=Print+News+Coverage+of+School-Based+Human+Papillomavirus+Vaccine+Mandates&rft.au=Casciotti%2C+Dana+M%3BSmith%2C+Katherine+C%3BAndon%2C+Lindsay%3BVernick%2C+Jon%3BTsui%2C+Amy%3BKlassen%2C+Ann+C&rft.aulast=Casciotti&rft.aufirst=Dana&rft.date=2014-02-01&rft.volume=84&rft.issue=2&rft.spage=71&rft.isbn=&rft.btitle=&rft.title=Journal+of+School+Health&rft.issn=00224391&rft_id=info:doi/10.1111%2Fjosh.12126
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Date revised - 2014-04-01
N1 - Last updated - 2016-09-27
N1 - SubjectsTermNotLitGenreText - Coverage; School based; Vaccines; Human papillomaviruses; Parents; Quantitative analysis
DO - http://dx.doi.org/10.1111/josh.12126
ER -
TY - JOUR
T1 - Biomechanics of Atherosclerotic Coronary Plaque: Site, Stability and In Vivo Elasticity Modeling
AN - 1505340384; 19348019
AB - Coronary atheroma develop in local sites that are widely variable among patients and are considerably variable in their vulnerability for rupture. This article summarizes studies conducted by our collaborative laboratories on predictive biomechanical modeling of coronary plaques. It aims to give insights into the role of biomechanics in the development and localization of atherosclerosis, the morphologic features that determine vulnerable plaque stability, and emerging in vivo imaging techniques that may detect and characterize vulnerable plaque. Composite biomechanical and hemodynamic factors that influence the actual site of development of plaques have been studied. Plaque vulnerability, in vivo, is more challenging to assess. Important steps have been made in defining the biomechanical factors that are predictive of plaque rupture and the likelihood of this occurring if characteristic features are known. A critical key in defining plaque vulnerability is the accurate quantification of both the morphology and the mechanical properties of the diseased arteries. Recently, an early IVUS based palpography technique developed to assess local strain, elasticity and mechanical instabilities has been successfully revisited and improved to account for complex plaque geometries. This is based on an initial best estimation of the plaque components' contours, allowing subsequent iteration for elastic modulus assessment as a basis for plaque stability determination. The improved method has also been preliminarily evaluated in patients with successful histologic correlation. Further clinical evaluation and refinement are on the horizon.
JF - Annals of Biomedical Engineering
AU - Ohayon, Jacques
AU - Finet, Gerard
AU - Floc'h, Simon
AU - Cloutier, Guy
AU - Gharib, Ahmed M
AU - Heroux, Julie
AU - Pettigrew, Roderic I
AD - Laboratory TIMC-IMAG/DyCTiM, UJF, CNRS UMR 5525, In3S, Grenoble, France, rpettigrew@nih.gov
Y1 - 2014/02//
PY - 2014
DA - Feb 2014
SP - 269
EP - 279
PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL - 42
IS - 2
SN - 0090-6964, 0090-6964
KW - Biotechnology and Bioengineering Abstracts
KW - Arteries
KW - Rupture
KW - Hemodynamics
KW - Plaques
KW - Arteriosclerosis
KW - imaging
KW - Biomechanics
KW - Mechanical properties
KW - W 30910:Imaging
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-03-01
N1 - Number of references - 83
N1 - Last updated - 2015-03-20
N1 - SubjectsTermNotLitGenreText - Arteries; Hemodynamics; Rupture; Plaques; Arteriosclerosis; imaging; Biomechanics; Mechanical properties
DO - http://dx.doi.org/10.1007/s10439-013-0888-1
ER -
TY - JOUR
T1 - Fighting Noise Pollution: A Public Health Strategy
AN - 1505339462; 19339770
AB - In this issue of EHP, investigators from the University of Michigan at Ann Arbor describe the most serious health effects of noise and propose a blueprint for an effective U.S. public health response. super(1) The team, led by Richard L. Neitzel, an assistant professor of environmental health sciences, estimated that nearly one-third of Americans are exposed to noise levels deemed injurious to hearing by the U.S. Environmental Protection Agency (EPA) - a 24-hour average noise level exceeding 70 dBA. super(1) The authors based this figure on 1981 estimates from the EPA. super(2)
JF - Environmental Health Perspectives
AU - Holzman, David C
AD - David C. Holzman writes on science, medicine, energy, economics, and cars from Lexington and Wellfleet, MA. His work has appeared in Smithsonian, The Atlantic Monthly, and the Journal of the National Cancer Institute.
Y1 - 2014/02/01/
PY - 2014
DA - 2014 Feb 01
SP - A58
PB - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States
VL - 122
IS - 2
SN - 0091-6765, 0091-6765
KW - Pollution Abstracts; Environment Abstracts; Health & Safety Science Abstracts; Sustainability Science Abstracts
KW - EPA
KW - Noise levels
KW - Environmental health
KW - Noise pollution
KW - Public health
KW - P 7000:NOISE
KW - M3 1010:Issues in Sustainable Development
KW - H 12000:Epidemiology and Public Health
KW - ENA 02:Toxicology & Environmental Safety
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-03-01
N1 - Last updated - 2015-05-13
N1 - SubjectsTermNotLitGenreText - EPA; Noise levels; Environmental health; Noise pollution; Public health
DO - http://dx.doi.org/10.1289/ehp.122-A58
ER -
TY - JOUR
T1 - Reduction of DNA mismatch repair protein expression in airway epithelial cells of premenopausal women chronically exposed to biomass smoke
AN - 1505330512; 19299307
AB - Biomass burning is a major source of indoor air pollution in rural India. This study examined whether chronic inhalation of biomass smoke causes change in the DNA mismatch repair (MMR) pathway in the airway cells. For this, airway cells exfoliated in sputum were collected from 72 premenopausal nonsmoking rural women (median age 34 years) who cooked with biomass (wood, dung, crop residues) and 68 control women who cooked with cleaner fuel liquefied petroleum gas (LPG) for the past 5 years or more. The levels of particulate matters with diameters less than 10 and 2.5 mu m (PM sub(10) and PM sub(2.5)) in indoor air were measured by real-time aerosol monitor. Benzene exposure was monitored by measuring trans,trans-muconic acid (t,t-MA) in urine by high-performance liquid chromatography with ultraviolet detector. Generation of reactive oxygen species (ROS) and level of superoxide dismutase (SOD) in airway cells were measured by flow cytometry and spectrophotometry, respectively. Immunocytochemical assay revealed lower percentage of airway epithelial cells expressing MMR proteins mutL homolog 1 (MLH1) and mutS homolog 2 (MSH2) in biomass-using women compared to LPG-using controls. Women who cooked with biomass had 6.7 times higher level of urinary t,t-MA, twofold increase in ROS generation, and 31 % depletion of SOD. Indoor air of biomass-using households had three times more particulate matters than that of controls. ROS, urinary t,t-MA, and particulate pollution in biomass-using kitchen had negative correlation, while SOD showed positive correlation with MSH2 and MLH1 expression. It appears that chronic exposure to biomass smoke reduces MMR response in airway epithelial cells, and oxidative stress plays an important role in the process.
JF - Environmental Science and Pollution Research International
AU - Mukherjee, Bidisha
AU - Dutta, Anindita
AU - Chowdhury, Saswati
AU - Roychoudhury, Sanghita
AU - Ray, Manas Ranjan
AD - Department of Experimental Hematology, Chittaranjan National Cancer Institute, 37, S. P. Mukherjee Road, Kolkata, 700 026, India, manasrray@rediffmail.com
PY - 2014
SP - 2826
EP - 2836
PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands
VL - 21
IS - 4
SN - 0944-1344, 0944-1344
KW - Biochemistry Abstracts 2: Nucleic Acids; Environment Abstracts; Pollution Abstracts
KW - High-performance liquid chromatography
KW - Inhalation
KW - Epithelial cells
KW - MLH1 protein
KW - Fuels
KW - Particulate matter
KW - Particulate pollution
KW - Particulates
KW - Benzene
KW - India
KW - Flow cytometry
KW - U.V. radiation
KW - Reactive oxygen species
KW - Oxidative stress
KW - Chronic exposure
KW - Superoxide dismutase
KW - Petroleum
KW - Spectrophotometry
KW - Respiratory tract
KW - MMR protein
KW - Aerosols
KW - MSH2 protein
KW - mismatch repair
KW - Wood
KW - Crop residues
KW - Biomass
KW - DNA repair
KW - Air pollution
KW - Smoke
KW - Liquid chromatography
KW - Urine
KW - Households
KW - DNA
KW - Dung
KW - Proteins
KW - Burning
KW - Sputum
KW - Indoor environments
KW - Rural areas
KW - P 0000:AIR POLLUTION
KW - N 14845:Miscellaneous
KW - ENA 01:Air Pollution
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-03-01
N1 - Number of references - 58
N1 - Last updated - 2016-01-21
N1 - SubjectsTermNotLitGenreText - Inhalation; High-performance liquid chromatography; MLH1 protein; Epithelial cells; Fuels; Particulate matter; Particulate pollution; Benzene; Flow cytometry; U.V. radiation; Reactive oxygen species; Superoxide dismutase; Chronic exposure; Oxidative stress; Petroleum; Spectrophotometry; Respiratory tract; MMR protein; MSH2 protein; Aerosols; mismatch repair; Crop residues; DNA repair; Biomass; Smoke; Air pollution; Urine; Dung; Sputum; Burning; Wood; Particulates; Liquid chromatography; Households; DNA; Proteins; Indoor environments; Rural areas; India
DO - http://dx.doi.org/10.1007/s11356-013-2218-4
ER -
TY - JOUR
T1 - Quantitative genetics of response to novelty and other stimuli by infant rhesus macaques (Macaca Mulatta) across three behavioral assessments
AN - 1504157079; 4535133
AB - Primate behavior is influenced by both heritable factors and environmental experience during development. Previous studies of rhesus macaques ( Macaca mulatta ) examined the effects of genetic variation on expressed behavior and related neurobiological traits (heritability and/or genetic association) using a variety of study designs. Most of these prior studies examined genetic effects on the behavior of adults or adolescent rhesus macaques, not in young macaques early in development. To assess environmental and additive genetic variation in behavioral reactivity and response to novelty among infants, we investigated a range of behavioral traits in a large number ( N = 428) of pedigreed infants born and housed in large outdoor corrals at the Oregon National Primate Research Center (ONPRC). We recorded the behavior of each subject during a series of brief tests, involving exposure of each infant to a novel environment, to a social threat without the mother present, and to a novel environment with its mother present but sedated. We found significant heritability ( h 2 ) for willingness to move away from the mother and explore a novel environment ( Italic h 2 = 0.25 ± 0.13; P = 0.003). The infants also exhibited a range of heritable behavioral reactions to separation stress or to threat when the mother was not present ( h Italic 2 = 0.23 ± 0.13-0.24 ± 0.15, P < 0.01). We observed no evidence of maternal environmental effects on these traits. Our results extend knowledge of genetic influences on temperament and reactivity in nonhuman primates by demonstrating that several measures of behavioral reactivity among infant rhesus macaques are heritable. Reprinted by permission of Springer
JF - International journal of primatology
AU - Fawcett, G L
AU - Dettmer, A M
AU - Kay, D
AU - Raveendran, M
AU - Higley, J D
AU - Ryan, N D
AU - Cameron, J L
AU - Rogers, J
AD - Baylor College of Medicine ; National Institutes of Health ; University of Florida ; Brigham Young University ; University of Pittsburgh
Y1 - 2014/02//
PY - 2014
DA - Feb 2014
SP - 325
EP - 339
VL - 35
IS - 1
SN - 0164-0291, 0164-0291
KW - Anthropology
KW - Genetics
KW - Primatology
KW - Anxiety
KW - Old World monkeys
KW - Primates
KW - Infants
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LA - English
DB - International Bibliography of the Social Sciences (IBSS)
N1 - Date revised - 2014-03-04
N1 - Last updated - 2014-03-05
N1 - SubjectsTermNotLitGenreText - 1147 4196; 5460 1615 8573 11325; 10149; 10148; 6495 2212; 8910 10148
DO - http://dx.doi.org/10.1007/s10764-014-9750-z
ER -
TY - JOUR
T1 - Consent under pressure: the puzzle of third party coercion
AN - 1504156823; 4535360
AB - Coercion by the recipient of consent renders that consent invalid. But what about when the coercive force comes from a third party, not from the person to whom consent would be proffered? In this paper I analyze how threats from a third party affect consent. I argue that, as with other cases of coercion, we should distinguish threats that render consent invalid from threats whose force is too weak to invalidate consent and threats that are legitimate. Illegitimate controlling third party threats render consent invalid just as they do in two party cases. However, knowing that the consent is invalid is not sufficient to tell the recipient of consent what she may or should do. I argue that when presented with a token of consent from someone whom she thinks is experiencing an illegitimate controlling threat, the recipient may act on that token if and only if doing so represents a reasonable joint decision for her and the victim of coercion. The appropriate action for someone faced with third party coercion therefore depends on the other options open to her and those open to the victim of coercion. Reprinted by permission of Springer
JF - Ethical theory and moral practice
AU - Millum, Joseph
AD - National Institutes of Health
Y1 - 2014/02//
PY - 2014
DA - Feb 2014
SP - 113
EP - 127
VL - 17
IS - 1
SN - 1386-2820, 1386-2820
KW - Sociology
KW - Two-party systems
KW - Legitimacy
KW - Medical research
KW - Third-party intervention
KW - Illegitimacy
KW - Victims of crime
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LA - English
DB - International Bibliography of the Social Sciences (IBSS)
N1 - Date revised - 2014-03-04
N1 - Last updated - 2014-03-05
N1 - SubjectsTermNotLitGenreText - 7886 10902; 12749 2703 2698 6828 7869 5200 5574 10472; 6216 13133 7253; 13035 9253; 13307 3015 11881; 7333 7315 9705
DO - http://dx.doi.org/10.1007/s10677-013-9419-2
ER -
TY - JOUR
T1 - Differential expression of p53 family proteins in colorectal adenomas and carcinomas: Prognostic and predictive values.
AN - 1503554675; 23996743
AB - We studied the contribution of p53 family proteins and their isoforms to the development and progression of colorectal carcinoma in relation to VEGF. p53, p63, p73 and VEGF proteins were assessed in 45 colorectal adenomas (CRAs), 80 carcinomas (CRCs) and 36 normal colonic tissue samples (NCT) by immunohistochemistry. Different p63 and p73 isoforms were assessed by RT-PCR. Aberrant protein and RNA expressions were correlated to patients' characteristics, disease free and overall survival (DFS and OS).
p53, p63, p73 and VEGF proteins were detected in 22.2%, 73.3%, 33.3%, 46.7% CRAs; in 68.8%, 38.8%, 62.5%, 62.5% CRCs and 16.7%, 83.3%; 13.9%, 41.7% NCT (p<0.05 except for VEGF). Commonest isoforms were TAp63α, ΔNp63, TAp73α in CRA and ΔNp63, TAp63α, ΔNp73, TAp73β in CRC. Significant correlations were found between aggressive tumor phenotypes and aberrations in p73, p53, p63, VEGF. DFS correlated with advanced stage, p73 and VEGF aberrations. While advanced stage, positive lymph nodes, p73 and p53 correlated with OS. Prognosis was worse in patients with aberrant p63 and p73 than in those with normal p63 and p73 expression regardless of p53 gene status (p⟨0.05).
p53 family proteins and VEGF play a pivotal role in colorectal carcinogenesis. p53 prognostic potential is augmented by p73 and p63 aberrations indicating a synergistic effect between the three family members. Nodal status, stage, p73, VEGF and p53 could be used as predictors of DFS and OS.
JF - Histology and histopathology
AU - Bahnassy, Abeer A
AU - Zekri, Abdel-Rahman N
AU - Salem, Salem E
AU - Abou-Bakr, Amany A
AU - Sakr, Mona A
AU - Abdel-Samiaa, Ayman G
AU - Al-Bradei, Manal
AD - Pathology Department, National Cancer Institute, Cairo University, Cairo, Egypt. chaya2000@hotmail.com. ; Cancer Biology Department, National Cancer Institute, Cairo University, Cairo, Egypt. ; Medical Oncology Department, National Cancer Institute, Cairo University, Cairo, Egypt. ; Pathology Department, National Cancer Institute, Cairo University, Cairo, Egypt. ; Radiotherapy Department, National Cancer Institute, Cairo University, Cairo, Egypt.
Y1 - 2014/02//
PY - 2014
DA - February 2014
SP - 207
EP - 216
VL - 29
IS - 2
KW - CKAP4 protein, human
KW - 0
KW - DNA-Binding Proteins
KW - Membrane Proteins
KW - Nuclear Proteins
KW - Tumor Protein p73
KW - Tumor Suppressor Protein p53
KW - Tumor Suppressor Proteins
KW - Vascular Endothelial Growth Factor A
KW - delta Np73 protein, human
KW - p73 protein, human
KW - Index Medicus
KW - Young Adult
KW - Colon -- pathology
KW - Humans
KW - Prognosis
KW - Intestinal Mucosa -- metabolism
KW - Predictive Value of Tests
KW - Prospective Studies
KW - Colon -- metabolism
KW - Adult
KW - Intestinal Mucosa -- pathology
KW - Middle Aged
KW - Female
KW - Male
KW - Nuclear Proteins -- genetics
KW - Colorectal Neoplasms -- metabolism
KW - Membrane Proteins -- metabolism
KW - Tumor Suppressor Proteins -- genetics
KW - DNA-Binding Proteins -- genetics
KW - Colorectal Neoplasms -- genetics
KW - Membrane Proteins -- genetics
KW - Tumor Suppressor Protein p53 -- metabolism
KW - Adenoma -- metabolism
KW - Carcinoma -- pathology
KW - Colorectal Neoplasms -- pathology
KW - Tumor Suppressor Proteins -- metabolism
KW - Tumor Suppressor Protein p53 -- genetics
KW - Nuclear Proteins -- metabolism
KW - Adenoma -- genetics
KW - Adenoma -- pathology
KW - Carcinoma -- metabolism
KW - Vascular Endothelial Growth Factor A -- genetics
KW - Vascular Endothelial Growth Factor A -- metabolism
KW - Carcinoma -- genetics
KW - DNA-Binding Proteins -- metabolism
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-09-19
N1 - Date created - 2014-02-04
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.14670/HH-29.207
ER -
TY - JOUR
T1 - Metabolism of synthetic cannabinoids PB-22 and its 5-fluoro analog, 5F-PB-22, by human hepatocyte incubation and high-resolution mass spectrometry.
AN - 1503550510; 24518903
AB - PB-22 (1-pentyl-8-quinolinyl ester-1H-indole-3-carboxylic acid) and 5F-PB-22 (1-(5-fluoropentyl)-8-quinolinyl ester-1H-indole-3-carboxylic acid) are new synthetic cannabinoids with a quinoline substructure and the first marketed substances with an ester bond linkage. No human metabolism data are currently available, making it difficult to document PB-22 and 5F-PB-22 intake from urine analysis, and complicating assessment of the drugs' pharmacodynamic and toxicological properties.
We incubated 10 μmol/l PB-22 and 5F-PB-22 with pooled cryopreserved human hepatocytes up to 3 h and analyzed samples on a TripleTOF 5600+ high-resolution mass spectrometer. Data were acquired via TOF scan, followed by information-dependent acquisition triggered product ion scans with mass defect filtering (MDF). The accurate mass full scan MS and MS/MS metabolite datasets were analyzed with multiple data processing techniques, including MDF, neutral loss and product ion filtering. The predominant metabolic pathway for PB-22 and 5F-PB-22 was ester hydrolysis yielding a wide variety of (5-fluoro)pentylindole-3-carboxylic acid metabolites. Twenty metabolites for PB-22 and 22 metabolites for 5F-PB-22 were identified, with the majority generated by oxidation with or without glucuronidation. For 5F-PB-22, oxidative defluorination occurred forming PB-22 metabolites. Both compounds underwent epoxide formation followed by internal hydrolysis and also produced a cysteine conjugate.
Human hepatic metabolic profiles were generated for PB-22 and 5F-PB-22. Pentylindole-3-carboxylic acid, hydroxypentyl-PB-22 and PB-22 pentanoic acid for PB-22, and 5'-fluoropentylindole-3-carboxylic acid, PB-22 pentanoic acid and the hydroxy-5F-PB-22 metabolite with oxidation at the quinoline system for 5F-PB-22 are likely the best targets to incorporate into analytical methods for urine to document PB-22 and 5F-PB-22 intake.
JF - Analytical and bioanalytical chemistry
AU - Wohlfarth, Ariane
AU - Gandhi, Adarsh S
AU - Pang, Shaokun
AU - Zhu, Mingshe
AU - Scheidweiler, Karl B
AU - Huestis, Marilyn A
AD - Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, 251 Bayview Boulevard, Baltimore, MD, 21224, USA.
Y1 - 2014/02//
PY - 2014
DA - February 2014
SP - 1763
EP - 1780
VL - 406
IS - 6
KW - Cannabinoids
KW - 0
KW - Indoles
KW - indole-3-carboxylic acid
KW - 771-50-6
KW - Index Medicus
KW - Oxidation-Reduction
KW - Spectrometry, Mass, Electrospray Ionization
KW - Cells, Cultured
KW - Humans
KW - Indoles -- metabolism
KW - Tandem Mass Spectrometry
KW - Indoles -- chemistry
KW - Hydrolysis
KW - Cannabinoids -- metabolism
KW - Cannabinoids -- chemistry
KW - Hepatocytes -- metabolism
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-10-21
N1 - Date created - 2014-02-27
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1007/s00216-014-7668-0
ER -
TY - JOUR
T1 - Assessment of CASP10 contact-assisted predictions
AN - 1500796382; 19044590
AB - In CASP10, for the first time, contact-assisted structure predictions have been assessed. Sets of pairs of contacting residues from target structures were provided to predictors for a second round of prediction after the initial round in which they were given only sequences. The objective of the experiment was to measure model quality improvement resulting from the added contact information and thereby assess and help develop so-called hybrid prediction methods-methods where some experimentally determined distance constraints are used to augment de novo computational prediction methods. The results of the experiment were, overall, quite promising. Proteins 2014; 82(Suppl 2):84-97. copyright 2013 Wiley Periodicals, Inc.
JF - Proteins: Structure, Function and Bioinformatics
AU - Taylor, Todd J
AU - Bai, Hongjun
AU - Tai, Chin-Hsien
AU - Lee, Byungkook
AD - Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland.
Y1 - 2014/02//
PY - 2014
DA - Feb 2014
SP - 84
EP - 97
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030 United States
VL - 82
SN - 0887-3585, 0887-3585
KW - Biotechnology and Bioengineering Abstracts
KW - Bioinformatics
KW - Hybrids
KW - W 30960:Bioinformatics & Computer Applications
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1500796382?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proteins%3A+Structure%2C+Function+and+Bioinformatics&rft.atitle=Assessment+of+CASP10+contact-assisted+predictions&rft.au=Taylor%2C+Todd+J%3BBai%2C+Hongjun%3BTai%2C+Chin-Hsien%3BLee%2C+Byungkook&rft.aulast=Taylor&rft.aufirst=Todd&rft.date=2014-02-01&rft.volume=82&rft.issue=&rft.spage=84&rft.isbn=&rft.btitle=&rft.title=Proteins%3A+Structure%2C+Function+and+Bioinformatics&rft.issn=08873585&rft_id=info:doi/10.1002%2Fprot.24367
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-02-01
N1 - Last updated - 2014-03-20
N1 - SubjectsTermNotLitGenreText - Hybrids
DO - http://dx.doi.org/10.1002/prot.24367
ER -
TY - JOUR
T1 - Assessment of template-free modeling in CASP10 and ROLL
AN - 1500784250; 19044580
AB - We present the assessment of predictions for Template-Free Modeling in CASP10 and a report on the first ROLL experiment wherein predictions are collected year round for review at the regular CASP season. Models were first clustered so that duplicated or very similar ones were grouped together and represented by one model in the cluster. The representatives were then compared with targets using GDT_TS, QCS, and three additional superposition-independent score functions newly developed for CASP10. For each target, the top 15 representatives by each score were pooled to form the Top15Union set. All models in this set were visually inspected by four of us independently using the new plugin, EvalScore, which we developed with the UCSF Chimera group. The best models were selected for each target after extensive debate among the four examiners. Groups were ranked by the number of targets (hits) for which a group's model was selected as one of the best models. The Keasar group had most hits in both categories, with four of 19 FM and eight of 36 ROLL targets. The most successful prediction servers were QUARK from Zhang's group for FM category with three hits and Zhang-server for the ROLL category with seven hits. As observed in CASP9, many successful groups were not true "template-free" modelers but used remote templates and/or server models to obtain their winning models. The results of the first ROLL experiment were broadly similar to those of the CASP10 FM exercise. Proteins 2014; 82(Suppl 2):57-83. copyright 2013 Wiley Periodicals, Inc.
JF - Proteins: Structure, Function and Bioinformatics
AU - Tai, Chin-Hsien
AU - Bai, Hongjun
AU - Taylor, Todd J
AU - Lee, Byungkook
AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, 20892.
Y1 - 2014/02//
PY - 2014
DA - Feb 2014
SP - 57
EP - 83
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030 United States
VL - 82
SN - 0887-3585, 0887-3585
KW - Biotechnology and Bioengineering Abstracts
KW - Bioinformatics
KW - Models
KW - W 30960:Bioinformatics & Computer Applications
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1500784250?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proteins%3A+Structure%2C+Function+and+Bioinformatics&rft.atitle=Assessment+of+template-free+modeling+in+CASP10+and+ROLL&rft.au=Tai%2C+Chin-Hsien%3BBai%2C+Hongjun%3BTaylor%2C+Todd+J%3BLee%2C+Byungkook&rft.aulast=Tai&rft.aufirst=Chin-Hsien&rft.date=2014-02-01&rft.volume=82&rft.issue=&rft.spage=57&rft.isbn=&rft.btitle=&rft.title=Proteins%3A+Structure%2C+Function+and+Bioinformatics&rft.issn=08873585&rft_id=info:doi/10.1002%2Fprot.24470
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-02-01
N1 - Last updated - 2014-03-20
N1 - SubjectsTermNotLitGenreText - Models
DO - http://dx.doi.org/10.1002/prot.24470
ER -
TY - JOUR
T1 - Evaluation of engraftment and immunological tolerance after reduced intensity conditioning in a rhesus hematopoietic stem cell gene therapy model
AN - 1500780058; 19282638
AB - Reduced intensity conditioning (RIC) is desirable for hematopoietic stem cell (HSC) targeted gene therapy; however, RIC may be insufficient for efficient engraftment and inducing immunological tolerance to transgenes. We previously established long-term gene marking in our rhesus macaque autologous HSC transplantation model following 10 Gy total body irradiation (TBI). In this study, we evaluated RIC transplantation with 4 Gy TBI in two rhesus macaques that received equal parts of CD34 super(+) cells transduced with green fluorescent protein (GFP)-expressing lentiviral vector and empty vector not expressing transgenes. In both animals, equivalently low gene marking between GFP and empty vectors was observed 6 months post-transplantation, even with efficient transduction of CD34 super(+) cells in vitro. Autologous lymphocyte infusion with GFP marking resulted in an increase of gene marking in lymphocytes in a control animal with GFP tolerance, but not in the two RIC-transplanted animals. In vitro assays revealed strong cellular and humoral immune responses to GFP protein in the two RIC-transplanted animals, but this was not observed in controls. In summary, 4 Gy TBI is insufficient to permit engraftment of genetically modified HSCs and induce immunological tolerance to transgenes. Our findings should help in the design of conditioning regimens in gene therapy trials.
JF - Gene Therapy
AU - Uchida, N
AU - Weitzel, R P
AU - Evans, M E
AU - Green, R
AU - Bonifacino, A C
AU - Krouse, A E
AU - Metzger, M E
AU - Hsieh, M M
AU - Donahue, R E
AU - Tisdale, J F
AD - Molecular and Clinical Hematology Branch, National Heart Lung and Blood Institutes (NHLBI)/National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), National Institutes of Health (NIH), Bethesda, MD, USA
Y1 - 2014/02//
PY - 2014
DA - Feb 2014
SP - 148
EP - 157
PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL - 21
IS - 2
SN - 0969-7128, 0969-7128
KW - Genetics Abstracts; Biotechnology and Bioengineering Abstracts
KW - Autografts
KW - Macaca mulatta
KW - Immunological tolerance
KW - W 30905:Medical Applications
KW - G 07730:Development & Cell Cycle
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gene+Therapy&rft.atitle=Evaluation+of+engraftment+and+immunological+tolerance+after+reduced+intensity+conditioning+in+a+rhesus+hematopoietic+stem+cell+gene+therapy+model&rft.au=Uchida%2C+N%3BWeitzel%2C+R+P%3BEvans%2C+M+E%3BGreen%2C+R%3BBonifacino%2C+A+C%3BKrouse%2C+A+E%3BMetzger%2C+M+E%3BHsieh%2C+M+M%3BDonahue%2C+R+E%3BTisdale%2C+J+F&rft.aulast=Uchida&rft.aufirst=N&rft.date=2014-02-01&rft.volume=21&rft.issue=2&rft.spage=148&rft.isbn=&rft.btitle=&rft.title=Gene+Therapy&rft.issn=09697128&rft_id=info:doi/10.1038%2Fgt.2013.67
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-02-01
N1 - Last updated - 2014-03-20
N1 - SubjectsTermNotLitGenreText - Immunological tolerance; Macaca mulatta
DO - http://dx.doi.org/10.1038/gt.2013.67
ER -
TY - JOUR
T1 - Definition and classification of evaluation units for CASP10
AN - 1500759241; 19044582
AB - For the 10th experiment on Critical Assessment of the techniques of protein Structure Prediction (CASP), the prediction target proteins were broken into independent evaluation units (EUs), which were then classified into template-based modeling (TBM) or free modeling (FM) categories. We describe here how the EUs were defined and classified, what issues arose in the process, and how we resolved them. EUs are frequently not the whole target proteins but the constituting structural domains. However, the assessors from CASP7 on combined more than one domain into 1 EU for some targets, which implied that the assessment also included evaluation of the prediction of the relative position and orientation of these domains. In CASP10, we followed and expanded this notion by defining multidomain EUs for a number of targets. These included 3 EUs, each made of two domains of familiar fold but arranged in a novel manner and for which the focus of evaluation was the interdomain arrangement. An EU was classified to the TBM category if a template could be found by sequence similarity searches and to FM if a structural template could not be found by structural similarity searches. The EUs that did not fall cleanly in either of these cases were classified case-by-case, often including consideration of the overall quality and characteristics of the predictions. Proteins 2014; 82(Suppl 2):14-25. copyright 2013 Wiley Periodicals, Inc.
JF - Proteins: Structure, Function and Bioinformatics
AU - Taylor, Todd J
AU - Tai, Chin-Hsien
AU - Huang, Yuanpeng J
AU - Block, Jeremy
AU - Bai, Hongjun
AU - Kryshtafovych, Andriy
AU - Montelione, Gaetano T
AU - Lee, Byungkook
AD - Laboratory of Molecular Biology, Center for Cancer Research National Cancer Institute National Institutes of Health, Bethesda, Maryland, 20892-4264.
Y1 - 2014/02//
PY - 2014
DA - Feb 2014
SP - 14
EP - 25
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030 United States
VL - 82
SN - 0887-3585, 0887-3585
KW - Biotechnology and Bioengineering Abstracts
KW - Bioinformatics
KW - Protein structure
KW - W 30960:Bioinformatics & Computer Applications
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1500759241?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proteins%3A+Structure%2C+Function+and+Bioinformatics&rft.atitle=Definition+and+classification+of+evaluation+units+for+CASP10&rft.au=Taylor%2C+Todd+J%3BTai%2C+Chin-Hsien%3BHuang%2C+Yuanpeng+J%3BBlock%2C+Jeremy%3BBai%2C+Hongjun%3BKryshtafovych%2C+Andriy%3BMontelione%2C+Gaetano+T%3BLee%2C+Byungkook&rft.aulast=Taylor&rft.aufirst=Todd&rft.date=2014-02-01&rft.volume=82&rft.issue=&rft.spage=14&rft.isbn=&rft.btitle=&rft.title=Proteins%3A+Structure%2C+Function+and+Bioinformatics&rft.issn=08873585&rft_id=info:doi/10.1002%2Fprot.24434
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-02-01
N1 - Last updated - 2014-03-20
N1 - SubjectsTermNotLitGenreText - Protein structure
DO - http://dx.doi.org/10.1002/prot.24434
ER -
TY - JOUR
T1 - Stereospecific PARP trapping by BMN 673 and comparison with olaparib and rucaparib.
AN - 1499149824; 24356813
AB - Anti-PARP drugs were initially developed as catalytic inhibitors to block the repair of DNA single-strand breaks. We recently reported that several PARP inhibitors have an additional cytotoxic mechanism by trapping PARP-DNA complexes, and that both olaparib and niraparib act as PARP poisons at pharmacologic concentrations. Therefore, we have proposed that PARP inhibitors should be evaluated based both on catalytic PARP inhibition and PARP-DNA trapping. Here, we evaluated the novel PARP inhibitor, BMN 673, and compared its effects on PARP1 and PARP2 with two other clinical PARP inhibitors, olaparib and rucaparib, using biochemical and cellular assays in genetically modified chicken DT40 and human cancer cell lines. Although BMN 673, olaparib, and rucaparib are comparable at inhibiting PARP catalytic activity, BMN 673 is ∼100-fold more potent at trapping PARP-DNA complexes and more cytotoxic as single agent than olaparib, whereas olaparib and rucaparib show similar potencies in trapping PARP-DNA complexes. The high level of resistance of PARP1/2 knockout cells to BMN 673 demonstrates the selectivity of BMN 673 for PARP1/2. Moreover, we show that BMN 673 acts by stereospecific binding to PARP1 as its enantiomer, LT674, is several orders of magnitude less efficient. BMN 673 is also approximately 100-fold more cytotoxic than olaparib and rucaparib in combination with the DNA alkylating agents methyl methane sulfonate (MMS) and temozolomide. Our study demonstrates that BMN 673 is the most potent clinical PARP inhibitor tested to date with the highest efficiency at trapping PARP-DNA complexes.
JF - Molecular cancer therapeutics
AU - Murai, Junko
AU - Huang, Shar-Yin N
AU - Renaud, Amèlie
AU - Zhang, Yiping
AU - Ji, Jiuping
AU - Takeda, Shunichi
AU - Morris, Joel
AU - Teicher, Beverly
AU - Doroshow, James H
AU - Pommier, Yves
AD - Corresponding Author: Yves Pommier, Developmental Therapeutics Branch, Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, 37 Convent Drive, Building 37, Room 5068, NIH, Bethesda, MD 20892-4255. pommier@nih.gov.
Y1 - 2014/02//
PY - 2014
DA - February 2014
SP - 433
EP - 443
VL - 13
IS - 2
KW - Enzyme Inhibitors
KW - 0
KW - Indoles
KW - Phthalazines
KW - Piperazines
KW - Poly(ADP-ribose) Polymerase Inhibitors
KW - talazoparib
KW - Dacarbazine
KW - 7GR28W0FJI
KW - rucaparib
KW - 8237F3U7EH
KW - Adenosine Triphosphate
KW - 8L70Q75FXE
KW - DNA
KW - 9007-49-2
KW - Methyl Methanesulfonate
KW - AT5C31J09G
KW - Poly(ADP-ribose) Polymerases
KW - EC 2.4.2.30
KW - olaparib
KW - WOH1JD9AR8
KW - temozolomide
KW - YF1K15M17Y
KW - Index Medicus
KW - Molecular Structure
KW - Immunoblotting
KW - Animals
KW - Stereoisomerism
KW - Poly(ADP-ribose) Polymerases -- chemistry
KW - Dose-Response Relationship, Drug
KW - Humans
KW - DNA -- metabolism
KW - Cell Line, Tumor
KW - Poly(ADP-ribose) Polymerases -- metabolism
KW - Methyl Methanesulfonate -- pharmacology
KW - Fluorescence Polarization
KW - Cell Survival -- drug effects
KW - Dacarbazine -- analogs & derivatives
KW - Dacarbazine -- pharmacology
KW - Adenosine Triphosphate -- metabolism
KW - DNA -- chemistry
KW - Enzyme Inhibitors -- pharmacology
KW - Inhibitory Concentration 50
KW - Drug Synergism
KW - Cell Cycle -- drug effects
KW - Phthalazines -- chemistry
KW - Indoles -- pharmacology
KW - Piperazines -- pharmacology
KW - Phthalazines -- pharmacology
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-02-19
N1 - Date created - 2014-02-11
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Nature. 2012 Jan 19;481(7381):287-94 [22258607]
J Biol Chem. 2012 Feb 3;287(6):4198-210 [22158865]
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Cancer Res. 2006 Aug 15;66(16):8109-15 [16912188]
Front Biosci. 2008;13:3046-82 [17981777]
Nat Rev Cancer. 2008 Mar;8(3):193-204 [18256616]
J Clin Oncol. 2008 Aug 1;26(22):3785-90 [18591545]
Clin Cancer Res. 2008 Dec 1;14(23):7917-23 [19047122]
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Cell. 2010 Apr 16;141(2):243-54 [20362325]
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Mol Oncol. 2011 Aug;5(4):387-93 [21821475]
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Breast Cancer Res Treat. 2012 Jul;134(2):649-59 [22678161]
Cancer Res. 2012 Nov 1;72(21):5588-99 [23118055]
Cancer Discov. 2013 Jan;3(1):68-81 [23103855]
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PLoS One. 2013;8(4):e61520 [23634208]
Clin Cancer Res. 2013 Sep 15;19(18):5003-15 [23881923]
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Mol Cell Biol. 2000 Jun;20(11):3977-87 [10805740]
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Mol Cancer Ther. 2006 Mar;5(3):564-74 [16546970]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1158/1535-7163.MCT-13-0803
ER -
TY - JOUR
T1 - The interactive roles of zinc and calcium in mitochondrial dysfunction and neurodegeneration.
AN - 1499140028; 24127746
AB - Zinc has been implicated in neurodegeneration following ischemia. In analogy with calcium, zinc has been proposed to induce toxicity via mitochondrial dysfunction, but the relative role of each cation in mitochondrial damage remains unclear. Here, we report that under conditions mimicking ischemia in hippocampal neurons - normal (2 mM) calcium plus elevated (> 100 μM) exogenous zinc - mitochondrial dysfunction evoked by glutamate, kainate or direct depolarization is, despite significant zinc uptake, primarily governed by calcium. Thus, robust mitochondrial ion accumulation, swelling, depolarization, and reactive oxygen species generation were only observed after toxic stimulation in calcium-containing media. This contrasts with the lack of any mitochondrial response in zinc-containing but calcium-free medium, even though zinc uptake and toxicity were strong under these conditions. Indeed, abnormally high, ionophore-induced zinc uptake was necessary to elicit any mitochondrial depolarization. In calcium- and zinc-containing media, depolarization-induced zinc uptake facilitated cell death and enhanced accumulation of mitochondrial calcium, which localized to characteristic matrix precipitates. Some of these contained detectable amounts of zinc. Together these data indicate that zinc uptake is generally insufficient to trigger mitochondrial dysfunction, so that mechanism(s) of zinc toxicity must be different from that of calcium. Published 2013. This article is a U.S. Government work and is in the public domain in the USA.
JF - Journal of neurochemistry
AU - Pivovarova, Natalia B
AU - Stanika, Ruslan I
AU - Kazanina, Galina
AU - Villanueva, Idalis
AU - Andrews, S Brian
AD - Laboratory of Neurobiology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA.
Y1 - 2014/02//
PY - 2014
DA - February 2014
SP - 592
EP - 602
VL - 128
IS - 4
KW - Calcium Channels
KW - 0
KW - Indicators and Reagents
KW - Reactive Oxygen Species
KW - Receptors, AMPA
KW - Zinc
KW - J41CSQ7QDS
KW - Calcium
KW - SY7Q814VUP
KW - Index Medicus
KW - cell death
KW - hippocampal neurons
KW - excitotoxicity
KW - ischemia
KW - electron microscopy
KW - Mitochondrial Swelling -- physiology
KW - Electron Probe Microanalysis
KW - Animals
KW - Cytosol -- metabolism
KW - Calcium Channels -- physiology
KW - Receptors, AMPA -- physiology
KW - Pregnancy
KW - Hippocampus -- drug effects
KW - Rats
KW - Microscopy, Fluorescence
KW - Electrophysiological Phenomena -- drug effects
KW - Rats, Sprague-Dawley
KW - Brain Ischemia -- pathology
KW - Cells, Cultured
KW - Hippocampus -- cytology
KW - Microscopy, Electron
KW - Female
KW - Neurodegenerative Diseases -- physiopathology
KW - Zinc -- pharmacology
KW - Calcium -- toxicity
KW - Mitochondrial Diseases -- physiopathology
KW - Mitochondrial Diseases -- metabolism
KW - Zinc -- physiology
KW - Zinc -- toxicity
KW - Neurodegenerative Diseases -- metabolism
KW - Calcium -- physiology
KW - Calcium -- pharmacology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+neurochemistry&rft.atitle=The+interactive+roles+of+zinc+and+calcium+in+mitochondrial+dysfunction+and+neurodegeneration.&rft.au=Pivovarova%2C+Natalia+B%3BStanika%2C+Ruslan+I%3BKazanina%2C+Galina%3BVillanueva%2C+Idalis%3BAndrews%2C+S+Brian&rft.aulast=Pivovarova&rft.aufirst=Natalia&rft.date=2014-02-01&rft.volume=128&rft.issue=4&rft.spage=592&rft.isbn=&rft.btitle=&rft.title=Journal+of+neurochemistry&rft.issn=1471-4159&rft_id=info:doi/10.1111%2Fjnc.12489
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-04-08
N1 - Date created - 2014-02-10
N1 - Date revised - 2017-01-13
N1 - SuppNotes - Cited By:
J Neurochem. 2008 Sep;106(5):2184-93 [18624907]
Ann Neurol. 2008 Jun;63(6):720-8 [18496842]
J Neurosci. 2009 Jan 28;29(4):1105-14 [19176819]
J Neurochem. 2009 Mar;108(5):1300-8 [19183267]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1111/jnc.12489
ER -
TY - JOUR
T1 - Lundep, a sand fly salivary endonuclease increases Leishmania parasite survival in neutrophils and inhibits XIIa contact activation in human plasma.
AN - 1499136132; 24516388
AB - Neutrophils are the host's first line of defense against infections, and their extracellular traps (NET) were recently shown to kill Leishmania parasites. Here we report a NET-destroying molecule (Lundep) from the salivary glands of Lutzomyia longipalpis. Previous analysis of the sialotranscriptome of Lu. longipalpis showed the potential presence of an endonuclease. Indeed, not only was the cloned cDNA (Lundep) shown to encode a highly active ss- and dsDNAse, but also the same activity was demonstrated to be secreted by salivary glands of female Lu. longipalpis. Lundep hydrolyzes both ss- and dsDNA with little sequence specificity with a calculated DNase activity of 300000 Kunitz units per mg of protein. Disruption of PMA (phorbol 12 myristate 13 acetate)- or parasite-induced NETs by treatment with recombinant Lundep or salivary gland homogenates increases parasite survival in neutrophils. Furthermore, co-injection of recombinant Lundep with metacyclic promastigotes significantly exacerbates Leishmania infection in mice when compared with PBS alone or inactive (mutagenized) Lundep. We hypothesize that Lundep helps the parasite to establish an infection by allowing it to escape from the leishmanicidal activity of NETs early after inoculation. Lundep may also assist blood meal intake by lowering the local viscosity caused by the release of host DNA and as an anticoagulant by inhibiting the intrinsic pathway of coagulation.
JF - PLoS pathogens
AU - Chagas, Andrezza C
AU - Oliveira, Fabiano
AU - Debrabant, Alain
AU - Valenzuela, Jesus G
AU - Ribeiro, José M C
AU - Calvo, Eric
AD - Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland, United States of America. ; Laboratory of Emerging Pathogens, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, Maryland, United States of America.
Y1 - 2014/02//
PY - 2014
DA - February 2014
SP - 1
VL - 10
IS - 2
KW - Endonucleases
KW - EC 3.1.-
KW - Factor XIIa
KW - EC 3.4.21.38
KW - Index Medicus
KW - Animals
KW - Disease Vectors
KW - Salivary Glands -- immunology
KW - Blood Coagulation -- physiology
KW - Neutrophils -- immunology
KW - Humans
KW - Amino Acid Sequence
KW - Mice
KW - Salivary Glands -- enzymology
KW - Polymerase Chain Reaction
KW - Leishmania
KW - Blotting, Western
KW - Neutrophils -- parasitology
KW - Factor XIIa -- metabolism
KW - Molecular Sequence Data
KW - Endonucleases -- metabolism
KW - Endonucleases -- immunology
KW - Leishmaniasis -- enzymology
KW - Host-Parasite Interactions -- physiology
KW - Psychodidae -- parasitology
KW - Psychodidae -- immunology
KW - Leishmaniasis -- immunology
KW - Psychodidae -- enzymology
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1499136132?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PLoS+pathogens&rft.atitle=Lundep%2C+a+sand+fly+salivary+endonuclease+increases+Leishmania+parasite+survival+in+neutrophils+and+inhibits+XIIa+contact+activation+in+human+plasma.&rft.au=Chagas%2C+Andrezza+C%3BOliveira%2C+Fabiano%3BDebrabant%2C+Alain%3BValenzuela%2C+Jesus+G%3BRibeiro%2C+Jos%C3%A9+M+C%3BCalvo%2C+Eric&rft.aulast=Chagas&rft.aufirst=Andrezza&rft.date=2014-02-01&rft.volume=10&rft.issue=2&rft.spage=e1003923&rft.isbn=&rft.btitle=&rft.title=PLoS+pathogens&rft.issn=1553-7374&rft_id=info:doi/10.1371%2Fjournal.ppat.1003923
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-10-03
N1 - Date created - 2014-02-11
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Infect Immun. 2011 Mar;79(3):1124-33 [21189319]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1371/journal.ppat.1003923
ER -
TY - JOUR
T1 - Evaluation in mice of a conjugate vaccine for cholera made from Vibrio cholerae O1 (Ogawa) O-specific polysaccharide.
AN - 1499136113; 24516685
AB - Protective immunity against cholera is serogroup specific. Serogroup specificity in Vibrio cholerae is determined by the O-specific polysaccharide (OSP) of lipopolysaccharide (LPS). Generally, polysaccharides are poorly immunogenic, especially in young children.
Here we report the evaluation in mice of a conjugate vaccine for cholera (OSP:TThc) made from V. cholerae O1 Ogawa O-Specific Polysaccharide-core (OSP) and recombinant tetanus toxoid heavy chain fragment (TThc). We immunized mice intramuscularly on days 0, 21, and 42 with OSP:TThc or OSP only, with or without dmLT, a non-toxigenic immunoadjuvant derived from heat labile toxin of Escherichia coli. We detected significant serum IgG antibody responses targeting OSP following a single immunization in mice receiving OSP:TThc with or without adjuvant. Anti-LPS IgG responses were detected following a second immunization in these cohorts. No anti-OSP or anti-LPS IgG responses were detected at any time in animals receiving un-conjugated OSP with or without immunoadjuvant, and in animals receiving immunoadjuvant alone. Responses were highest following immunization with adjuvant. Serum anti-OSP IgM responses were detected in mice receiving OSP:TThc with or without immunoadjuvant, and in mice receiving unconjugated OSP. Serum anti-LPS IgM and vibriocidal responses were detected in all vaccine cohorts except in mice receiving immunoadjuvant alone. No significant IgA anti-OSP or anti-LPS responses developed in any group. Administration of OSP:TThc and adjuvant also induced memory B cell responses targeting OSP and resulted in 95% protective efficacy in a mouse lethality cholera challenge model.
We describe a protectively immunogenic cholera conjugate in mice. Development of a cholera conjugate vaccine could assist in inducing long-term protective immunity, especially in young children who respond poorly to polysaccharide antigens.
JF - PLoS neglected tropical diseases
AU - Alam, Mohammad Murshid
AU - Bufano, Megan Kelly
AU - Xu, Peng
AU - Kalsy, Anuj
AU - Yu, Y
AU - Freeman, Y Wu
AU - Sultana, Tania
AU - Rashu, Md Rasheduzzaman
AU - Desai, Ishaan
AU - Eckhoff, Grace
AU - Leung, Daniel T
AU - Charles, Richelle C
AU - LaRocque, Regina C
AU - Harris, Jason B
AU - Clements, John D
AU - Calderwood, Stephen B
AU - Qadri, Firdausi
AU - Vann, W F
AU - Kováč, Pavol
AU - Ryan, Edward T
AD - Division of Infectious Diseases, Massachusetts General Hospital, Boston, Massachusetts, United States of America ; International Centre for Diarrheal Disease Research, Bangladesh (ICDDR,B), Dhaka, Bangladesh. ; Division of Infectious Diseases, Massachusetts General Hospital, Boston, Massachusetts, United States of America. ; NIDDK, LBC, National Institutes of Health, Bethesda, Maryland, United States of America. ; Division of Infectious Diseases, Massachusetts General Hospital, Boston, Massachusetts, United States of America ; International Centre for Diarrheal Disease Research, Bangladesh (ICDDR,B), Dhaka, Bangladesh ; Department of Medicine, Harvard Medical School, Boston, Massachusetts, United States of America. ; Division of Infectious Diseases, Massachusetts General Hospital, Boston, Massachusetts, United States of America ; Department of Medicine, Harvard Medical School, Boston, Massachusetts, United States of America. ; Division of Infectious Diseases, Massachusetts General Hospital, Boston, Massachusetts, United States of America ; Department of Pediatrics, Harvard Medical School, Boston, Massachusetts, United States of America. ; Tulane University School of Medicine, New Orleans, Louisiana, United States of America. ; Division of Infectious Diseases, Massachusetts General Hospital, Boston, Massachusetts, United States of America ; Department of Medicine, Harvard Medical School, Boston, Massachusetts, United States of America ; Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts, United States of America. ; International Centre for Diarrheal Disease Research, Bangladesh (ICDDR,B), Dhaka, Bangladesh. ; CBER, FDA, Laboratory of Bacterial Toxins, Bethesda, Maryland, United States of America. ; Division of Infectious Diseases, Massachusetts General Hospital, Boston, Massachusetts, United States of America ; Department of Medicine, Harvard Medical School, Boston, Massachusetts, United States of America ; Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts, United States of America.
Y1 - 2014/02//
PY - 2014
DA - February 2014
SP - 1
VL - 8
IS - 2
KW - Antibodies, Bacterial
KW - 0
KW - Cholera Vaccines
KW - O Antigens
KW - Recombinant Proteins
KW - Vaccines, Conjugate
KW - Index Medicus
KW - Animals
KW - Recombinant Proteins -- metabolism
KW - Recombinant Proteins -- immunology
KW - Antibodies, Bacterial -- blood
KW - Disease Models, Animal
KW - Mice
KW - Recombinant Proteins -- chemistry
KW - Female
KW - Cholera Vaccines -- chemistry
KW - Cholera -- mortality
KW - Vaccines, Conjugate -- immunology
KW - Cholera -- immunology
KW - Cholera Vaccines -- immunology
KW - O Antigens -- metabolism
KW - O Antigens -- immunology
KW - Cholera -- prevention & control
KW - Vaccines, Conjugate -- chemistry
KW - O Antigens -- chemistry
KW - Cholera Vaccines -- metabolism
KW - Vaccines, Conjugate -- metabolism
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1499136113?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PLoS+neglected+tropical+diseases&rft.atitle=Evaluation+in+mice+of+a+conjugate+vaccine+for+cholera+made+from+Vibrio+cholerae+O1+%28Ogawa%29+O-specific+polysaccharide.&rft.au=Alam%2C+Mohammad+Murshid%3BBufano%2C+Megan+Kelly%3BXu%2C+Peng%3BKalsy%2C+Anuj%3BYu%2C+Y%3BFreeman%2C+Y+Wu%3BSultana%2C+Tania%3BRashu%2C+Md+Rasheduzzaman%3BDesai%2C+Ishaan%3BEckhoff%2C+Grace%3BLeung%2C+Daniel+T%3BCharles%2C+Richelle+C%3BLaRocque%2C+Regina+C%3BHarris%2C+Jason+B%3BClements%2C+John+D%3BCalderwood%2C+Stephen+B%3BQadri%2C+Firdausi%3BVann%2C+W+F%3BKov%C3%A1%C4%8D%2C+Pavol%3BRyan%2C+Edward+T&rft.aulast=Alam&rft.aufirst=Mohammad&rft.date=2014-02-01&rft.volume=8&rft.issue=2&rft.spage=e2683&rft.isbn=&rft.btitle=&rft.title=PLoS+neglected+tropical+diseases&rft.issn=1935-2735&rft_id=info:doi/10.1371%2Fjournal.pntd.0002683
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-11-03
N1 - Date created - 2014-02-11
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Infect Immun. 2000 Feb;68(2):977-81 [10639476]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1371/journal.pntd.0002683
ER -
TY - JOUR
T1 - Inhibition of tumorigenesis by the thyroid hormone receptor β in xenograft models.
AN - 1499136035; 23731250
AB - Previous studies showed a close association between several types of human cancers and somatic mutations of thyroid hormone receptor β (TRβ) and reduced expression of TRβ due to epigenetic inactivation and/or deletion of the THRB gene. These observations suggest that TRβ could act as a tumor suppressor in carcinogenesis. However, the mechanisms by which TRβ could function to inhibit tumorigenesis are less well understood.
We used the human follicular thyroid cancer cell lines (FTC-133 and FTC-236 cells) to elucidate how functional expression of the THRB gene could affect tumorigenesis. We stably expressed the THRB gene in FTC cells and evaluated the effects of the expressed TRβ on cancer cell proliferation, migration, and tumor growth in cell-based studies and xenograft models. Expression of TRβ in FTC-133 cells, as compared with control FTC cells without TRβ, reduced cancer cell proliferation and impeded migration of tumor cells through inhibition of the AKT-mTOR-p70 S6K pathway. TRβ expression in FTC-133 and FTC-236 led to less tumor growth in xenograft models. Importantly, new vessel formation was significantly suppressed in tumors induced by FTC cells expressing TRβ compared with control FTC cells without TRβ. The decrease in vessel formation was mediated by the downregulation of vascular endothelial growth factor in FTC cells expressing TRβ.
These findings indicate that TRβ acts as a tumor suppressor through downregulation of the AKT-mTOR-p70 S6K pathway and decreased vascular endothelial growth factor expression in FTC cells. The present results raise the possibility that TRβ could be considered as a potential therapeutic target for thyroid cancer.
JF - Thyroid : official journal of the American Thyroid Association
AU - Kim, Won Gu
AU - Zhao, Li
AU - Kim, Dong Wook
AU - Willingham, Mark C
AU - Cheng, Sheue-yann
AD - Laboratory of Molecular Biology, Center for Cancer Research , National Cancer Institute, Bethesda, Maryland.
Y1 - 2014/02//
PY - 2014
DA - February 2014
SP - 260
EP - 269
VL - 24
IS - 2
KW - Angiogenesis Inhibitors
KW - 0
KW - Thyroid Hormone Receptors beta
KW - Tumor Suppressor Proteins
KW - VEGFA protein, human
KW - Vascular Endothelial Growth Factor A
KW - Triiodothyronine
KW - 06LU7C9H1V
KW - MTOR protein, human
KW - EC 2.7.1.1
KW - TOR Serine-Threonine Kinases
KW - Index Medicus
KW - Heterografts
KW - Angiogenesis Inhibitors -- physiology
KW - Animals
KW - Vascular Endothelial Growth Factor A -- biosynthesis
KW - Triiodothyronine -- pharmacology
KW - Humans
KW - Cell Line, Tumor
KW - Mice
KW - Mice, Nude
KW - Vascular Endothelial Growth Factor A -- antagonists & inhibitors
KW - Neoplasm Transplantation
KW - Adenocarcinoma, Follicular -- pathology
KW - Thyroid Neoplasms -- pathology
KW - Male
KW - Tumor Suppressor Proteins -- physiology
KW - Thyroid Hormone Receptors beta -- biosynthesis
KW - Thyroid Hormone Receptors beta -- physiology
KW - Thyroid Hormone Receptors beta -- genetics
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1499136035?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Thyroid+%3A+official+journal+of+the+American+Thyroid+Association&rft.atitle=Inhibition+of+tumorigenesis+by+the+thyroid+hormone+receptor+%CE%B2+in+xenograft+models.&rft.au=Kim%2C+Won+Gu%3BZhao%2C+Li%3BKim%2C+Dong+Wook%3BWillingham%2C+Mark+C%3BCheng%2C+Sheue-yann&rft.aulast=Kim&rft.aufirst=Won&rft.date=2014-02-01&rft.volume=24&rft.issue=2&rft.spage=260&rft.isbn=&rft.btitle=&rft.title=Thyroid+%3A+official+journal+of+the+American+Thyroid+Association&rft.issn=1557-9077&rft_id=info:doi/10.1089%2Fthy.2013.0054
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-10-21
N1 - Date created - 2014-02-12
N1 - Date revised - 2017-01-13
N1 - SuppNotes - Cited By:
Cancer Lett. 2000 Jul 31;155(2):145-52 [10822129]
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Carcinogenesis. 2002 Jan;23(1):25-33 [11756220]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1089/thy.2013.0054
ER -
TY - JOUR
T1 - The naturally occurring luteinizing hormone surge is diminished in mice lacking estrogen receptor Beta in the ovary.
AN - 1499120417; 24337314
AB - Female ESR2-null mice (betaERKO) display defects in ovarian function and are subfertile. Follicular maturation is impaired and explains smaller litters, but betaERKO also produce fewer litters, which may be partially due to inadequate ovulatory signals. To test this, the amplitude and timing of the naturally occurring luteinizing hormone (LH) surge was measured in individual intact betaERKO and wild-type (WT) mice. Vaginal cytology was evaluated daily, and blood samples were taken from mice in proestrus. The amplitude of the LH surge was severely blunted in betaERKO mice compared to WT, but pituitary LH levels revealed no differences. The betaERKO mice did not produce a preovulatory estradiol surge. To determine if the smaller LH surges and the reduced number of litters in betaERKO were due to the lack of ESR2 in the hypothalamic-pituitary axis or due to the absence of ESR2 in the ovary, ovaries were transplanted from WT into betaERKO mice and vice versa. The size of the LH surge was reduced only in mice lacking ESR2 within the ovary, and these mice had fewer litters. Fertility and size of the LH surge were rescued in betaERKO mice receiving a WT ovary. These data provide the first experimental evidence that the LH surge is impaired in betaERKO females and may contribute to their reduced fertility. ESR2 is not necessary within the pituitary and hypothalamus for the generation of a normal LH surge and for normal fertility, but ESR2 is essential within the ovary to provide proper signals.
JF - Biology of reproduction
AU - Jayes, Friederike L
AU - Burns, Katherine A
AU - Rodriguez, Karina F
AU - Kissling, Grace E
AU - Korach, Kenneth S
AD - Receptor Biology Section, Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina.
Y1 - 2014/02//
PY - 2014
DA - February 2014
SP - 24
VL - 90
IS - 2
KW - Estrogen Receptor beta
KW - 0
KW - Luteinizing Hormone
KW - 9002-67-9
KW - Index Medicus
KW - positive feedback
KW - naturally occurring luteinizing hormone surge
KW - ovarian transplants
KW - fertility
KW - HPO axis
KW - estrogen receptor beta
KW - ESR2
KW - Animals
KW - Infertility, Female -- blood
KW - Mice
KW - Estrous Cycle -- blood
KW - Estrous Cycle -- genetics
KW - Mice, Knockout
KW - Down-Regulation
KW - Hypothalamus -- metabolism
KW - Mice, Inbred C57BL
KW - Pituitary Gland -- metabolism
KW - Infertility, Female -- genetics
KW - Female
KW - Male
KW - Luteinizing Hormone -- secretion
KW - Ovary -- metabolism
KW - Luteinizing Hormone -- blood
KW - Estrogen Receptor beta -- metabolism
KW - Ovary -- transplantation
KW - Estrogen Receptor beta -- genetics
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1499120417?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biology+of+reproduction&rft.atitle=The+naturally+occurring+luteinizing+hormone+surge+is+diminished+in+mice+lacking+estrogen+receptor+Beta+in+the+ovary.&rft.au=Jayes%2C+Friederike+L%3BBurns%2C+Katherine+A%3BRodriguez%2C+Karina+F%3BKissling%2C+Grace+E%3BKorach%2C+Kenneth+S&rft.aulast=Jayes&rft.aufirst=Friederike&rft.date=2014-02-01&rft.volume=90&rft.issue=2&rft.spage=24&rft.isbn=&rft.btitle=&rft.title=Biology+of+reproduction&rft.issn=1529-7268&rft_id=info:doi/10.1095%2Fbiolreprod.113.113316
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-11-21
N1 - Date created - 2014-02-07
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1095/biolreprod.113.113316
ER -
TY - JOUR
T1 - Risk of ovarian cancer and the NF-κB pathway: genetic association with IL1A and TNFSF10.
AN - 1499115951; 24272484
AB - A missense single-nucleotide polymorphism (SNP) in the immune modulatory gene IL1A has been associated with ovarian cancer risk (rs17561). Although the exact mechanism through which this SNP alters risk of ovarian cancer is not clearly understood, rs17561 has also been associated with risk of endometriosis, an epidemiologic risk factor for ovarian cancer. Interleukin-1α (IL1A) is both regulated by and able to activate NF-κB, a transcription factor family that induces transcription of many proinflammatory genes and may be an important mediator in carcinogenesis. We therefore tagged SNPs in more than 200 genes in the NF-κB pathway for a total of 2,282 SNPs (including rs17561) for genotype analysis of 15,604 cases of ovarian cancer in patients of European descent, including 6,179 of high-grade serous (HGS), 2,100 endometrioid, 1,591 mucinous, 1,034 clear cell, and 1,016 low-grade serous, including 23,235 control cases spanning 40 studies in the Ovarian Cancer Association Consortium. In this large population, we confirmed the association between rs17561 and clear cell ovarian cancer [OR, 0.84; 95% confidence interval (CI), 0.76-0.93; P = 0.00075], which remained intact even after excluding participants in the prior study (OR, 0.85; 95% CI, 0.75-0.95; P = 0.006). Considering a multiple-testing-corrected significance threshold of P < 2.5 × 10(-5), only one other variant, the TNFSF10 SNP rs6785617, was associated significantly with a risk of ovarian cancer (low malignant potential tumors OR, 0.85; 95% CI, 0.79-0.91; P = 0.00002). Our results extend the evidence that borderline tumors may have a distinct genetic etiology. Further investigation of how these SNPs might modify ovarian cancer associations with other inflammation-related risk factors is warranted.
JF - Cancer research
AU - Charbonneau, Bridget
AU - Block, Matthew S
AU - Bamlet, William R
AU - Vierkant, Robert A
AU - Kalli, Kimberly R
AU - Fogarty, Zachary
AU - Rider, David N
AU - Sellers, Thomas A
AU - Tworoger, Shelley S
AU - Poole, Elizabeth
AU - Risch, Harvey A
AU - Salvesen, Helga B
AU - Kiemeney, Lambertus A
AU - Baglietto, Laura
AU - Giles, Graham G
AU - Severi, Gianluca
AU - Trabert, Britton
AU - Wentzensen, Nicolas
AU - Chenevix-Trench, Georgia
AU - for AOCS/ACS group
AU - Whittemore, Alice S
AU - Sieh, Weiva
AU - Chang-Claude, Jenny
AU - Bandera, Elisa V
AU - Orlow, Irene
AU - Terry, Kathryn
AU - Goodman, Marc T
AU - Thompson, Pamela J
AU - Cook, Linda S
AU - Rossing, Mary Anne
AU - Ness, Roberta B
AU - Narod, Steven A
AU - Kupryjanczyk, Jolanta
AU - Lu, Karen
AU - Butzow, Ralf
AU - Dörk, Thilo
AU - Pejovic, Tanja
AU - Campbell, Ian
AU - Le, Nhu D
AU - Bunker, Clareann H
AU - Bogdanova, Natalia
AU - Runnebaum, Ingo B
AU - Eccles, Diana
AU - Paul, James
AU - Wu, Anna H
AU - Gayther, Simon A
AU - Hogdall, Estrid
AU - Heitz, Florian
AU - Kaye, Stanley B
AU - Karlan, Beth Y
AU - Anton-Culver, Hoda
AU - Gronwald, Jacek
AU - Hogdall, Claus K
AU - Lambrechts, Diether
AU - Fasching, Peter A
AU - Menon, Usha
AU - Schildkraut, Joellen
AU - Pearce, Celeste Leigh
AU - Levine, Douglas A
AU - Kjaer, Susanne Kruger
AU - Cramer, Daniel
AU - Flanagan, James M
AU - Phelan, Catherine M
AU - Brown, Robert
AU - Massuger, Leon F A G
AU - Song, Honglin
AU - Doherty, Jennifer A
AU - Krakstad, Camilla
AU - Liang, Dong
AU - Odunsi, Kunle
AU - Berchuck, Andrew
AU - Jensen, Allan
AU - Lubinski, Jan
AU - Nevanlinna, Heli
AU - Bean, Yukie T
AU - Lurie, Galina
AU - Ziogas, Argyrios
AU - Walsh, Christine
AU - Despierre, Evelyn
AU - Brinton, Louise
AU - Hein, Alexander
AU - Rudolph, Anja
AU - Dansonka-Mieszkowska, Agnieszka
AU - Olson, Sara H
AU - Harter, Philipp
AU - Tyrer, Jonathan
AU - Vitonis, Allison F
AU - Brooks-Wilson, Angela
AU - Aben, Katja K
AU - Pike, Malcolm C
AU - Ramus, Susan J
AU - Wik, Elisabeth
AU - Cybulski, Cezary
AU - Lin, Jie
AU - Sucheston, Lara
AU - Edwards, Robert
AU - McGuire, Valerie
AU - Lester, Jenny
AU - du Bois, Andreas
AU - Lundvall, Lene
AU - Wang-Gohrke, Shan
AU - Szafron, Lukasz M
AU - Lambrechts, Sandrina
AU - Yang, Hannah
AU - Beckmann, Matthias W
AU - Pelttari, Liisa M
AU - Van Altena, Anne M
AU - van den Berg, David
AU - Halle, Mari K
AU - Gentry-Maharaj, Aleksandra
AU - Schwaab, Ira
AU - Chandran, Urmila
AU - Menkiszak, Janusz
AU - Ekici, Arif B
AU - Wilkens, Lynne R
AU - Leminen, Arto
AU - Modugno, Francesmary
AU - Friel, Grace
AU - Rothstein, Joseph H
AU - Vergote, Ignace
AU - Garcia-Closas, Montserrat
AU - Hildebrandt, Michelle A T
AU - Sobiczewski, Piotr
AU - Kelemen, Linda E
AU - Pharoah, Paul D P
AU - Moysich, Kirsten
AU - Knutson, Keith L
AU - Cunningham, Julie M
AU - Fridley, Brooke L
AU - Goode, Ellen L
AD - Authors' Affiliations: Departments of Health Sciences Research, Division of Epidemiology, Medical Oncology, Health Sciences Research, Division of Biomedical Statistics and Informatics, Immunology, and Laboratory Medicine and Pathology, Division of Experimental Pathology, Mayo Clinic, Rochester, Minnesota; Department of Cancer Epidemiology, Division of Population Sciences, Moffitt Cancer Center, Tampa, Florida; Channing Division of Network Medicine, Obstetrics and Gynecology Epidemiology Center, Brigham and Women's Hospital, Harvard Medical School; Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts; Department of Chronic Disease Epidemiology, Yale School of Public Health, New Haven, Connecticut; Department of Clinical Science, University of Bergen; Departments of Gynecology and Obstetrics, and Pathology, Haukeland University Hospital, Bergen, Norway; Departments for Health Evidence, Urology, and Gynaecology, Radboud University Medical Centre, Nijmegen; Comprehensive Cancer Center The Netherlands, Utrecht, the Netherlands; Cancer Epidemiology Centre, The Cancer Council Victoria; Centre for Molecular, Environmental, Genetic and Analytical Epidemiology, Department of Pathology, and Sir Peter MacCallum Department of Oncology, University of Melbourne; Department of Epidemiology and Preventive Medicine, Monash University; Peter MacCallum Cancer Institute; Research Division, Peter MacCallum Cancer Centre, Melbourne, Victoria; Cancer Division, Queensland Institute of Medical Research, Herston, Queensland, Australia; Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland; Department of Health Research and Policy, Division of Epidemiology, Stanford University School of Medicine, Palo Alto; Samuel Oschin Comprehensive Cancer Institute; Women's Cancer Program, Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center; Department of Preventive Medicine, Keck School of Medicine, University of Sout ; for AOCS/ACS group
Y1 - 2014/02/01/
PY - 2014
DA - 2014 Feb 01
SP - 852
EP - 861
VL - 74
IS - 3
KW - Interleukin-1alpha
KW - 0
KW - NF-kappa B
KW - TNF-Related Apoptosis-Inducing Ligand
KW - TNFSF10 protein, human
KW - Index Medicus
KW - Risk
KW - Polymorphism, Single Nucleotide
KW - Humans
KW - Genetic Association Studies
KW - Case-Control Studies
KW - Female
KW - TNF-Related Apoptosis-Inducing Ligand -- genetics
KW - Ovarian Neoplasms -- metabolism
KW - Ovarian Neoplasms -- genetics
KW - Ovarian Neoplasms -- pathology
KW - Signal Transduction
KW - NF-kappa B -- metabolism
KW - Interleukin-1alpha -- genetics
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Risk+of+ovarian+cancer+and+the+NF-%CE%BAB+pathway%3A+genetic+association+with+IL1A+and+TNFSF10.&rft.au=Charbonneau%2C+Bridget%3BBlock%2C+Matthew+S%3BBamlet%2C+William+R%3BVierkant%2C+Robert+A%3BKalli%2C+Kimberly+R%3BFogarty%2C+Zachary%3BRider%2C+David+N%3BSellers%2C+Thomas+A%3BTworoger%2C+Shelley+S%3BPoole%2C+Elizabeth%3BRisch%2C+Harvey+A%3BSalvesen%2C+Helga+B%3BKiemeney%2C+Lambertus+A%3BBaglietto%2C+Laura%3BGiles%2C+Graham+G%3BSeveri%2C+Gianluca%3BTrabert%2C+Britton%3BWentzensen%2C+Nicolas%3BChenevix-Trench%2C+Georgia%3Bfor+AOCS%2FACS+group%3BWhittemore%2C+Alice+S%3BSieh%2C+Weiva%3BChang-Claude%2C+Jenny%3BBandera%2C+Elisa+V%3BOrlow%2C+Irene%3BTerry%2C+Kathryn%3BGoodman%2C+Marc+T%3BThompson%2C+Pamela+J%3BCook%2C+Linda+S%3BRossing%2C+Mary+Anne%3BNess%2C+Roberta+B%3BNarod%2C+Steven+A%3BKupryjanczyk%2C+Jolanta%3BLu%2C+Karen%3BButzow%2C+Ralf%3BD%C3%B6rk%2C+Thilo%3BPejovic%2C+Tanja%3BCampbell%2C+Ian%3BLe%2C+Nhu+D%3BBunker%2C+Clareann+H%3BBogdanova%2C+Natalia%3BRunnebaum%2C+Ingo+B%3BEccles%2C+Diana%3BPaul%2C+James%3BWu%2C+Anna+H%3BGayther%2C+Simon+A%3BHogdall%2C+Estrid%3BHeitz%2C+Florian%3BKaye%2C+Stanley+B%3BKarlan%2C+Beth+Y%3BAnton-Culver%2C+Hoda%3BGronwald%2C+Jacek%3BHogdall%2C+Claus+K%3BLambrechts%2C+Diether%3BFasching%2C+Peter+A%3BMenon%2C+Usha%3BSchildkraut%2C+Joellen%3BPearce%2C+Celeste+Leigh%3BLevine%2C+Douglas+A%3BKjaer%2C+Susanne+Kruger%3BCramer%2C+Daniel%3BFlanagan%2C+James+M%3BPhelan%2C+Catherine+M%3BBrown%2C+Robert%3BMassuger%2C+Leon+F+A+G%3BSong%2C+Honglin%3BDoherty%2C+Jennifer+A%3BKrakstad%2C+Camilla%3BLiang%2C+Dong%3BOdunsi%2C+Kunle%3BBerchuck%2C+Andrew%3BJensen%2C+Allan%3BLubinski%2C+Jan%3BNevanlinna%2C+Heli%3BBean%2C+Yukie+T%3BLurie%2C+Galina%3BZiogas%2C+Argyrios%3BWalsh%2C+Christine%3BDespierre%2C+Evelyn%3BBrinton%2C+Louise%3BHein%2C+Alexander%3BRudolph%2C+Anja%3BDansonka-Mieszkowska%2C+Agnieszka%3BOlson%2C+Sara+H%3BHarter%2C+Philipp%3BTyrer%2C+Jonathan%3BVitonis%2C+Allison+F%3BBrooks-Wilson%2C+Angela%3BAben%2C+Katja+K%3BPike%2C+Malcolm+C%3BRamus%2C+Susan+J%3BWik%2C+Elisabeth%3BCybulski%2C+Cezary%3BLin%2C+Jie%3BSucheston%2C+Lara%3BEdwards%2C+Robert%3BMcGuire%2C+Valerie%3BLester%2C+Jenny%3Bdu+Bois%2C+Andreas%3BLundvall%2C+Lene%3BWang-Gohrke%2C+Shan%3BSzafron%2C+Lukasz+M%3BLambrechts%2C+Sandrina%3BYang%2C+Hannah%3BBeckmann%2C+Matthias+W%3BPelttari%2C+Liisa+M%3BVan+Altena%2C+Anne+M%3Bvan+den+Berg%2C+David%3BHalle%2C+Mari+K%3BGentry-Maharaj%2C+Aleksandra%3BSchwaab%2C+Ira%3BChandran%2C+Urmila%3BMenkiszak%2C+Janusz%3BEkici%2C+Arif+B%3BWilkens%2C+Lynne+R%3BLeminen%2C+Arto%3BModugno%2C+Francesmary%3BFriel%2C+Grace%3BRothstein%2C+Joseph+H%3BVergote%2C+Ignace%3BGarcia-Closas%2C+Montserrat%3BHildebrandt%2C+Michelle+A+T%3BSobiczewski%2C+Piotr%3BKelemen%2C+Linda+E%3BPharoah%2C+Paul+D+P%3BMoysich%2C+Kirsten%3BKnutson%2C+Keith+L%3BCunningham%2C+Julie+M%3BFridley%2C+Brooke+L%3BGoode%2C+Ellen+L&rft.aulast=Charbonneau&rft.aufirst=Bridget&rft.date=2014-02-01&rft.volume=74&rft.issue=3&rft.spage=852&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=1538-7445&rft_id=info:doi/10.1158%2F0008-5472.CAN-13-1051
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-04-15
N1 - Date created - 2014-02-04
N1 - Date revised - 2017-01-13
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1158/0008-5472.CAN-13-1051
ER -
TY - JOUR
T1 - Cognitive and affective perceptions of vulnerability as predictors of exercise intentions among people with type 2 diabetes
AN - 1496959934; 4521778
AB - Most conventional measures of risk perception such as perceived likelihood address largely deliberative or cognitive perceptions of vulnerability. Nevertheless, affective perceptions of vulnerability such as worry may have different antecedents and consequences than do these conventional measures, serve as stronger predictors of behavior, and qualify effects of conventional deliberative risk perceptions on behavior. In this study, we assessed how worry - the most common measure of affective perceptions of vulnerability compared with three conventional measures of risk (absolute risk, comparative risk, and conditional risk) in predicting behavioral intentions. Participants were 83 adults with type 2 diabetes who assessed their risk of heart disease and reported their intentions to increase physical activity (which reduces heart disease risk). As predicted, worry was the only significant predictor of exercise intentions such that higher worry was associated with higher intentions. Importantly, this relationship was stronger among individuals who perceived their absolute risk to be relatively higher and those who perceived their comparative risk to be relatively lower, demonstrating that cognitive and affective perceptions interact. These findings highlight the importance of not conflating affective and cognitive perceptions of vulnerability when assessing perceived risk and suggest the need for more research on how to best conceptualize perceived risk in different samples and settings. Reprinted by permission of Carfax Publishing, Taylor & Francis Ltd
JF - Journal of risk research
AU - Portnoy, David B
AU - Kaufman, Annette R
AU - Klein, William M.P.
AU - Doyle, Todd A
AU - Groot, Mary de
AD - US National Cancer Institute ; Ohio University ; Indiana University, Indianapolis
Y1 - 2014/02//
PY - 2014
DA - Feb 2014
SP - 177
EP - 193
VL - 17
IS - 2
SN - 1366-9877, 1366-9877
KW - Sociology
KW - Comparative analysis
KW - Perception
KW - Physical activity
KW - Diseases
KW - Cognition
KW - Risk theory
KW - Diabetes
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1496959934?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+risk+research&rft.atitle=Cognitive+and+affective+perceptions+of+vulnerability+as+predictors+of+exercise+intentions+among+people+with+type+2+diabetes&rft.au=Portnoy%2C+David+B%3BKaufman%2C+Annette+R%3BKlein%2C+William+M.P.%3BDoyle%2C+Todd+A%3BGroot%2C+Mary+de&rft.aulast=Portnoy&rft.aufirst=David&rft.date=2014-02-01&rft.volume=17&rft.issue=2&rft.spage=177&rft.isbn=&rft.btitle=&rft.title=Journal+of+risk+research&rft.issn=13669877&rft_id=info:doi/10.1080%2F13669877.2013.794153
LA - English
DB - International Bibliography of the Social Sciences (IBSS)
N1 - Date revised - 2014-01-23
N1 - Last updated - 2014-02-11
N1 - SubjectsTermNotLitGenreText - 9506; 3524 6220; 11040 11035; 9382; 3617 6220; 2630 971; 2449 10404
DO - http://dx.doi.org/10.1080/13669877.2013.794153
ER -
TY - JOUR
T1 - Role of neuroticism and coping strategies in psychological reactions to a racist incident among African American University students
AN - 1496951074; 4522728
AB - A total of 562 African American university students provided data on individual differences in neuroticism; coping with a recent experience being the target of prejudice, racism, and/or discrimination; and psychological reactions to the incident. Higher negative affect, lower positive affect, more intrusive thoughts about the incident, and lack of forgiveness for the perpetrator were used to index distress in response to the racist incident. Using factor analyses, we determined the factor structure of the Brief COPE in our sample. Using structural equation modeling, we then examined neuroticism and each coping factor as unique predictors of reactions to the race-related incident. We documented that there were direct and indirect associations (via the selection of coping strategies) between neuroticism and the outcome measures. Neuroticism also moderated the association between particular coping strategies and reactions to the racist incident. There was also evidence for direct associations between various coping strategies and the outcome measures. The research, though preliminary, suggests the importance of neuroticism and coping strategies in understanding psychological reactions to being the target of racism. Reprinted by permission of Sage Publications, Inc.
JF - Journal of black psychology
AU - Pearson, Matthew R
AU - Derlega, Valerian J
AU - Henson, James M
AU - Holmes, Karen Y
AU - Ferrer, Rebecca A
AU - Harrison, Scott B
AD - Old Dominion University ; Norfolk State University ; National Cancer Institute, Rockville
Y1 - 2014/02//
PY - 2014
DA - Feb 2014
SP - 81
EP - 111
VL - 40
IS - 1
SN - 0095-7984, 0095-7984
KW - Sociology
KW - Racism
KW - Social psychology
KW - Survival strategy
KW - Personality
KW - Africa
KW - Discrimination
KW - U.S.A.
KW - Students
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1496951074?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+black+psychology&rft.atitle=Role+of+neuroticism+and+coping+strategies+in+psychological+reactions+to+a+racist+incident+among+African+American+University+students&rft.au=Pearson%2C+Matthew+R%3BDerlega%2C+Valerian+J%3BHenson%2C+James+M%3BHolmes%2C+Karen+Y%3BFerrer%2C+Rebecca+A%3BHarrison%2C+Scott+B&rft.aulast=Pearson&rft.aufirst=Matthew&rft.date=2014-02-01&rft.volume=40&rft.issue=1&rft.spage=81&rft.isbn=&rft.btitle=&rft.title=Journal+of+black+psychology&rft.issn=00957984&rft_id=info:doi/10.1177%2F0095798412471682
LA - English
DB - International Bibliography of the Social Sciences (IBSS)
N1 - Date revised - 2014-01-23
N1 - Last updated - 2014-02-11
N1 - SubjectsTermNotLitGenreText - 3612 3549 2688 2449 10404; 9416 2153; 12432; 10575 10566 3612 3549 2688 2449 10404 9680; 11901 10404; 12334 4049; 2; 433 293 14
DO - http://dx.doi.org/10.1177/0095798412471682
ER -
TY - JOUR
T1 - A High-Throughput Screening Assay for Fungicidal Compounds against Cryptococcus neoformans
AN - 1496898167; 19022822
AB - Cryptococcus neoformans is a pathogenic fungus that causes meningitis worldwide, particularly in human immunodeficiency virus (HIV)-infected individuals. Although amphotericin B is the "gold standard" treatment for cryptococcal meningitis, the toxicity and inconvenience of intravenous injection emphasize a need for development of new anticryptocccal drugs. Recent data from humans and animal studies suggested that a nutrient-deprived host environment may exist in cryptococcal meningitis. Thus, a screening assay for identifying fungicidal compounds under nutrient-deprived conditions may provide an alternative strategy to develop new anticryptococcal drugs for this disease. A high-throughput fungicidal assay was developed using a profluorescent dye, alamarBlue, to detect residual metabolic activity of C. neoformans under nutrient-limiting conditions. Screening the Library of Pharmacologically Active Compounds (LOPAC) with this assay identified a potential chemical scaffold, 10058-F4, that exhibited fungicidal activity in the low micromolar range. These results thus demonstrate the feasibility of this alamarBlue-based assay for high-throughput screening of fungicidal compounds under nutrient-limiting conditions for new anticryptococcal drug development.
JF - Journal of Biomolecular Screening
AU - Rabjohns, Jennifer LA
AU - Park, Yoon-Dong
AU - Dehdashti, Jean
AU - Sun, Wei
AU - Henderson, Christina
AU - Zelazny, Adrian
AU - Metallo, Steven J
AU - Zheng, Wei
AU - Williamson, Peter R
AD - Laboratory of Clinical Infectious Diseases, National Institutes of Health, Bethesda, MD, USA
Y1 - 2014/02//
PY - 2014
DA - Feb 2014
SP - 270
EP - 277
PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom
VL - 19
IS - 2
SN - 1087-0571, 1087-0571
KW - Toxicology Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology; Microbiology Abstracts C: Algology, Mycology & Protozoology; Biotechnology and Bioengineering Abstracts
KW - Amphotericin B
KW - Intravenous administration
KW - Data processing
KW - Fungicidal activity
KW - Drug development
KW - Toxicity
KW - scaffolds
KW - Meningitis
KW - Cryptococcus neoformans
KW - Human immunodeficiency virus
KW - high-throughput screening
KW - Drugs
KW - A 01380:Plant Protection, Fungicides & Seed Treatments
KW - K 03400:Human Diseases
KW - W 30965:Miscellaneous, Reviews
KW - X 24330:Agrochemicals
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biomolecular+Screening&rft.atitle=A+High-Throughput+Screening+Assay+for+Fungicidal+Compounds+against+Cryptococcus+neoformans&rft.au=Rabjohns%2C+Jennifer+LA%3BPark%2C+Yoon-Dong%3BDehdashti%2C+Jean%3BSun%2C+Wei%3BHenderson%2C+Christina%3BZelazny%2C+Adrian%3BMetallo%2C+Steven+J%3BZheng%2C+Wei%3BWilliamson%2C+Peter+R&rft.aulast=Rabjohns&rft.aufirst=Jennifer&rft.date=2014-02-01&rft.volume=19&rft.issue=2&rft.spage=270&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biomolecular+Screening&rft.issn=10870571&rft_id=info:doi/10.1177%2F1087057113496847
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-02-01
N1 - Number of references - 30
N1 - Last updated - 2014-06-12
N1 - SubjectsTermNotLitGenreText - Amphotericin B; Intravenous administration; Data processing; Fungicidal activity; high-throughput screening; Drug development; Toxicity; Drugs; scaffolds; Meningitis; Cryptococcus neoformans; Human immunodeficiency virus
DO - http://dx.doi.org/10.1177/1087057113496847
ER -
TY - JOUR
T1 - Characterization of the Noncoding Regions of the 1918 Influenza A H1N1 Virus
AN - 1496895963; 19010477
AB - The terminal noncoding region (NCR) sequences of the eight gene segments of the influenza A/Brevig Mission/1/1918 (H1N1) virus were determined by rapid amplification of cDNA ends (RACE). Chimeric viruses encoding the open reading frames of the 1918 virus but flanked by either the wild-type 1918 NCR sequences or the NCR sequences of two other H1N1 virus strains, A/WSN/1933 and A/New York/312/2001, were produced. No growth differences between the NCR variant 1918 influenza viruses were noted.
JF - Journal of Virology
AU - Wang, Ruixue
AU - Taubenberger, Jeffery K
Y1 - 2014/02//
PY - 2014
DA - Feb 2014
SP - 1815
EP - 1818
PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States
VL - 88
IS - 3
SN - 0022-538X, 0022-538X
KW - Health & Safety Science Abstracts; Virology & AIDS Abstracts
KW - Influenza
KW - Influenza A
KW - Viruses
KW - Open reading frames
KW - USA, New York
KW - H 0500:General
KW - V 22310:Genetics, Taxonomy & Structure
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1496895963?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Virology&rft.atitle=Characterization+of+the+Noncoding+Regions+of+the+1918+Influenza+A+H1N1+Virus&rft.au=Wang%2C+Ruixue%3BTaubenberger%2C+Jeffery+K&rft.aulast=Wang&rft.aufirst=Ruixue&rft.date=2014-02-01&rft.volume=88&rft.issue=3&rft.spage=1815&rft.isbn=&rft.btitle=&rft.title=Journal+of+Virology&rft.issn=0022538X&rft_id=info:doi/10.1128%2FJVI.03098-13
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-02-01
N1 - Number of references - 22
N1 - Last updated - 2015-04-02
N1 - SubjectsTermNotLitGenreText - Influenza A; Open reading frames; Influenza; Viruses; USA, New York
DO - http://dx.doi.org/10.1128/JVI.03098-13
ER -
TY - JOUR
T1 - A possible outbreak of swine influenza, 1892
AN - 1496894068; 19028604
AB - Influenza A viruses are globally enzootic in swine populations. Swine influenza has been recognised only since 1918, but an anecdotal report suggests that a swine-influenza epizootic might have occurred in England in 1892, at the same time as an explosive epidemic (or pandemic recurrence) of human influenza. This outbreak suggests that the ecobiological association between human and swine influenza could extend to before 1918. By contrast with the recent documentation of swine influenza, influenza in horses has been well documented for hundreds of years, and was often linked temporally and geographically to epidemics of human influenza. Both decreased contact between people and horses, and the concomitant increase in swine production over the past century, might have altered the character and dynamics of influenza host-switch events between people and domestic mammals.
JF - Lancet Infectious Diseases
AU - Morens, David M
AU - Taubenberger, Jeffery K
AD - Office of the Director, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA
Y1 - 2014/02//
PY - 2014
DA - Feb 2014
SP - 169
EP - 172
PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands
VL - 14
IS - 2
SN - 1473-3099, 1473-3099
KW - Health & Safety Science Abstracts; Virology & AIDS Abstracts
KW - Epidemics
KW - Influenza
KW - British Isles, England
KW - Swine influenza
KW - H 6000:Natural Disasters/Civil Defense/Emergency Management
KW - V 22400:Human Diseases
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1496894068?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Lancet+Infectious+Diseases&rft.atitle=A+possible+outbreak+of+swine+influenza%2C+1892&rft.au=Morens%2C+David+M%3BTaubenberger%2C+Jeffery+K&rft.aulast=Morens&rft.aufirst=David&rft.date=2014-02-01&rft.volume=14&rft.issue=2&rft.spage=169&rft.isbn=&rft.btitle=&rft.title=Lancet+Infectious+Diseases&rft.issn=14733099&rft_id=info:doi/10.1016%2FS1473-3099%2813%2970227-5
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-02-01
N1 - Last updated - 2014-03-20
N1 - SubjectsTermNotLitGenreText - Swine influenza; Influenza; British Isles, England
DO - http://dx.doi.org/10.1016/S1473-3099(13)70227-5
ER -
TY - JOUR
T1 - Social Theory Applied to Body Image and Chronic Illness in Youth
AN - 1496883676; 19002616
AB - Changes in appearance and functional limitations of youth with chronic illness place them at greater risk for negative body image and poor psychosocial and medical outcomes compared with their healthy peers. Sociocultural pressures from the media, family, and peers, as well as social comparison processes to some extent explain the development of negative or positive body image in young people. This article discusses social theories applied to body image in young people with chronic illness, an overlooked population. A review of risk and protective factors of body dissatisfaction in this population and suggested treatment strategies/interventions in the prevention of body dissatisfaction are also considered. Reported findings may help health care providers become more aware of body image issues their young patients with chronic illness face, and posit the importance of regularly monitoring their psychosocial well-being in the efforts to curtail development of body dissatisfaction and consequential poor health outcomes.
JF - American Journal of Lifestyle Medicine
AU - Quick, Virginia
AD - Eunice Kennedy Shriver National Institute of Child Health and Human Development/National Institutes of Health, Division of Intramural Population Health Research, Bethesda, Maryland
Y1 - 2014/02//
PY - 2014
DA - Feb 2014
SP - 15
EP - 20
PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom
VL - 8
IS - 1
SN - 1559-8276, 1559-8276
KW - Health & Safety Science Abstracts; Risk Abstracts
KW - Prevention
KW - Health care
KW - Risk factors
KW - Reviews
KW - Intervention
KW - H 0500:General
KW - R2 23110:Psychological aspects
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1496883676?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Lifestyle+Medicine&rft.atitle=Social+Theory+Applied+to+Body+Image+and+Chronic+Illness+in+Youth&rft.au=Quick%2C+Virginia&rft.aulast=Quick&rft.aufirst=Virginia&rft.date=2014-02-01&rft.volume=8&rft.issue=1&rft.spage=15&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Lifestyle+Medicine&rft.issn=15598276&rft_id=info:doi/10.1177%2F1559827613505408
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-02-01
N1 - Number of references - 45
N1 - Last updated - 2014-06-26
N1 - SubjectsTermNotLitGenreText - Prevention; Health care; Reviews; Risk factors; Intervention
DO - http://dx.doi.org/10.1177/1559827613505408
ER -
TY - JOUR
T1 - Circulating estrogens and estrogens within the breast among postmenopausal BRCA1/2 mutation carriers.
AN - 1493798895; 24442642
AB - Accurately quantifying parent estrogens (PE) estrone (E1) and estradiol (E2) and their metabolites (EM) within breast tissue and serum may permit detailed investigations of their contributions to breast carcinogenesis among BRCA1/2 mutation carriers. We conducted a study of PE/EM in serum, nipple aspirate fluid (NAF), and ductal lavage supernatant (DLS) among postmenopausal BRCA1/2 mutation carriers. PE/EM (conjugated and unconjugated) were measured in paired serum/NAF (n = 22 women) and paired serum/DLS samples (n = 24 women) using quantitative liquid chromatography-tandem mass spectrometry (LC/MS/MS). The relationships between serum and tissue-specific PE/EM were measured using Pearson's correlation coefficients. Conjugated forms of PE/EM constituted the majority of estrogen in serum (88 %), NAF (59 %) and DLS (69 %). PE/EM in NAF and serum were highly correlated [E1 (r = 0.97, p < 0.0001), E2 (r = 0.90, p < 0.0001) and estriol (E3) (r = 0.74, p < 0.0001)] as they were in DLS and serum [E1 (r = 0.92, p < 0.0001; E2 (r = 0.70, p = 0.0001; E3 (r = 0.67, p = 0.0004)]. Analyses of paired total estrogen values for NAF and serum, and DLS and serum yielded ratios of 0.22 (95 % CI 0.19-0.25) and 0.28 (95 % CI 0.24-0.32), respectively. This report is the first to employ LC/MS/MS to quantify PE/EM in novel breast tissue-derived biospecimens (i.e., NAF and DLS). We demonstrate that circulating PE and EM are strongly and positively correlated with tissue-specific PE and EM measured in NAF and DLS among postmenopausal BRCA1/2 mutation carriers. If confirmed, future etiologic studies could utilize the more readily obtainable serum hormone levels as a reliable surrogate measure of exposure at the tissue level.
JF - Breast cancer research and treatment
AU - Loud, Jennifer T
AU - Gierach, Gretchen L
AU - Veenstra, Timothy D
AU - Falk, Roni T
AU - Nichols, Kathryn
AU - Guttmann, Allison
AU - Xu, Xia
AU - Greene, Mark H
AU - Gail, Mitchell H
AD - Clinical Genetics Branch (CGB), Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, 9609 Medical Center Drive, Room 6E536, Bethesda, MD, 20850-9772, USA, loudj@mail.nih.gov.
Y1 - 2014/02//
PY - 2014
DA - February 2014
SP - 517
EP - 529
VL - 143
IS - 3
KW - BRCA1 Protein
KW - 0
KW - BRCA1 protein, human
KW - BRCA2 Protein
KW - BRCA2 protein, human
KW - Estrone
KW - 2DI9HA706A
KW - Estradiol
KW - 4TI98Z838E
KW - Index Medicus
KW - Nipple Aspirate Fluid
KW - Carcinogenesis -- metabolism
KW - Carcinogenesis -- genetics
KW - Postmenopause
KW - Premenopause
KW - Humans
KW - Heterozygote
KW - Adult
KW - Middle Aged
KW - Tandem Mass Spectrometry
KW - Mutation
KW - Female
KW - Breast Neoplasms -- genetics
KW - Estradiol -- blood
KW - BRCA1 Protein -- genetics
KW - Breast Neoplasms -- metabolism
KW - Estrone -- blood
KW - Estrone -- metabolism
KW - Breast Neoplasms -- blood
KW - BRCA2 Protein -- genetics
KW - Estradiol -- metabolism
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Breast+cancer+research+and+treatment&rft.atitle=Circulating+estrogens+and+estrogens+within+the+breast+among+postmenopausal+BRCA1%2F2+mutation+carriers.&rft.au=Loud%2C+Jennifer+T%3BGierach%2C+Gretchen+L%3BVeenstra%2C+Timothy+D%3BFalk%2C+Roni+T%3BNichols%2C+Kathryn%3BGuttmann%2C+Allison%3BXu%2C+Xia%3BGreene%2C+Mark+H%3BGail%2C+Mitchell+H&rft.aulast=Loud&rft.aufirst=Jennifer&rft.date=2014-02-01&rft.volume=143&rft.issue=3&rft.spage=517&rft.isbn=&rft.btitle=&rft.title=Breast+cancer+research+and+treatment&rft.issn=1573-7217&rft_id=info:doi/10.1007%2Fs10549-013-2821-6
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-09-19
N1 - Date created - 2014-01-31
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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Comment In:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1007/s10549-013-2821-6
ER -
TY - JOUR
T1 - Cixutumumab for patients with recurrent or refractory advanced thymic epithelial tumours: a multicentre, open-label, phase 2 trial.
AN - 1493797390; 24439931
AB - No standard treatment exists for refractory or relapsed advanced thymic epithelial tumours. We investigated the efficacy of cixutumumab, a fully human IgG1 monoclonal antibody targeting the insulin-like growth factor 1 receptor in thymic epithelial tumours after failure of previous chemotherapy.
Between Aug 25, 2009, and March 27, 2012, we did a multicentre, open-label, phase 2 trial in patients aged 18 years or older with histologically confirmed recurrent or refractory thymic epithelial tumours. We enrolled individuals who had progressed after at least one previous regimen of platinum-containing chemotherapy, had an Eastern Cooperative Oncology Group performance status of 0 or 1, and had measurable disease and adequate organ function. Eligible patients received intravenous cixutumumab (20 mg/kg) every 3 weeks until disease progression or development of intolerable toxic effects. The primary endpoint was the frequency of response, analysed on an intention-to-treat basis. We also did pharmacodynamic studies. This trial is registered with ClinicalTrials.gov, number NCT00965250. 49 patients were enrolled (37 with thymomas and 12 with thymic carcinomas) who received a median of eight cycles of cixutumumab (range 1-46). At the final actuarial analysis when follow-up data were updated (Nov 30, 2012), median potential follow-up (from on-study date to most current follow-up date) was 24·0 months (IQR 17·3-36·9). In the thymoma cohort, five (14%) of 37 patients (95% CI 5-29) achieved a partial response, 28 had stable disease, and four had progressive disease. In the thymic carcinoma cohort, none of 12 patients (95% CI 0-26) had a partial response, five had stable disease, and seven had progressive disease. The most common grade 3-4 adverse events in both cohorts combined were hyperglycaemia (five [10%]), lipase elevation (three [6%]), and weight loss, tumour pain, and hyperuricaemia (two each [4%]). Nine (24%) of 37 patients with thymoma developed autoimmune conditions during treatment (five were new-onset disorders), the most common of which was pure red-cell aplasia. Two (4%) patients died; one was attributed to disease progression and the other to disease-related complications (respiratory failure, myositis, and an acute coronary event), which could have been precipitated by treatment with cixutumumab. Cixutumumab monotherapy is well-tolerated and active in relapsed thymoma. Development of autoimmunity during treatment needs further investigation.
Division of Cancer Treatment and Diagnosis at the National Cancer Institute (National Institutes of Health), ImClone Systems. Copyright © 2014 Elsevier Ltd. All rights reserved.
JF - The Lancet. Oncology
AU - Rajan, Arun
AU - Carter, Corey A
AU - Berman, Arlene
AU - Cao, Liang
AU - Kelly, Ronan J
AU - Thomas, Anish
AU - Khozin, Sean
AU - Chavez, Ariel Lopez
AU - Bergagnini, Isabella
AU - Scepura, Barbara
AU - Szabo, Eva
AU - Lee, Min-Jung
AU - Trepel, Jane B
AU - Browne, Sarah K
AU - Rosen, Lindsey B
AU - Yu, Yunkai
AU - Steinberg, Seth M
AU - Chen, Helen X
AU - Riely, Gregory J
AU - Giaccone, Giuseppe
AD - Medical Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. ; Genetics Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. ; Memorial Sloan-Kettering Cancer Center, New York, NY, USA. ; National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA. ; Biostatistics and Data Management Section, Office of the Clinical Director, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. ; Medical Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. Electronic address: gg496@Georgetown.edu.
Y1 - 2014/02//
PY - 2014
DA - February 2014
SP - 191
EP - 200
VL - 15
IS - 2
KW - Antibodies, Monoclonal
KW - 0
KW - Antineoplastic Agents
KW - anti-IGF-1R antibody A12
KW - Receptor, IGF Type 1
KW - EC 2.7.10.1
KW - Index Medicus
KW - Receptor, IGF Type 1 -- immunology
KW - Disease-Free Survival
KW - Humans
KW - Disease Progression
KW - Aged
KW - Kaplan-Meier Estimate
KW - Aged, 80 and over
KW - Adult
KW - Intention to Treat Analysis
KW - Treatment Outcome
KW - Autoimmunity -- drug effects
KW - Receptor, IGF Type 1 -- antagonists & inhibitors
KW - Middle Aged
KW - Time Factors
KW - Female
KW - Male
KW - Neoplasms, Glandular and Epithelial -- mortality
KW - Thymus Neoplasms -- immunology
KW - Thymus Neoplasms -- pathology
KW - Antibodies, Monoclonal -- therapeutic use
KW - Antineoplastic Agents -- adverse effects
KW - Neoplasms, Glandular and Epithelial -- pathology
KW - Neoplasm Recurrence, Local -- immunology
KW - Neoplasms, Glandular and Epithelial -- drug therapy
KW - Neoplasm Recurrence, Local -- drug therapy
KW - Neoplasms, Glandular and Epithelial -- immunology
KW - Antibodies, Monoclonal -- adverse effects
KW - Thymus Neoplasms -- drug therapy
KW - Antineoplastic Agents -- therapeutic use
KW - Thymus Neoplasms -- mortality
KW - Neoplasm Recurrence, Local -- mortality
KW - Neoplasm Recurrence, Local -- pathology
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1493797390?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Lancet.+Oncology&rft.atitle=Cixutumumab+for+patients+with+recurrent+or+refractory+advanced+thymic+epithelial+tumours%3A+a+multicentre%2C+open-label%2C+phase+2+trial.&rft.au=Rajan%2C+Arun%3BCarter%2C+Corey+A%3BBerman%2C+Arlene%3BCao%2C+Liang%3BKelly%2C+Ronan+J%3BThomas%2C+Anish%3BKhozin%2C+Sean%3BChavez%2C+Ariel+Lopez%3BBergagnini%2C+Isabella%3BScepura%2C+Barbara%3BSzabo%2C+Eva%3BLee%2C+Min-Jung%3BTrepel%2C+Jane+B%3BBrowne%2C+Sarah+K%3BRosen%2C+Lindsey+B%3BYu%2C+Yunkai%3BSteinberg%2C+Seth+M%3BChen%2C+Helen+X%3BRiely%2C+Gregory+J%3BGiaccone%2C+Giuseppe&rft.aulast=Rajan&rft.aufirst=Arun&rft.date=2014-02-01&rft.volume=15&rft.issue=2&rft.spage=191&rft.isbn=&rft.btitle=&rft.title=The+Lancet.+Oncology&rft.issn=1474-5488&rft_id=info:doi/10.1016%2FS1470-2045%2813%2970596-5
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-03-27
N1 - Date created - 2014-01-31
N1 - Date revised - 2017-01-14
N1 - Genetic sequence - NCT00965250; ClinicalTrials.gov
N1 - SuppNotes - Cited By:
Clin Cancer Res. 2003 Jan;9(1):377-82 [12538491]
Clin Exp Immunol. 2003 Apr;132(1):128-36 [12653847]
Clin Cancer Res. 2013 Aug 1;19(15):4282-9 [23741071]
Invest New Drugs. 2012 Aug;30(4):1548-56 [21748299]
J Clin Oncol. 2012 May 20;30(15):1849-56 [22508822]
J Clin Immunol. 2012 Apr;32(2):238-45 [22170314]
Clin Cancer Res. 2012 Mar 15;18(6):1808-17 [22287600]
Nat Rev Cancer. 2012 Mar;12(3):159-69 [22337149]
J Clin Oncol. 2012 Jan 20;30(3):256-62 [22184397]
J Clin Oncol. 2011 May 20;29(15):2052-9 [21502553]
Cancer. 2010 Oct 15;116(20):4686-95 [20597130]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/S1470-2045(13)70596-5
ER -
TY - JOUR
T1 - Methylarsonous acid causes oxidative DNA damage in cells independent of the ability to biomethylate inorganic arsenic.
AN - 1493797081; 24091636
AB - Inorganic arsenic (iAs) and its toxic methylated metabolite, methylarsonous acid (MMA(III)), both have carcinogenic potential. Prior study shows iAs-induced malignant transformation in both arsenic methylation-proficient (liver) and methylation-deficient (prostate) cells, but only methylation-proficient cells show oxidative DNA damage (ODD) during this transformation. To further define whether arsenic methylation is necessary for transformation or ODD induction, here we chronically exposed these same liver or prostate cell lines to MMA(III) (0.25-1.0 μM) and tested for acquired malignant phenotype. Various metrics of oncogenic transformation were periodically assessed along with ODD during chronic MMA(III) exposure. Methylation-deficient and methylation-proficient cells both acquired a cancer phenotype with MMA(III) exposure at about 20 weeks, based on increased matrix metalloproteinase secretion, colony formation, and invasion. In contrast, prior work showed iAs-induced transformation took longer in biomethylation-deficient cells (~30 weeks) than in biomethylation-proficient cells (~18 weeks). In the present study, MMA(III) caused similar peak ODD levels at similar concentrations and at similar exposure times (18-22 weeks) in both cell types. At the approximate peak of ODD production, both cell types showed similar alterations in arsenic and oxidative stress adaptation factors (i.e., ABCC1, ABCC2, GST-π, SOD-1). Thus, MMA(III) causes oncogenic transformation associated with ODD in methylation-deficient cells, indicating that further methylation is not required to induce ODD. Together, these results show that MMA(III) and iAs cause an acquired malignant phenotype in methylation-deficient cells, yet iAs does not induce ODD. This indicates iAs likely has both genotoxic and non-genotoxic mechanisms dictated by the target cell's ability to methylate arsenic.
JF - Archives of toxicology
AU - Tokar, Erik J
AU - Kojima, Chikara
AU - Waalkes, Michael P
AD - National Toxicology Program (NTP) Laboratory, Division of the National Toxicology Program, National Institute of Environmental Health Sciences (NIEHS), 111 Alexander Drive, MD E1-07, P.O. Box 12233, Research Triangle Park, NC, 27709, USA.
Y1 - 2014/02//
PY - 2014
DA - February 2014
SP - 249
EP - 261
VL - 88
IS - 2
KW - Arsenicals
KW - 0
KW - PTEN Phosphohydrolase
KW - EC 3.1.3.67
KW - PTEN protein, human
KW - Pten protein, rat
KW - monomethylarsonic acid
KW - J37VJ5709S
KW - Index Medicus
KW - Animals
KW - Arsenic Poisoning -- pathology
KW - Liver -- cytology
KW - Cell Line -- drug effects
KW - Humans
KW - Prostate -- metabolism
KW - PTEN Phosphohydrolase -- genetics
KW - Rats
KW - Oxidation-Reduction
KW - Adaptation, Physiological -- drug effects
KW - Adaptation, Physiological -- physiology
KW - Liver -- drug effects
KW - Toxicity Tests, Chronic
KW - Prostate -- cytology
KW - Methylation
KW - Male
KW - Cell Transformation, Neoplastic -- chemically induced
KW - Arsenicals -- pharmacology
KW - DNA Damage -- drug effects
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1493797081?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+toxicology&rft.atitle=Methylarsonous+acid+causes+oxidative+DNA+damage+in+cells+independent+of+the+ability+to+biomethylate+inorganic+arsenic.&rft.au=Tokar%2C+Erik+J%3BKojima%2C+Chikara%3BWaalkes%2C+Michael+P&rft.aulast=Tokar&rft.aufirst=Erik&rft.date=2014-02-01&rft.volume=88&rft.issue=2&rft.spage=249&rft.isbn=&rft.btitle=&rft.title=Archives+of+toxicology&rft.issn=1432-0738&rft_id=info:doi/10.1007%2Fs00204-013-1141-2
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-09-30
N1 - Date created - 2014-01-30
N1 - Date revised - 2017-01-13
N1 - SuppNotes - Cited By:
Toxicol Appl Pharmacol. 2012 Jun 1;261(2):204-16 [22521957]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1007/s00204-013-1141-2
ER -
TY - JOUR
T1 - Arsenic-induced cancer cell phenotype in human breast epithelia is estrogen receptor-independent but involves aromatase activation.
AN - 1493795270; 24068038
AB - Accumulating data suggest arsenic may be an endocrine disruptor and tentatively linked to breast cancer by some studies. Therefore, we tested the effects of chronic inorganic arsenic exposure on the normal estrogen receptor (ER)-negative breast epithelial cell line, MCF-10A. Cells were chronically exposed to a low-level arsenite (500 nM) for up to 24 weeks. Markers of cancer cell phenotype and the expression of critical genes relevant to breast cancer or stem cells (SCs) were examined. After 24 weeks, chronic arsenic-exposed breast epithelial (CABE) cells showed increases in secreted MMP activity, colony formation, invasion, and proliferation rate, indicating an acquired cancer cell phenotype. These CABE cells presented with basal-like breast cancer characteristics, including ER-α, HER-2, and progesterone receptor negativity, and overexpression of K5 and p63. Putative CD44(+)/CD24(-/low) breast SCs were increased to 80 % over control in CABE cells. CABE cells also formed multilayer cell mounds, indicative of loss of contact inhibition. These mounds showed high levels of K5 and p63, indicating the potential presence of cancer stem cells (CSCs). Epithelial-to-mesenchymal transition occurred during arsenic exposure. Overexpression of aromatase, a key rate-limiting enzyme in estrogen synthesis, occurred with arsenic starting early on in exposure. Levels of 17β-estradiol increased in CABE cells and their conditioned medium. The aromatase inhibitor letrozole abolished arsenic-induced increases in 17β-estradiol production and reversed cancer cell phenotype. Thus, chronic arsenic exposure drives human breast epithelia into a cancer cell phenotype with an apparent overabundance of putative CSCs. Arsenic appears to transform breast epithelia through overexpression of aromatase, thereby activating oncogenic processes independent of ER.
JF - Archives of toxicology
AU - Xu, Yuanyuan
AU - Tokar, Erik J
AU - Waalkes, Michael P
AD - National Toxicology Program Laboratory, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA.
Y1 - 2014/02//
PY - 2014
DA - February 2014
SP - 263
EP - 274
VL - 88
IS - 2
KW - Estrogen Receptor alpha
KW - 0
KW - Receptors, Estrogen
KW - estrogen receptor alpha, human
KW - Estradiol
KW - 4TI98Z838E
KW - Aromatase
KW - EC 1.14.14.1
KW - Matrix Metalloproteinase 2
KW - EC 3.4.24.24
KW - Matrix Metalloproteinase 9
KW - EC 3.4.24.35
KW - Arsenic
KW - N712M78A8G
KW - Index Medicus
KW - Cell Line -- drug effects
KW - Humans
KW - Epithelial-Mesenchymal Transition -- drug effects
KW - Estrogen Receptor alpha -- metabolism
KW - Matrix Metalloproteinase 2 -- metabolism
KW - Estradiol -- metabolism
KW - Neoplastic Stem Cells -- drug effects
KW - Matrix Metalloproteinase 9 -- metabolism
KW - Epithelial Cells -- drug effects
KW - Epithelial Cells -- pathology
KW - Toxicity Tests, Chronic
KW - Cell Transformation, Neoplastic -- chemically induced
KW - Female
KW - Mammary Glands, Human -- cytology
KW - Arsenic -- toxicity
KW - Breast Neoplasms -- pathology
KW - Aromatase -- metabolism
KW - Breast Neoplasms -- metabolism
KW - Receptors, Estrogen -- metabolism
KW - Breast Neoplasms -- chemically induced
KW - Mammary Glands, Human -- drug effects
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1493795270?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+toxicology&rft.atitle=Arsenic-induced+cancer+cell+phenotype+in+human+breast+epithelia+is+estrogen+receptor-independent+but+involves+aromatase+activation.&rft.au=Xu%2C+Yuanyuan%3BTokar%2C+Erik+J%3BWaalkes%2C+Michael+P&rft.aulast=Xu&rft.aufirst=Yuanyuan&rft.date=2014-02-01&rft.volume=88&rft.issue=2&rft.spage=263&rft.isbn=&rft.btitle=&rft.title=Archives+of+toxicology&rft.issn=1432-0738&rft_id=info:doi/10.1007%2Fs00204-013-1131-4
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-09-30
N1 - Date created - 2014-01-30
N1 - Date revised - 2017-01-13
N1 - SuppNotes - Cited By:
Environ Health Perspect. 2010 Jan;118(1):108-15 [20056578]
Environ Health Perspect. 2009 Dec;117(12):1847-52 [20049202]
Crit Rev Toxicol. 2010 Nov;40(10):912-27 [20812815]
Toxicol Sci. 2011 Jan;119(1):73-83 [20937726]
J Steroid Biochem Mol Biol. 2011 May;125(1-2):13-22 [21335088]
Cancer Res. 2011 Aug 15;71(16):5477-87 [21840986]
Biol Trace Elem Res. 2011 Dec;144(1-3):360-79 [21660533]
Cancer Res. 2012 Mar 15;72(6):1459-66 [22422990]
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Steroids. 2013 Feb;78(2):161-70 [23178278]
J Mammary Gland Biol Neoplasia. 2013 Mar;18(1):25-42 [23392570]
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PLoS One. 2008;3(8):e2888 [18682804]
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Environ Sci Technol. 2008 Oct 1;42(19):7187-92 [18939545]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1007/s00204-013-1131-4
ER -
TY - JOUR
T1 - S-(-)equol producing status not associated with breast cancer risk among low isoflavone-consuming US postmenopausal women undergoing a physician-recommended breast biopsy.
AN - 1492703557; 24461312
AB - Soy foods are the richest sources of isoflavones, mainly daidzein and genistein. Soy isoflavones are structurally similar to the steroid hormone 17β-estradiol and may protect against breast cancer. S-(-)equol, a metabolite of the soy isoflavone daidzein, has a higher bioavailability and greater affinity for estrogen receptor β than daidzein. Approximately one-third of the Western population is able to produce S-(-)equol, and the ability is linked to certain gut microbes. We hypothesized that the prevalence of breast cancer, ductal hyperplasia, and overall breast pathology will be lower among S-(-)equol producing, as compared with nonproducing, postmenopausal women undergoing a breast biopsy. We tested our hypothesis using a cross-sectional study design. Usual diets of the participants were supplemented with 1 soy bar per day for 3 consecutive days. Liquid chromatography-multiple reaction ion monitoring mass spectrometry analysis of urine from 143 subjects revealed 25 (17.5%) as S-(-)equol producers. We found no statistically significant associations between S-(-)equol producing status and overall breast pathology (odds ratio [OR], 0.68; 95% confidence interval [CI], 0.23-1.89), ductal hyperplasia (OR, 0.84; 95% CI, 0.20-3.41), or breast cancer (OR, 0.56; 95% CI, 0.16-1.87). However, the mean dietary isoflavone intake was much lower (0.3 mg/d) than in previous reports. Given that the amount of S-(-)equol produced in the gut depends on the amount of daidzein exposure, the low soy intake coupled with lower prevalence of S-(-)equol producing status in the study population favors toward null associations. Findings from our study could be used for further investigations on S-(-)equol producing status and disease risk.
Published by Elsevier Inc.
JF - Nutrition research (New York, N.Y.)
AU - Virk-Baker, Mandeep K
AU - Barnes, Stephen
AU - Krontiras, Helen
AU - Nagy, Tim R
AD - Department of Nutrition Sciences, University of Alabama at Birmingham, Birmingham, AL, USA. Electronic address: mandeep.virk-baker@nih.gov. ; Department of Pharmacology and Toxicology, University of Alabama at Birmingham, Birmingham, AL, USA; The UAB Comprehensive Cancer Center, Birmingham, AL, USA. Electronic address: sbarnes@uab.edu. ; The UAB Comprehensive Cancer Center, Birmingham, AL, USA; Department of Surgery, Surgical Oncology, University of Alabama at Birmingham, Birmingham, AL, USA. Electronic address: helen.krontiras@ccc.uab.edu. ; Department of Nutrition Sciences, University of Alabama at Birmingham, Birmingham, AL, USA; The UAB Comprehensive Cancer Center, Birmingham, AL, USA. Electronic address: tnagy@uab.edu.
Y1 - 2014/02//
PY - 2014
DA - February 2014
SP - 116
EP - 125
VL - 34
IS - 2
KW - Estrogen Receptor beta
KW - 0
KW - Isoflavones
KW - Phytoestrogens
KW - Equol
KW - 531-95-3
KW - Index Medicus
KW - ER+
KW - Soy Screen Questionnaire
KW - liquid chromatography–multiple reaction ion monitoring mass spectrometry
KW - Dietary soy isoflavones
KW - body mass index
KW - estrogen receptor positive
KW - Ductal hyperplasia
KW - University of Alabama at Birmingham.
KW - BMI
KW - Food Frequency Questionnaire
KW - estrogen receptor negative
KW - UAB
KW - S-(−)equol status
KW - ER–
KW - Breast biopsy
KW - AS
KW - FFQ
KW - confidence interval
KW - OR
KW - African American
KW - estrogen receptor
KW - CI
KW - Postmenopausal women
KW - AA
KW - odds ratio
KW - ER
KW - LC-MRM-MS
KW - SSQ
KW - Asian American
KW - Breast cancer
KW - United States
KW - Cross-Sectional Studies
KW - Odds Ratio
KW - Postmenopause
KW - Humans
KW - Soy Foods
KW - Aged
KW - Middle Aged
KW - Dietary Supplements
KW - Biopsy
KW - Estrogen Receptor beta -- metabolism
KW - Feeding Behavior
KW - Female
KW - Biological Availability
KW - Isoflavones -- pharmacology
KW - Phytoestrogens -- pharmacology
KW - Isoflavones -- administration & dosage
KW - Soybeans -- chemistry
KW - Breast Neoplasms -- etiology
KW - Equol -- urine
KW - Breast Neoplasms -- metabolism
KW - Breast -- pathology
KW - Diet
KW - Phytoestrogens -- administration & dosage
KW - Equol -- metabolism
KW - Equol -- biosynthesis
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nutrition+research+%28New+York%2C+N.Y.%29&rft.atitle=S-%28-%29equol+producing+status+not+associated+with+breast+cancer+risk+among+low+isoflavone-consuming+US+postmenopausal+women+undergoing+a+physician-recommended+breast+biopsy.&rft.au=Virk-Baker%2C+Mandeep+K%3BBarnes%2C+Stephen%3BKrontiras%2C+Helen%3BNagy%2C+Tim+R&rft.aulast=Virk-Baker&rft.aufirst=Mandeep&rft.date=2014-02-01&rft.volume=34&rft.issue=2&rft.spage=116&rft.isbn=&rft.btitle=&rft.title=Nutrition+research+%28New+York%2C+N.Y.%29&rft.issn=1879-0739&rft_id=info:doi/10.1016%2Fj.nutres.2013.12.002
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-09-11
N1 - Date created - 2014-01-27
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.nutres.2013.12.002
ER -
TY - JOUR
T1 - Endometrial thickness and risk of breast and endometrial carcinomas in the prostate, lung, colorectal and ovarian cancer screening trial
AN - 1492633661; 18888730
AB - Postmenopausal women with higher circulating estrogen levels are at increased risk of developing breast and endometrial carcinomas. In the endometrium, excess estrogen relative to progesterone produces a net proliferative stimulus, which may result in endometrial thickening. Therefore, the hypothesis that endometrial thickness is a biological marker of excess estrogen stimulation that is associated with risk of breast and endometrial carcinomas was tested. Endometrial thickness was measured in 1,272 postmenopausal women, aged 55-74 years, who underwent transvaginal ultrasound (TVU) screening as part of the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. Serial endometrial thickness measurements were available for a subset of women at 1 year (n=1,018), 2 years (n=869) and 3 years (n=641) after baseline. The associations between endometrial thickness and breast (n=91) and endometrial (n=14) carcinoma were evaluated by estimating relative risks (RRs) and 95% confidence intervals (CIs) using Cox proportional hazards regression with age as the time metric. Models incorporating baseline endometrial thickness and as a time-varying covariate using all measurements were examined. Median follow-up among study participants was 12.5 years (range: 0.3-13.8 years). Compared to baseline endometrial thickness of 1.0-2.99 mm, women with baseline endometrial thickness greater than or equal to 5.0 mm had an increased risk of breast (RR=2.00, 95% CI=1.15-3.48) and endometrial (RR=5.02, 95% CI=0.96-26.36) carcinomas in models adjusted for menopausal hormone use and BMI. These data suggest that increased endometrial thickness as assessed by TVU was associated with increased risk of breast and endometrial carcinomas. What's new? Endometrial thickness is related to obesity and menopausal hormone use, factors associated with a higher incidence of breast and endometrial carcinomas. Given these associations, the authors of this study investigated whether endometrial thickness was independently associated with incident breast or endometrial carcinoma risk. In a cohort of 1,272 women, an endometrial thickness greater than five millimeters was associated with a two-fold increase in risk for breast carcinoma and a five-fold increase in risk for endometrial carcinoma.
JF - International Journal of Cancer
AU - Felix, Ashley S
AU - Weissfeld, Joel L
AU - Pfeiffer, Ruth M
AU - Modugno, Francesmary
AU - Black, Amanda
AU - Hill, Lyndon M
AU - Martin, Jerry
AU - Sit, Anita S
AU - Sherman, Mark E
AU - Brinton, Louise A
AD - Cancer Prevention Fellowship Program, Division of Cancer Prevention, National Cancer Institute, National Institutes of Health, Rockville, MD.
Y1 - 2014/02//
PY - 2014
DA - Feb 2014
SP - 954
EP - 960
PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States
VL - 134
IS - 4
SN - 0020-7136, 0020-7136
KW - Health & Safety Science Abstracts; Risk Abstracts
KW - Age
KW - Risk assessment
KW - H 11000:Diseases/Injuries/Trauma
KW - R2 23060:Medical and environmental health
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492633661?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Cancer&rft.atitle=Endometrial+thickness+and+risk+of+breast+and+endometrial+carcinomas+in+the+prostate%2C+lung%2C+colorectal+and+ovarian+cancer+screening+trial&rft.au=Felix%2C+Ashley+S%3BWeissfeld%2C+Joel+L%3BPfeiffer%2C+Ruth+M%3BModugno%2C+Francesmary%3BBlack%2C+Amanda%3BHill%2C+Lyndon+M%3BMartin%2C+Jerry%3BSit%2C+Anita+S%3BSherman%2C+Mark+E%3BBrinton%2C+Louise+A&rft.aulast=Felix&rft.aufirst=Ashley&rft.date=2014-02-01&rft.volume=134&rft.issue=4&rft.spage=954&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.28404
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-01-01
N1 - Last updated - 2014-02-11
N1 - SubjectsTermNotLitGenreText - Risk assessment
DO - http://dx.doi.org/10.1002/ijc.28404
ER -
TY - JOUR
T1 - Role of Myc in hepatocellular proliferation and hepatocarcinogenesis.
AN - 1490900417; 24096051
AB - Myc is involved in cell growth, proliferation, apoptosis, energy metabolism, and differentiation. Whether it is essential for hepatocellular proliferation and carcinogenesis is unclear due to a lack of an efficient hepatocyte-specific Myc disruption model. This study used a novel genetic model to investigate the involvement of Myc in hepatocellular proliferation and hepatocarcinogenesis in mice.
Temporal hepatocyte-specific Myc disruption was achieved by use of the tamoxifen-inducible Cre-ER(T2) recombinase system under control of the serum albumin promoter. Hepatocyte proliferation was assessed by administering peroxisome proliferator-activated receptor α (PPARα) agonist Wy-14,643. A diethylnitrosamine-induced liver cancer model was used to evaluate the role of Myc in hepatocarcinogenesis. Tamoxifen administration induced recombination of Myc specifically in hepatocytes of Myc(fl/fl,ERT2-Cre) mice. When treated with a known hepatocellular proliferative stimulus Wy-14,643, Myc(fl/fl,ERT2-Cre) mice showed a lower liver/body weight ratio and suppressed hepatocyte proliferation as compared to Myc(fl/fl) mice. Hepatic expression of cell cycle control genes, DNA repair genes, and Myc target gene miRNAs were upregulated in Wy-14,643-treated Myc(fl/fl) mouse livers, but not in Wy-14,643-treated Myc(fl/fl,ERT2-Cre) livers. However, no differences were observed in the lipid-lowering effect of Wy-14,643 between Myc(fl/fl,ERT2-Cre) and Myc(fl/fl) mice, consistent with no differences in the expression of several PPARα target genes involved in fatty acid β-oxidation. Moreover, when subjected to the diethylnitrosamine liver cancer bioassay, Myc(fl/fl,ERT2-Cre) mice exhibited a markedly lower incidence of tumor formation compared with Myc(fl/fl) mice.
Myc plays an essential role in hepatocellular proliferation and liver tumorigenesis. Published by Elsevier B.V.
JF - Journal of hepatology
AU - Qu, Aijuan
AU - Jiang, Changtao
AU - Cai, Yan
AU - Kim, Jung-Hwan
AU - Tanaka, Naoki
AU - Ward, Jerrold M
AU - Shah, Yatrik M
AU - Gonzalez, Frank J
AD - Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, United States. ; Global VetPathology, Montgomery Village, MD 20866, United States. ; Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, United States; Department of Molecular and Integrative Physiology and Internal Medicine, Division of Gastroenterology, University of Michigan School of Medicine, Ann Arbor, MI 48109, United States. ; Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, United States. Electronic address: gonzalef@mail.nih.gov.
Y1 - 2014/02//
PY - 2014
DA - February 2014
SP - 331
EP - 338
VL - 60
IS - 2
KW - Fatty Acids
KW - 0
KW - MIRN17-92 microRNA, mouse
KW - MicroRNAs
KW - PPAR alpha
KW - Pyrimidines
KW - RNA, Messenger
KW - pirinixic acid
KW - 86C4MRT55A
KW - Index Medicus
KW - peroxisome proliferator-activated receptor α
KW - Cyp4a10 and Cyp4a14
KW - diethynitrosamine
KW - Rad51
KW - cre recombinase, tamoxifen-inducible estrogen receptor ligand-binding domain fusion protein
KW - minichromosome maintenance
KW - DEN
KW - α/β interferon-inducible Mx-promoter driving Cre recombinase
KW - floxed Myc allele
KW - cytochromes P450 4a10 and 4a14
KW - bromodeoxyuridine
KW - CDK
KW - RAD51 homolog (S. cerevisiae)
KW - bHLH
KW - acyl-CoA oxidase
KW - cyclin-dependent kinase
KW - Myc(fl/fl)
KW - Myc
KW - inducible liver-specific Myc knockout mouse
KW - Tumorigenesis
KW - Mcm
KW - Myc(fl/fl,ERT2-Cre)
KW - PPARα
KW - Cre-ER(T2)
KW - serum albumin promoter
KW - BrdU
KW - Acox1
KW - checkpoint kinase 1 homologue
KW - Chek1
KW - Cell cycle control
KW - basic helix-loop-helix leucine zipper
KW - Cell proliferation
KW - Myc(fl/fl)Mx-Cre
KW - SA
KW - Cell Proliferation -- drug effects
KW - Animals
KW - MicroRNAs -- genetics
KW - Pyrimidines -- pharmacology
KW - Mice
KW - RNA, Messenger -- genetics
KW - PPAR alpha -- agonists
KW - Fatty Acids -- metabolism
KW - Mice, Knockout
KW - Gene Knockout Techniques
KW - MicroRNAs -- metabolism
KW - RNA, Messenger -- metabolism
KW - Models, Genetic
KW - Male
KW - Liver Neoplasms, Experimental -- genetics
KW - Hepatocytes -- drug effects
KW - Liver Neoplasms, Experimental -- pathology
KW - Liver Neoplasms, Experimental -- etiology
KW - Genes, myc
KW - Hepatocytes -- pathology
KW - Hepatocytes -- metabolism
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-09-26
N1 - Date created - 2014-01-20
N1 - Date revised - 2017-01-13
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.jhep.2013.09.024
ER -
TY - JOUR
T1 - The potential of hyperpolarized (13)C MRI in assessing signaling pathways in cancer.
AN - 1490899543; 24439335
AB - Advances in genomics are enabling integration of various -omics to reveal the complexities underneath carcinogenesis. Multivariate signaling pathways are deregulated and evolve spatially and temporally depending on the tumor microenvironment. This finding shifts the focus of cancer research from "one disease-one target and drug" to "one disease-multiple pathway targets and combinational therapy" and imposes new challenges on the imaging community in terms of imaging targets, scales and information levels. In current clinical settings, most imaging modalities assess cancer risk through alternations in anatomy, function, metabolism, cellularity, or limited molecular events. Few clinical-translatable imaging modalities are capable of detecting aberrations in signaling pathways at the level of tissue biology. An exception to this is hyperpolarized (13)C magnetic resonance spectroscopic imaging (HP (13)C MRI), which is capable of imaging the molecular signatures of special metabolic enzymes using HP (13)C-labeled substrates. HP (13)C MRI can identify multiple metabolites including intermediates and products simultaneously to allow extraction of critical parameters such as flux alterations for multiple metabolic pathways. Meanwhile, recent progress in cancer metabolism research affirms that metabolic alterations are directly controlled by signaling pathways. Thus, in vivo assessment of aberrations occurring in signaling pathways becomes feasible through HP (13)C imaging. This report briefly reviews the connections between signaling pathways and cancer metabolic phenotypes, the current status of HP (13)C MRI in assessing signal pathways, and recent advances in HP (13)C MRI techniques. Integrated with cancer genomics and animal models, HP (13)C MRI may hold high promise in exploring important issues in cancer that are linked to functionality of signaling pathways. Examples include genomic-driven therapy, intratumoral heterogeneity, and drug resistances. Published by Elsevier Inc.
JF - Academic radiology
AU - Zhang, Huiming
AD - Division of Cancer Treatment and Diagnosis, Cancer Imaging Program, National Cancer Institute, National Institutes of Health, Bethesda, MD. Electronic address: zhanghui@mail.nih.gov.
Y1 - 2014/02//
PY - 2014
DA - February 2014
SP - 215
EP - 222
VL - 21
IS - 2
KW - Carbon Isotopes
KW - 0
KW - Neoplasm Proteins
KW - Index Medicus
KW - cancer genomics–driven approach
KW - cancer metabolism
KW - signaling pathways
KW - metabolic imaging
KW - Hyperpolarized (13)C MRI
KW - Image Interpretation, Computer-Assisted -- methods
KW - Animals
KW - Feasibility Studies
KW - Humans
KW - Molecular Imaging -- methods
KW - Carbon Isotopes -- pharmacokinetics
KW - Magnetic Resonance Spectroscopy -- methods
KW - Magnetic Resonance Imaging -- methods
KW - Algorithms
KW - Neoplasm Proteins -- metabolism
KW - Signal Transduction
KW - Neoplasms -- metabolism
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1490899543?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Academic+radiology&rft.atitle=The+potential+of+hyperpolarized+%2813%29C+MRI+in+assessing+signaling+pathways+in+cancer.&rft.au=Zhang%2C+Huiming&rft.aulast=Zhang&rft.aufirst=Huiming&rft.date=2014-02-01&rft.volume=21&rft.issue=2&rft.spage=215&rft.isbn=&rft.btitle=&rft.title=Academic+radiology&rft.issn=1878-4046&rft_id=info:doi/10.1016%2Fj.acra.2013.11.015
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-11-06
N1 - Date created - 2014-01-20
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.acra.2013.11.015
ER -
TY - JOUR
T1 - A phase II study of cixutumumab (IMC-A12, NSC742460) in advanced hepatocellular carcinoma.
AN - 1490899263; 24045151
AB - IGF-IR is implicated in hepatic carcinogenesis. This and preliminary evidence of biological activity of anti-IGF-1R monoclonal antibody cixutumumab in phase I trials prompted this phase II study.
Patients with advanced HCC, Child-Pugh A-B8, received cixutumumab 6mg/kg weekly, in a Simon two-stage design study, with the primary endpoints being 4-month PFS and RECIST-defined response rate. Tissue and circulating markers plus different HCC scoring systems were evaluated for correlation with PFS and OS. As a result of pre-specified futility criteria, only stage 1 was accrued: N=24: median age 67.5 years (range 49-83), KPS 80% (70-90%), 20 males (83%), 9 stage III (37%)/15 stage IV (63%), 18 Child-Pugh A (75%), 11 HBV (46%)/10 HCV (42%)/11 alcoholic cirrhosis (46%)/2 NASH (8%), 11 (46%) diabetic. Median number of doses: 7 (range 1-140). Grade 3/4 toxicities >10% included: diabetes, elevated liver function tests, hyponatremia, and lymphopenia. Four-month PFS was 30% (95% CI 13-48), and there were no objective responses. Median overall survival was 8 months (95% CI 5.8-14). IGF-R1 staining did not correlate with outcome. Elevated IGFBP-1 correlated with improved PFS (1.2 [95% CI 1-1.4]; p 0.009) and OS (1.2 [95% CI 1.1-1.4]; p 0.003).
Cixutumumab monotherapy did not have clinically meaningful activity in this unselected HCC population. Grade 3-4 hyperglycemia occurred in 46% of patients. Elevated IGFBP-1 correlated with improved PFS and OS. Copyright © 2013 European Association for the Study of the Liver. All rights reserved.
JF - Journal of hepatology
AU - Abou-Alfa, Ghassan K
AU - Capanu, Marinela
AU - O'Reilly, Eileen M
AU - Ma, Jennifer
AU - Chou, Joanne F
AU - Gansukh, Bolorsukh
AU - Shia, Jinru
AU - Kalin, Marcia
AU - Katz, Seth
AU - Abad, Leslie
AU - Reidy-Lagunes, Diane L
AU - Kelsen, David P
AU - Chen, Helen X
AU - Saltz, Leonard B
AD - Department of Internal Medicine, Memorial Sloan-Kettering Cancer Center, New York, NY, United States; Department of Internal Medicine, Weill Medical College at Cornell University, New York, NY, United States. Electronic address: abou-alg@mskcc.org. ; Department of Epidemiology and Biostatistics, Memorial Sloan-Kettering Cancer Center, New York, NY, United States. ; Department of Internal Medicine, Memorial Sloan-Kettering Cancer Center, New York, NY, United States; Department of Internal Medicine, Weill Medical College at Cornell University, New York, NY, United States. ; Department of Internal Medicine, Memorial Sloan-Kettering Cancer Center, New York, NY, United States. ; Department of Pathology, Memorial Sloan-Kettering Cancer Center, New York, NY, United States. ; Department of Radiology, Memorial Sloan-Kettering Cancer Center, New York, NY, United States. ; Research Department, ImClone Systems, a wholly-owned subsidiary of Eli Lilly & Company, New York, NY, United States. ; Cancer Therapy Evaluation Program (CTEP), National Cancer Institute, Bethesda, MD, United States.
Y1 - 2014/02//
PY - 2014
DA - February 2014
SP - 319
EP - 324
VL - 60
IS - 2
KW - Antibodies, Monoclonal
KW - 0
KW - Biomarkers, Tumor
KW - IGFBP1 protein, human
KW - IGFBP3 protein, human
KW - Insulin-Like Growth Factor Binding Protein 1
KW - Insulin-Like Growth Factor Binding Protein 3
KW - anti-IGF-1R antibody A12
KW - Insulin-Like Growth Factor I
KW - 67763-96-6
KW - Insulin-Like Growth Factor II
KW - 67763-97-7
KW - Receptor, IGF Type 1
KW - EC 2.7.10.1
KW - Index Medicus
KW - HR
KW - LOH
KW - CTEP/NCI
KW - Units/Liter
KW - Insulin growth factor 1 receptor
KW - Cell conditioning 1
KW - Insulin-like growth factor binding protein 1
KW - ELISA
KW - progression free survival
KW - Insulin-like growth factor binding protein 3
KW - mcl
KW - IGFBP 1
KW - Enzyme-linked immunosorbent assay
KW - RECIST
KW - Mitogen activated protein
KW - ALT
KW - Insulin growth factor 2
KW - ADCC
KW - IGFBP 3
KW - Loss of heterozygosity
KW - Insulin growth factor 1
KW - Karnofsky performance status
KW - Free IGF1
KW - Cixutumumab (IMC-A12, NSC742460)
KW - PFS
KW - mg/kg
KW - Milliliter per minute
KW - Alanine aminotransferase
KW - HIV
KW - Response evaluation criteria in solid tumors
KW - Antibody-dependent complement-mediated cytotoxicity
KW - Aspartate aminotransferase
KW - Insulin growth factor 2 receptor
KW - CALGB
KW - AJCC
KW - IRB
KW - milligram/kilogram
KW - Overall urvival
KW - American Joint Committee on Cancer
KW - IGF-1R
KW - mg/dl
KW - IgG1
KW - CTCAE
KW - PT/INR
KW - CDC
KW - Hepatocellular Carcinoma
KW - Complement-dependent cytotoxicity
KW - Prothrombin time/International normalized ratio
KW - Non-alcoholic steatohepatitis
KW - Immunoglobulin 1
KW - Hepatocellular carcinoma
KW - units/L
KW - KPS
KW - OS
KW - Cells per microliter
KW - IGF2
KW - Institutional Review Board
KW - Cancer Leukemia Group B
KW - IGF-IR
KW - IGF-2
KW - ml/min
KW - IGF-1
KW - MAP
KW - Diabetes
KW - Hazard ratio
KW - Common terminology criteria for adverse events
KW - Milligram/deciliter
KW - Human immunodeficiency virus
KW - AST
KW - IGF-2R
KW - CC1
KW - Cancer Therapy Evaluation Program (CTEP)/National Cancer Institute
KW - NASH
KW - HCC
KW - Receptor, IGF Type 1 -- metabolism
KW - Humans
KW - Aged
KW - Insulin-Like Growth Factor I -- metabolism
KW - Insulin-Like Growth Factor II -- metabolism
KW - Biomarkers, Tumor -- metabolism
KW - Kaplan-Meier Estimate
KW - Aged, 80 and over
KW - Middle Aged
KW - Insulin-Like Growth Factor Binding Protein 1 -- blood
KW - Biomarkers, Tumor -- blood
KW - Insulin-Like Growth Factor Binding Protein 3 -- blood
KW - Female
KW - Male
KW - Liver Neoplasms -- pathology
KW - Liver Neoplasms -- therapy
KW - Carcinoma, Hepatocellular -- therapy
KW - Carcinoma, Hepatocellular -- blood
KW - Carcinoma, Hepatocellular -- pathology
KW - Liver Neoplasms -- blood
KW - Antibodies, Monoclonal -- therapeutic use
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1490899263?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+hepatology&rft.atitle=A+phase+II+study+of+cixutumumab+%28IMC-A12%2C+NSC742460%29+in+advanced+hepatocellular+carcinoma.&rft.au=Abou-Alfa%2C+Ghassan+K%3BCapanu%2C+Marinela%3BO%27Reilly%2C+Eileen+M%3BMa%2C+Jennifer%3BChou%2C+Joanne+F%3BGansukh%2C+Bolorsukh%3BShia%2C+Jinru%3BKalin%2C+Marcia%3BKatz%2C+Seth%3BAbad%2C+Leslie%3BReidy-Lagunes%2C+Diane+L%3BKelsen%2C+David+P%3BChen%2C+Helen+X%3BSaltz%2C+Leonard+B&rft.aulast=Abou-Alfa&rft.aufirst=Ghassan&rft.date=2014-02-01&rft.volume=60&rft.issue=2&rft.spage=319&rft.isbn=&rft.btitle=&rft.title=Journal+of+hepatology&rft.issn=1600-0641&rft_id=info:doi/10.1016%2Fj.jhep.2013.09.008
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-09-26
N1 - Date created - 2014-01-20
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
J Natl Cancer Inst. 2000 Feb 2;92(3):205-16 [10655437]
J Clin Oncol. 2011 Jul 20;29(21):e638-40 [21606420]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.jhep.2013.09.008
ER -
TY - JOUR
T1 - Pain-related depression of the mesolimbic dopamine system in rats: expression, blockade by analgesics, and role of endogenous κ-opioids.
AN - 1490758611; 24008352
AB - Pain is often associated with depression of behavior and mood, and relief of pain-related depression is a common goal of treatment. This study tested the hypothesis that pain-related behavioral depression is mediated by activation of endogenous κ-opioid systems and subsequent depression of mesolimbic dopamine release. Adult male Sprague-Dawley rats were implanted with electrodes targeting the medial forebrain bundle (for behavior studies of intracranial self-stimulation (ICSS)) or with cannulae for microdialysis measures of nucleus accumbens dopamine (NAc DA). Changes in ICSS and NAc DA were examined after treatment with a visceral noxious stimulus (intraperitoneal injection of dilute lactic acid) or an exogenous κ-agonist (U69593). Additional studies examined the sensitivity of acid and U69593 effects to blockade by two analgesics (the nonsteroidal antiinflammatory drug ketoprofen and the μ-opioid agonist morphine) or by the κ-antagonist norbinaltorphimine (norBNI). The effects of acid were also examined on mRNA expression for prodynorphin (PDYN) and κ-opioid receptors (KORs) in mesocorticolimbic brain regions. Both acid and U69593 depressed ICSS and extracellular levels of NAc DA. Pain-related acid effects were blocked by ketoprofen and morphine but not by norBNI. The U69593 effects were blocked by norBNI but not by ketoprofen, and were only attenuated by morphine. Acid did not significantly alter PDYN or KOR in NAc, but it produced a delayed increase in PDYN in prefrontal cortex. These results support a key role for the mesolimbic DA system, but a more nuanced role for endogenous κ-opioid systems, in mediating acute pain-related behavioral depression in rats.
JF - Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology
AU - Leitl, Michael D
AU - Onvani, Sara
AU - Bowers, M Scott
AU - Cheng, Kejun
AU - Rice, Kenner C
AU - Carlezon, William A
AU - Banks, Matthew L
AU - Negus, S Stevens
AD - Department of Pharmacology and Toxicology, Virginia Commonwealth University, Richmond, VA, USA. ; Behavioral Genetics Laboratory, McLean Hospital, Harvard Medical School, Belmont, MA, USA. ; Department of Psychiatry, Virginia Commonwealth University, Richmond, VA, USA. ; Chemical Biology Research Branch, National Institute on Drug Abuse and National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA.
Y1 - 2014/02//
PY - 2014
DA - February 2014
SP - 614
EP - 624
VL - 39
IS - 3
KW - Analgesics, Opioid
KW - 0
KW - Benzeneacetamides
KW - Narcotic Antagonists
KW - Pyrrolidines
KW - Receptors, Opioid, kappa
KW - Lactic Acid
KW - 33X04XA5AT
KW - norbinaltorphimine
KW - 36OOQ86QM1
KW - Naltrexone
KW - 5S6W795CQM
KW - Morphine
KW - 76I7G6D29C
KW - Ketoprofen
KW - 90Y4QC304K
KW - U 69593
KW - J5S4K6TKTG
KW - Dopamine
KW - VTD58H1Z2X
KW - Index Medicus
KW - Animals
KW - Benzeneacetamides -- pharmacology
KW - Self Stimulation
KW - Medial Forebrain Bundle -- drug effects
KW - Medial Forebrain Bundle -- physiology
KW - Naltrexone -- analogs & derivatives
KW - Disease Models, Animal
KW - Ketoprofen -- pharmacology
KW - Morphine -- pharmacology
KW - Rats
KW - Rats, Sprague-Dawley
KW - Analgesics, Opioid -- pharmacology
KW - Naltrexone -- pharmacology
KW - Pyrrolidines -- pharmacology
KW - Time Factors
KW - Narcotic Antagonists -- pharmacology
KW - Lactic Acid -- pharmacology
KW - Male
KW - Pain -- complications
KW - Pain -- drug therapy
KW - Depression -- pathology
KW - Receptors, Opioid, kappa -- genetics
KW - Nucleus Accumbens -- drug effects
KW - Depression -- etiology
KW - Depression -- metabolism
KW - Receptors, Opioid, kappa -- metabolism
KW - Nucleus Accumbens -- metabolism
KW - Dopamine -- metabolism
KW - Gene Expression Regulation -- drug effects
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuropsychopharmacology+%3A+official+publication+of+the+American+College+of+Neuropsychopharmacology&rft.atitle=Pain-related+depression+of+the+mesolimbic+dopamine+system+in+rats%3A+expression%2C+blockade+by+analgesics%2C+and+role+of+endogenous+%CE%BA-opioids.&rft.au=Leitl%2C+Michael+D%3BOnvani%2C+Sara%3BBowers%2C+M+Scott%3BCheng%2C+Kejun%3BRice%2C+Kenner+C%3BCarlezon%2C+William+A%3BBanks%2C+Matthew+L%3BNegus%2C+S+Stevens&rft.aulast=Leitl&rft.aufirst=Michael&rft.date=2014-02-01&rft.volume=39&rft.issue=3&rft.spage=614&rft.isbn=&rft.btitle=&rft.title=Neuropsychopharmacology+%3A+official+publication+of+the+American+College+of+Neuropsychopharmacology&rft.issn=1740-634X&rft_id=info:doi/10.1038%2Fnpp.2013.236
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-09-10
N1 - Date created - 2014-01-16
N1 - Date revised - 2017-01-13
N1 - SuppNotes - Cited By:
J Pharmacol Exp Ther. 2012 Nov;343(2):389-400 [22892341]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1038/npp.2013.236
ER -
TY - JOUR
T1 - Approaches and considerations for the assessment of immunotoxicity for environmental chemicals: a workshop summary.
AN - 1490704678; 24280359
AB - As experience is gained with toxicology testing and as new assays and technologies are developed, it is critical for stakeholders to discuss opportunities to advance our overall testing strategies. To facilitate these discussions, a workshop on practices for assessing immunotoxicity for environmental chemicals was held with the goal of sharing perspectives on immunotoxicity testing strategies and experiences, developmental immunotoxicity (DIT), and integrated and alternative approaches to immunotoxicity testing. Experiences across the chemical and pharmaceutical industries suggested that standard toxicity studies, combined with triggered-based testing approaches, represent an effective and efficient approach to evaluate immunotoxic potential. Additionally, discussions on study design, critical windows, and new guideline approaches and experiences identified important factors to consider before initiating DIT evaluations including assay choice and timing and the impact of existing adult data. Participants agreed that integrating endpoints into standard repeat-dose studies should be considered for fulfilling any immunotoxicity testing requirements, while also maximizing information and reducing animal use. Participants also acknowledged that in vitro evaluation of immunosuppression is complex and may require the use of multiple assays that are still being developed. These workshop discussions should contribute to developing an effective but more resource and animal efficient approach for evaluating chemical immunotoxicity.
Copyright © 2013 Elsevier Inc. All rights reserved.
JF - Regulatory toxicology and pharmacology : RTP
AU - Boverhof, Darrell R
AU - Ladics, Greg
AU - Luebke, Bob
AU - Botham, Jane
AU - Corsini, Emanuela
AU - Evans, Ellen
AU - Germolec, Dori
AU - Holsapple, Michael
AU - Loveless, Scott E
AU - Lu, Haitian
AU - van der Laan, Jan Willem
AU - White, Kimber L
AU - Yang, Yung
AD - The Dow Chemical Company, Midland, MI, United States. Electronic address: rboverhof@dow.com. ; DuPont Pioneer, Wilmington, DE, United States. ; Cardiopulmonary and Immunotoxicology Branch, US Environmental Protection Agency, Research Triangle Park, NC, United States. ; Syngenta Ltd., Macclesfield, UK. ; Laboratory of Toxicology, Dipartimento di Scienze Farmacologiche e Biomolecolari, Università degli Studi di Milano, Milan, Italy. ; Pfizer, Inc., Groton, CT, United States. ; National Toxicology Program, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC, United States. ; Battelle Memorial Institute, Columbus, OH, United States. ; DuPont Haskell Global Centers for Health and Environmental Sciences, Newark, DE, United States. ; Dow AgroSciences, Indianapolis, IN, United States. ; Medicines Evaluation Board, Utrecht, The Netherlands. ; ImmunoTox® Inc., Richmond, VA, United States. ; Office of Pesticides Programs, US Environmental Protection Agency, Washington, DC, United States.
Y1 - 2014/02//
PY - 2014
DA - February 2014
SP - 96
EP - 107
VL - 68
IS - 1
KW - Environmental Pollutants
KW - 0
KW - Index Medicus
KW - AFC
KW - keyhole limpet hemocyanin
KW - agricultural chemical safety assessment
KW - NIEHS
KW - European union
KW - developmental and reproductive toxicology
KW - NOAEL
KW - NIOSH
KW - T-cell dependent antibody reaction
KW - PND
KW - Environmental chemicals
KW - ELISA
KW - RIVM
KW - national institute of environmental health sciences
KW - US
KW - STS
KW - DART
KW - antibody forming cell
KW - EU
KW - weight-of-evidence
KW - SRBC
KW - allergic contact dermatitis
KW - EPA
KW - national institute for occupational safety and health
KW - standard toxicology studies
KW - WoE
KW - NK
KW - FDA
KW - HESI
KW - ACSA
KW - EOGRTS
KW - developmental immunotoxicity
KW - international life sciences institute
KW - United States
KW - 2,4-D
KW - postnatal day
KW - no observed adverse effect level
KW - national toxicology program
KW - organisation for economic cooperation and development
KW - natural killer
KW - environmental protection agency
KW - Testing
KW - local lymph node assay
KW - enzyme linked immunosorbent assay
KW - cyclophosphamide
KW - ACD
KW - 2,4-dichlorophenoxyacetic acid
KW - international conference on harmonization
KW - NRC
KW - national research council
KW - KLH
KW - sheep red blood cells
KW - CT
KW - DIT
KW - food and drug administration
KW - ICH
KW - health and environmental sciences institute
KW - carbon tetrachloride
KW - Immunotoxicity
KW - NTP
KW - extended one-generation reproductive toxicity study
KW - TDAR
KW - OECD
KW - LLNA
KW - CP
KW - dutch national institute of public health and the environment
KW - ILSI
KW - Animals
KW - Humans
KW - Toxicity Tests
KW - Environmental Exposure -- adverse effects
KW - Female
KW - Risk Assessment
KW - Prenatal Exposure Delayed Effects
KW - Pregnancy
KW - Immune System -- drug effects
KW - Environmental Pollutants -- toxicity
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1490704678?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Regulatory+toxicology+and+pharmacology+%3A+RTP&rft.atitle=Approaches+and+considerations+for+the+assessment+of+immunotoxicity+for+environmental+chemicals%3A+a+workshop+summary.&rft.au=Boverhof%2C+Darrell+R%3BLadics%2C+Greg%3BLuebke%2C+Bob%3BBotham%2C+Jane%3BCorsini%2C+Emanuela%3BEvans%2C+Ellen%3BGermolec%2C+Dori%3BHolsapple%2C+Michael%3BLoveless%2C+Scott+E%3BLu%2C+Haitian%3Bvan+der+Laan%2C+Jan+Willem%3BWhite%2C+Kimber+L%3BYang%2C+Yung&rft.aulast=Boverhof&rft.aufirst=Darrell&rft.date=2014-02-01&rft.volume=68&rft.issue=1&rft.spage=96&rft.isbn=&rft.btitle=&rft.title=Regulatory+toxicology+and+pharmacology+%3A+RTP&rft.issn=1096-0295&rft_id=info:doi/10.1016%2Fj.yrtph.2013.11.012
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-09-04
N1 - Date created - 2014-01-13
N1 - Date revised - 2017-01-14
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.yrtph.2013.11.012
ER -
TY - JOUR
T1 - Targeting notch signaling pathway in cancer: clinical development advances and challenges.
AN - 1490702251; 24076266
AB - Notch signaling plays an important role in development and cell fate determination, and it is deregulated in human hematologic malignancies and solid tumors. This review includes a brief introduction of the relevant pathophysiology of Notch signaling pathway and primarily focuses on the clinical development of promising agents that either obstruct Notch receptor cleavages such as γ-secretase inhibitors (GSIs) or interfere with the Notch ligand-receptor interaction by monoclonal antibodies (mAbs). Antitumor activity by GSIs and mAbs administered as single agent in early phases of clinical trials has been observed in advanced or metastatic thyroid cancer, non-small cell lung cancer, intracranial tumors, sarcoma or desmoid tumors, colorectal cancer with neuroendocrine features, melanoma and ovarian cancer. A number of mechanism-based adverse events particularly gastrointestinal toxicities emerged and mitigation strategies are developed after testing multiple GSIs and Notch targeting mAbs. We also discuss pharmacodynamic biomarkers in conjunction with methods of assessment of the molecular target inhibition validation. Biomarkers of efficacy or benefit may be of importance for a successful development of this class of drugs. Published by Elsevier Inc.
JF - Pharmacology & therapeutics
AU - Takebe, Naoko
AU - Nguyen, Dat
AU - Yang, Sherry X
AD - Cancer Therapy Evaluation Program, Division of Cancer Treatment and Diagnosis, National Cancer Institute, National Institutes of Health, Bethesda, United States. Electronic address: takeben@mail.nih.gov. ; National Clinical Target Validation Laboratory, Division of Cancer Treatment and Diagnosis, National Cancer Institute, National Institutes of Health, Bethesda, United States. ; National Clinical Target Validation Laboratory, Division of Cancer Treatment and Diagnosis, National Cancer Institute, National Institutes of Health, Bethesda, United States. Electronic address: Sherry.Yang@nih.gov.
Y1 - 2014/02//
PY - 2014
DA - February 2014
SP - 140
EP - 149
VL - 141
IS - 2
KW - Antineoplastic Agents
KW - 0
KW - Biomarkers
KW - Receptors, Notch
KW - Index Medicus
KW - JAG
KW - cancer stem cells
KW - MSFE
KW - T-LL
KW - Clinical trials
KW - a disintegrin and metalloproteases
KW - MTD
KW - partial response
KW - ethylenediaminetetraacetic acid
KW - dose limiting toxicity
KW - stable disease
KW - maximum tolerated dose
KW - T-cell lymphoblastic lymphoma
KW - TICs
KW - tumor initiating cells
KW - mAb
KW - RECIST
KW - Diarrhea
KW - Jagged
KW - Monoclonal antibodies (mAbs)
KW - GSI
KW - metalloproteinase tumor necrosis factor-α-converting enzyme
KW - mammosphere-forming efficiency
KW - TACE
KW - PR
KW - MAML
KW - Notch intracellular domain
KW - T-cell acute lymphoblastic leukemia
KW - DLT
KW - DLL
KW - GBM
KW - EDTA
KW - response evaluation criteria in solid tumors
KW - pharmacodynamics
KW - γ-Secretase inhibitors
KW - CSCs
KW - NICD
KW - γ-secretase inhibitor
KW - SD
KW - mastermind-like
KW - non-small cell lung cancer
KW - glioblastoma multiforme
KW - ADAM
KW - T-ALL
KW - NSCLC
KW - Delta-like ligand
KW - PK
KW - PD
KW - Notch signaling
KW - CR
KW - pharmacokinetics
KW - complete response
KW - monoclonal antibody
KW - Animals
KW - Humans
KW - Biomarkers -- metabolism
KW - Neovascularization, Pathologic
KW - Antineoplastic Agents -- therapeutic use
KW - Signal Transduction
KW - Neoplastic Stem Cells -- metabolism
KW - Neoplasms -- drug therapy
KW - Receptors, Notch -- metabolism
KW - Neoplasms -- metabolism
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacology+%26+therapeutics&rft.atitle=Targeting+notch+signaling+pathway+in+cancer%3A+clinical+development+advances+and+challenges.&rft.au=Takebe%2C+Naoko%3BNguyen%2C+Dat%3BYang%2C+Sherry+X&rft.aulast=Takebe&rft.aufirst=Naoko&rft.date=2014-02-01&rft.volume=141&rft.issue=2&rft.spage=140&rft.isbn=&rft.btitle=&rft.title=Pharmacology+%26+therapeutics&rft.issn=1879-016X&rft_id=info:doi/10.1016%2Fj.pharmthera.2013.09.005
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-08-24
N1 - Date created - 2014-01-10
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.pharmthera.2013.09.005
ER -
TY - JOUR
T1 - Prevalence and predictors of elevated aspartate aminotransferase-to-platelet ratio index in Latin American perinatally HIV-infected children.
AN - 1490694003; 23799515
AB - Chronic liver disease has emerged as an important problem in adults with longstanding HIV infection, but data are lacking for children. We characterized elevated aspartate aminotransferase-to-platelet ratio index (APRI), a marker of possible liver fibrosis, in perinatally HIV-infected children.
The National Institute of Child Health and Human Development International Site Development Initiative enrolled HIV-infected children (ages 0.1-20.1 years) from 5 Latin American countries in an observational cohort from 2002 to 2009. Twice yearly visits included medical history, physical examination and laboratory evaluations. The prevalence (95% confidence interval) of APRI > 1.5 was calculated, and associations with demographic, HIV-related and liver-related variables were investigated in bivariate analyses.
APRI was available for 1012 of 1032 children. APRI was >1.5 in 32 (3.2%, 95% confidence interval: 2.2%-4.4%) including 2 of 4 participants with hepatitis B virus infection. Factors significantly associated with APRI > 1.5 (P 1.5 varied significantly by current ARV regimen (P = 0.0002), from 8.0% for no ARV to 3.2% for non-protease inhibitor regimens to 1.5% for protease inhibitor-based regimens.
Elevated APRI occurred in approximately 3% of perinatally HIV-infected children. Protease inhibitor-based ARVs appeared protective whereas inadequate HIV control appeared to increase risk of elevated APRI. Additional investigations are needed to better assess potential subclinical, chronic liver disease in HIV-infected children.
JF - The Pediatric infectious disease journal
AU - Siberry, George K
AU - Cohen, Rachel A
AU - Harris, D Robert
AU - Cruz, Maria Leticia Santos
AU - Oliveira, Ricardo
AU - Peixoto, Mario F
AU - Cervi, Maria Celia
AU - Hazra, Rohan
AU - Pinto, Jorge A
AU - NISDI PLACES Protocol
AD - From the *Maternal and Pediatric Infectious Disease Branch, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda; †Westat, Rockville, MD; ‡Department of Infectious Diseases, Hospital Federal dos Servidores do Estado; §Instituto de Puericultura e Pediatria Martagão Gesteira, Universidade Federal do Rio de Janeiro, Rio de Janeiro; ¶Vertical Transmission Unit, Femina Hospital, Porto Alegre; ‖Department of Pediatrics, University of São Paulo Faculty of Medicine of Ribeirão Preto, Ribeirão Preto; and **Department of Pediatrics, Federal University of Minas Gerais, Belo Horizonte, Brazil. ; NISDI PLACES Protocol
Y1 - 2014/02//
PY - 2014
DA - February 2014
SP - 177
EP - 182
VL - 33
IS - 2
KW - Aspartate Aminotransferases
KW - EC 2.6.1.1
KW - Index Medicus
KW - Sensitivity and Specificity
KW - Infectious Disease Transmission, Vertical
KW - Liver Cirrhosis -- virology
KW - Latin America -- epidemiology
KW - Humans
KW - Child
KW - Liver Cirrhosis -- blood
KW - Liver Cirrhosis -- enzymology
KW - Child, Preschool
KW - Infant
KW - Female
KW - Male
KW - Prevalence
KW - Platelet Count
KW - Aspartate Aminotransferases -- blood
KW - HIV Infections -- blood
KW - HIV Infections -- enzymology
KW - Blood Platelets -- cytology
KW - HIV Infections -- epidemiology
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1490694003?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Pediatric+infectious+disease+journal&rft.atitle=Prevalence+and+predictors+of+elevated+aspartate+aminotransferase-to-platelet+ratio+index+in+Latin+American+perinatally+HIV-infected+children.&rft.au=Siberry%2C+George+K%3BCohen%2C+Rachel+A%3BHarris%2C+D+Robert%3BCruz%2C+Maria+Leticia+Santos%3BOliveira%2C+Ricardo%3BPeixoto%2C+Mario+F%3BCervi%2C+Maria+Celia%3BHazra%2C+Rohan%3BPinto%2C+Jorge+A%3BNISDI+PLACES+Protocol&rft.aulast=Siberry&rft.aufirst=George&rft.date=2014-02-01&rft.volume=33&rft.issue=2&rft.spage=177&rft.isbn=&rft.btitle=&rft.title=The+Pediatric+infectious+disease+journal&rft.issn=1532-0987&rft_id=info:doi/10.1097%2FINF.0b013e3182a01dfb
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-09-25
N1 - Date created - 2014-01-13
N1 - Date revised - 2017-01-13
N1 - SuppNotes - Cited By:
J Hepatol. 2005 Jul;43(1):78-84 [15894397]
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Hepatology. 2006 Jun;43(6):1317-25 [16729309]
AIDS. 2007 Nov 30;21(18):2483-91 [18025885]
J Pediatr Gastroenterol Nutr. 2007 Oct;45(4):443-50 [18030211]
BMC Public Health. 2007;7:338 [18031586]
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PLoS Med. 2009 Apr 28;6(4):e1000066 [19399157]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1097/INF.0b013e3182a01dfb
ER -
TY - JOUR
T1 - Blockade of D3 receptors by YQA14 inhibits cocaine's rewarding effects and relapse to drug-seeking behavior in rats.
AN - 1469214824; 24176392
AB - Preclinical studies suggest that dopamine D3 receptor (D3R) antagonists are promising for the treatment of drug abuse and addiction. However, few D3R antagonists have potential to be tested in humans due to short half-life, toxicity or limited preclinical research into pharmacotherapeutic efficacy. Here, we report on a novel D3R antagonist YQA14, which has improved half-life and pharmacokinetic profile and which displays potent pharmacotherapeutic efficacy in attenuating cocaine reward and relapse to drug-seeking behavior. Electrical brain-stimulation reward (BSR) in laboratory animals is a highly sensitive experimental approach to evaluate a drug's rewarding effects. We found that cocaine (2 mg/kg) significantly enhanced electrical BSR in rats (i.e., decreased stimulation threshold for BSR), while YQA14 alone had no effect on BSR. Pretreatment with YQA14 significantly and dose-dependently attenuated cocaine-enhanced BSR. YQA14 also facilitated extinction from drug-seeking behavior in rats during early behavioral extinction, and attenuated cocaine- or contextual cue-induced relapse to drug-seeking behavior. YQA14 alone did not maintain self-administration in either naïve rats or in rats experienced at cocaine self-administration. YQA14 also inhibited expression of repeated cocaine-induced behavioral sensitization. These findings suggest that YQA14 may have pharmacotherapeutic potential in attenuating cocaine-taking and cocaine-seeking behavior. Thus, YQA14 deserves further investigation as a promising agent for treatment of cocaine addiction.
Published by Elsevier Ltd.
JF - Neuropharmacology
AU - Song, Rui
AU - Bi, Guo-Hua
AU - Zhang, Hai-Ying
AU - Yang, Ri-Fang
AU - Gardner, Eliot L
AU - Li, Jin
AU - Xi, Zheng-Xiong
AD - Intramural Research Program, National Institute on Drug Abuse, Baltimore, MD 21224, USA; Beijing Institute of Pharmacology and Toxicology, Beijing 100850, China. ; Intramural Research Program, National Institute on Drug Abuse, Baltimore, MD 21224, USA. ; Beijing Institute of Pharmacology and Toxicology, Beijing 100850, China. ; Beijing Institute of Pharmacology and Toxicology, Beijing 100850, China. Electronic address: jinli9802@163.com. ; Intramural Research Program, National Institute on Drug Abuse, Baltimore, MD 21224, USA. Electronic address: zxi@intra.nida.nih.gov.
Y1 - 2014/02//
PY - 2014
DA - February 2014
SP - 398
EP - 405
VL - 77
KW - Benzoxazoles
KW - 0
KW - Dopamine Antagonists
KW - Dopamine Uptake Inhibitors
KW - Piperazines
KW - Receptors, Dopamine D3
KW - YQA14
KW - Cocaine
KW - I5Y540LHVR
KW - Index Medicus
KW - Dopamine
KW - Reward
KW - Reinstatement
KW - D3 receptors
KW - Rats
KW - Behavior, Animal -- drug effects
KW - Animals
KW - Rats, Long-Evans
KW - Dose-Response Relationship, Drug
KW - Brain -- drug effects
KW - Cocaine-Related Disorders -- drug therapy
KW - Behavior, Addictive -- drug therapy
KW - Electric Stimulation
KW - Recurrence
KW - Male
KW - Drug-Seeking Behavior -- drug effects
KW - Benzoxazoles -- pharmacology
KW - Benzoxazoles -- therapeutic use
KW - Piperazines -- therapeutic use
KW - Dopamine Antagonists -- pharmacology
KW - Receptors, Dopamine D3 -- antagonists & inhibitors
KW - Piperazines -- pharmacology
KW - Cocaine -- pharmacology
KW - Dopamine Uptake Inhibitors -- pharmacology
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-08-26
N1 - Date created - 2013-12-16
N1 - Date revised - 2017-01-13
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.neuropharm.2013.10.010
ER -
TY - JOUR
T1 - Simultaneous quantification of 20 synthetic cannabinoids and 21 metabolites, and semi-quantification of 12 alkyl hydroxy metabolites in human urine by liquid chromatography-tandem mass spectrometry.
AN - 1492681123; 24418231
AB - Clandestine laboratories constantly produce new synthetic cannabinoids to circumvent legislative efforts, complicating toxicological analysis. No extensive synthetic cannabinoid quantitative urinary methods are reported in the literature. We developed and validated a liquid chromatography-tandem mass spectrometric (LC-MS/MS) method for simultaneously quantifying JWH-018, JWH-019, JWH-073, JWH-081, JWH-122, JWH-200, JWH-210, JWH-250, JWH-398, RCS-4, AM-2201, MAM-2201, UR-144, CP 47,497-C7, CP 47,497-C8 and their metabolites, and JWH-203, AM-694, RCS-8, XLR-11 and HU-210 parent compounds in urine. Non-chromatographically resolved alkyl hydroxy metabolite isomers were considered semi-quantitative. β-Glucuronidase hydrolyzed urine was extracted with 1ml Biotage SLE+ columns. Specimens were reconstituted in 150μL mobile phase consisting of 50% A (0.01% formic acid in water) and 50% B (0.01% formic acid in 50:50 methanol:acetonitrile). 4 and 25μL injections were performed to acquire data in positive and negative ionization modes, respectively. The LC-MS/MS instrument consisted of a Shimadzu UFLCxr system and an ABSciex 5500 Qtrap mass spectrometer with an electrospray source. Gradient chromatographic separation was achieved utilizing a Restek Ultra Biphenyl column with a 0.5ml/min flow rate and an overall run time of 19.5 and 11.4min for positive and negative mode methods, respectively. Quantification was by multiple reaction monitoring with CP 47,497 compounds and HU-210 ionized via negative polarity; all other analytes were acquired in positive mode. Lower and upper limits of linearity were 0.1-1.0 and 50-100μg/l (r(2)>0.994). Validation parameters were evaluated at three concentrations spanning linear dynamic ranges. Inter-day analytical recovery (bias) and imprecision (N=20) were 88.3-112.2% and 4.3-13.5% coefficient of variation, respectively. Extraction efficiencies and matrix effect (N=10) were 44-110 and -73 to 52%, respectively. We present a novel LC-MS/MS method for simultaneously quantifying 20 synthetic cannabinoids and 21 metabolites, and semi-quantifying 12 alkyl hydroxy metabolites in urine.
Published by Elsevier B.V.
JF - Journal of chromatography. A
AU - Scheidweiler, Karl B
AU - Huestis, Marilyn A
AD - Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD 21224, USA. ; Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD 21224, USA. Electronic address: mhuestis@intra.nida.nih.gov.
Y1 - 2014/01/31/
PY - 2014
DA - 2014 Jan 31
SP - 105
EP - 117
VL - 1327
KW - Cannabinoids
KW - 0
KW - Index Medicus
KW - Urine
KW - Analytical method
KW - Synthetic cannabinoids
KW - Metabolites
KW - LC–MS/MS
KW - Sensitivity and Specificity
KW - Chromatography, Liquid -- methods
KW - Humans
KW - Tandem Mass Spectrometry -- methods
KW - Cannabinoids -- metabolism
KW - Cannabinoids -- urine
KW - Substance Abuse Detection -- methods
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492681123?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+chromatography.+A&rft.atitle=Simultaneous+quantification+of+20+synthetic+cannabinoids+and+21+metabolites%2C+and+semi-quantification+of+12+alkyl+hydroxy+metabolites+in+human+urine+by+liquid+chromatography-tandem+mass+spectrometry.&rft.au=Scheidweiler%2C+Karl+B%3BHuestis%2C+Marilyn+A&rft.aulast=Scheidweiler&rft.aufirst=Karl&rft.date=2014-01-31&rft.volume=1327&rft.issue=&rft.spage=105&rft.isbn=&rft.btitle=&rft.title=Journal+of+chromatography.+A&rft.issn=1873-3778&rft_id=info:doi/10.1016%2Fj.chroma.2013.12.067
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-07-15
N1 - Date created - 2014-01-21
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.chroma.2013.12.067
ER -
TY - JOUR
T1 - Biomarkers and neurodevelopment in perinatally HIV-infected or exposed youth: a structural equation model analysis
AN - 1765970385; PQ0002559384
AB - Objective: To examine the relationship between markers of vascular dysfunction and neurodevelopmental outcomes in perinatally HIV-infected (PHIV+) and perinatally HIV-exposed but uninfected (PHEU) youth. Design: Cross-sectional design within a prospective, 15-site US-based cohort study. Methods: Neurodevelopmental outcomes were evaluated in relation to nine selected vascular biomarkers in 342 youth (212 PHIV+, 130 PHEU). Serum levels were assessed for adiponectin, C-reactive protein (CRP), fibrinogen, interleukin-6 (IL-6), soluble vascular cell adhesion molecule-1 (sVCAM-1), E-selectin (sE-selectin), monocyte chemoattractant protein (sMCP-1), intercellular adhesion molecule-1 (slCAM-1), and P-selectin (sP-selectin). The Wechsler Intelligence Scale for Children-Fourth Edition (WISC-IV) was administered at entry, yielding a Full-Scale IQ score, and four index scores. Factor analysis was conducted to reduce the biomarkers to fewer factors with related biological roles. Structural equation models (SEMs) were used to measure associations between resulting factors and WISC-IV scores. Results: Mean participant age was 11.4 years, 54% were female, 70% black. The nine biomarkers were clustered into three factor groups: F1 (fibrinogen, CRP, and IL-6); F2 (slCAM-1 and sVCAM-1); and F3 (MCP-1, sP-selectin, and sE-selectin). Adiponectin showed little correlation with any factor. SEMs revealed significant negative association of F1 with WISC-IV processing speed score in the total cohort. This effect remained significant after adjusting for HIV status and other potential confounders. A similar association was observed when restricted to PHIV+ participants in both unadjusted and adjusted SEMs. Conclusion: Aggregate measures of fibrinogen, CRP, and IL-6 may serve as a latent biomarker associated with relatively decreased processing speed in both PHIV+ and PHEU youth.
JF - AIDS
AU - Kapetanovic, Suad
AU - Griner, Ray
AU - Zeldow, Bret
AU - Nichols, Sharon
AU - Leister, Erin
AU - Gelbard, Harris A
AU - Miller, Tracie L
AU - Hazra, Rohan
AU - Mendez, Armando J
AU - Malee, Kathleen
AU - Kammerer, Betsy
AU - Williams, Paige L
AD - National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland, suad.kapetanovic@nih.gov
Y1 - 2014/01/28/
PY - 2014
DA - 2014 Jan 28
SP - 355
EP - 364
PB - Lippincott Williams & Wilkins, Inc, 530 Walnut Street Philadelphia PA 19106-3621 United States
VL - 28
IS - 3
SN - 0269-9370, 0269-9370
KW - Health & Safety Science Abstracts; Immunology Abstracts; Virology & AIDS Abstracts
KW - HIV-affected children
KW - inflammatory markers
KW - neurodevelopmental outcomes
KW - perinatal HIV infection
KW - Bioindicators
KW - Interleukin 6
KW - Acquired immune deficiency syndrome
KW - Age
KW - Monocyte chemoattractant protein 1
KW - Mathematical models
KW - Factor analysis
KW - Fibrinogen
KW - P-selectin
KW - Adhesion
KW - biomarkers
KW - Monocyte chemoattractant protein
KW - Serum levels
KW - Intelligence
KW - vascular cell adhesion molecule 1
KW - Human immunodeficiency virus
KW - intercellular adhesion molecule 1
KW - Proteins
KW - Adiponectin
KW - E-selectin
KW - C-reactive protein
KW - V 22360:AIDS and HIV
KW - H 11000:Diseases/Injuries/Trauma
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1765970385?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS&rft.atitle=Biomarkers+and+neurodevelopment+in+perinatally+HIV-infected+or+exposed+youth%3A+a+structural+equation+model+analysis&rft.au=Kapetanovic%2C+Suad%3BGriner%2C+Ray%3BZeldow%2C+Bret%3BNichols%2C+Sharon%3BLeister%2C+Erin%3BGelbard%2C+Harris+A%3BMiller%2C+Tracie+L%3BHazra%2C+Rohan%3BMendez%2C+Armando+J%3BMalee%2C+Kathleen%3BKammerer%2C+Betsy%3BWilliams%2C+Paige+L&rft.aulast=Kapetanovic&rft.aufirst=Suad&rft.date=2014-01-28&rft.volume=28&rft.issue=3&rft.spage=355&rft.isbn=&rft.btitle=&rft.title=AIDS&rft.issn=02699370&rft_id=info:doi/10.1097%2FQAD.0000000000000072
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2016-02-01
N1 - Last updated - 2016-03-17
N1 - SubjectsTermNotLitGenreText - Interleukin 6; Age; Mathematical models; Monocyte chemoattractant protein 1; Factor analysis; Fibrinogen; P-selectin; Monocyte chemoattractant protein; biomarkers; Serum levels; vascular cell adhesion molecule 1; Intelligence; intercellular adhesion molecule 1; Adiponectin; E-selectin; C-reactive protein; Bioindicators; Acquired immune deficiency syndrome; Human immunodeficiency virus; Proteins; Adhesion
DO - http://dx.doi.org/10.1097/QAD.0000000000000072
ER -
TY - JOUR
T1 - Factors associated with survival among patients with AIDS-related primary central nervous system lymphoma
AN - 1765970192; PQ0002559388
AB - Objective: AIDS-related primary central nervous system lymphoma (AR-PCNSL) has a poor prognosis. Improved understanding of specific patient, infectious, diagnostic, and treatment-related factors that affect overall survival (OS) is required to improve outcomes. Design: Population-based registry linkage study. Methods: Adult cases from the San Francisco AIDS registry (1990-2000) were matched with the California Cancer Registry (1985-2002) to ascertain AR-PCNSL data. Survival time was assessed through 31 December 2007. Risk factors and temporal trends for death were measured using two-sided Kaplan-Meier and Cox analyses. Results: Two hundred and seven AR-PCNSL patients were identified: 68% were white, 20% Hispanic, 10% African-American, and 2% Asian. Nineteen percent of patients had central nervous system (CNS) opportunistic infections diagnosed prior to AR-PCNSL. Fifty-seven percent of patients received radiation and/or chemotherapy and 12% used HAART prior to or within 30 days of AR-PCNSL diagnosis. One hundred and ninety-nine patients died (34 deaths/100 person-years). In adjusted analysis, prior CNS opportunistic infection diagnosis increased risk of death (hazard ratio 1.9, P = 0.0006) whereas radiation and/or chemotherapy decreased risk (hazard ratio 0.6, P < 0.0001). AR-PCNSL diagnosis 1999-2002 had a lower mortality risk (hazard ratio = 0.4, P = 0.02) compared to 1990-1995. African-Americans had an increased risk of death compared to whites or Asians (hazard ratio = 2.0, P = 0.007). Conclusion: OS among AR-PCNSL patients improved over time but remains poor, especially among African-Americans. Prospective evaluation of curative therapy in AR-PCNSL is urgently needed. Accurate diagnosis of CNS mass lesions in patients with AIDS is required and for those with AR-PCNSL, antiretroviral therapy with concomitant AR-PCNSL therapy, and antimicrobial supportive care may improve OS.
JF - AIDS
AU - Uldrick, Thomas S
AU - Pipkin, Sharon
AU - Scheer, Susan
AU - Hessol, Nancy A
AD - HIV & AIDS Malignancy Branch, Center for Cancer Research, National Cancer Institute at the National Institutes of Health, Bethesda, Maryland, uldrickts@mail.nih.gov
Y1 - 2014/01/28/
PY - 2014
DA - 2014 Jan 28
SP - 397
EP - 405
PB - Lippincott Williams & Wilkins, Inc, 530 Walnut Street Philadelphia PA 19106-3621 United States
VL - 28
IS - 3
SN - 0269-9370, 0269-9370
KW - Health & Safety Science Abstracts; Immunology Abstracts; Virology & AIDS Abstracts
KW - AIDS
KW - AIDS-related lymphoma
KW - brain neoplasms
KW - HAART
KW - prognosis
KW - risk factors
KW - time factors
KW - Risk assessment
KW - Central nervous system
KW - Acquired immune deficiency syndrome
KW - Chemotherapy
KW - Survival
KW - Infection
KW - Radiation
KW - Risk factors
KW - Lesions
KW - Lymphoma
KW - Ethnic groups
KW - Mortality
KW - Data processing
KW - Prognosis
KW - Antiretroviral agents
KW - Cancer
KW - Antimicrobial agents
KW - Opportunist infection
KW - Health risks
KW - highly active antiretroviral therapy
KW - INE, USA, California, San Francisco
KW - V 22360:AIDS and HIV
KW - H 8000:Radiation Safety/Electrical Safety
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1765970192?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS&rft.atitle=Factors+associated+with+survival+among+patients+with+AIDS-related+primary+central+nervous+system+lymphoma&rft.au=Uldrick%2C+Thomas+S%3BPipkin%2C+Sharon%3BScheer%2C+Susan%3BHessol%2C+Nancy+A&rft.aulast=Uldrick&rft.aufirst=Thomas&rft.date=2014-01-28&rft.volume=28&rft.issue=3&rft.spage=397&rft.isbn=&rft.btitle=&rft.title=AIDS&rft.issn=02699370&rft_id=info:doi/10.1097%2FQAD.0000000000000030
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2016-02-01
N1 - Last updated - 2016-03-17
N1 - SubjectsTermNotLitGenreText - Central nervous system; Mortality; Acquired immune deficiency syndrome; Data processing; Chemotherapy; Prognosis; Survival; Cancer; Opportunist infection; Antimicrobial agents; Radiation; highly active antiretroviral therapy; Risk factors; Lymphoma; Risk assessment; Infection; Antiretroviral agents; Health risks; Lesions; Ethnic groups; INE, USA, California, San Francisco
DO - http://dx.doi.org/10.1097/QAD.0000000000000030
ER -
TY - JOUR
T1 - The role of a Schiff base scaffold, N-(2-hydroxy acetophenone) glycinate-in overcoming multidrug resistance in cancer.
AN - 1459563804; 24044945
AB - Drug resistance is a problem that hinders the numerous successes of chemotherapeutic intervention of cancer and continues to be a major obstacle for cures. Till date, several attempts have been made to develop suitable multidrug resistance (MDR) reversing agents. But, throughout the clinical development of MDR reversing agents, patients repeatedly suffer from toxicities. So far, some anticancer activity of Schiff bases which are the condensation products of carbonyl compounds and primary amines and their metal complexes has been described. But, overcoming multidrug resistance, by the use of such small molecules still remain unexplored. Under this backdrop, in search of less toxic and more effective MDR reversing agents our laboratory has developed the different metal chelates of Schiff base N-(2-hydroxy acetophenone)glycinate (NG) which is structurally similar to azatyrosine [L-β-(5-hydroxy-2-pyridyl)-alanine] that inhibits tumor formation by deactivating the c-Raf-1 kinase and c-Ha-ras signalling pathway. A decade-long research proposes possible strategies to overcome MDR by exploiting the chemical nature of such metal chelates. In this review we have catalogued the success of metal chelates of NG to overcome MDR in cancer. The review depict that the problem of MDR can be circumvent by synchronized activation of immunogenic cell death pathways that utilize the components of a host's immune system to kill cancer cells in combination with other conventional strategies. The current wealth of preclinical information promises better understanding of the cellular processes underlying MDR reversing activity of metal derivatives of NG and thus exposes several cellular targets for rational designing of new generation of Schiff base metal chelates as MDR reversing agents. Copyright © 2013 Elsevier B.V. All rights reserved.
JF - European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences
AU - Ganguly, Avishek
AU - Chakraborty, Paramita
AU - Banerjee, Kaushik
AU - Choudhuri, Soumitra Kumar
AD - Department of In Vitro Carcinogenesis and Cellular Chemotherapy, Chittaranjan National Cancer Institute, Kolkata, India.
Y1 - 2014/01/23/
PY - 2014
DA - 2014 Jan 23
SP - 96
EP - 109
VL - 51
KW - Chelating Agents
KW - 0
KW - Coordination Complexes
KW - Schiff Bases
KW - Index Medicus
KW - N-(2-hydroxy acetophenone)glycinate
KW - MAPK
KW - MDR
KW - FoxP3
KW - Apoptosis
KW - ROS
KW - Glutathione
KW - EAC/Dox
KW - Reactive oxygen species
KW - CuNG
KW - Schiff base metal chelates
KW - Multidrug Resistance-associated Protein 1
KW - Myeloid derived suppressor cell
KW - Iron N-(2-hydroxy acetophenone)glycinate
KW - ABC transporter
KW - reactive oxygen species
KW - GSH
KW - ZnNG
KW - TAM
KW - FeNG
KW - Zn N-(2-hydroxyacetophenone)glycinate.
KW - T regulatory cell (CD4(+)CD25(+)FoxP3(+))
KW - NG
KW - MDSC
KW - Tumor-associated macrophage
KW - MAP kinase signalling
KW - Forkhead box P3
KW - Copper N-(2-hydroxyacetophenone)glycinate
KW - Multidrug resistance
KW - T(Reg)
KW - Mitogen-activated protein kinase
KW - Doxorubicin resistant Ehrlich ascites carcinoma cells
KW - MRP1
KW - Animals
KW - Humans
KW - Chelating Agents -- metabolism
KW - Coordination Complexes -- metabolism
KW - Schiff Bases -- therapeutic use
KW - Drug Resistance, Multiple -- drug effects
KW - Schiff Bases -- pharmacology
KW - Drug Resistance, Neoplasm -- drug effects
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-06-23
N1 - Date created - 2013-11-18
N1 - Date revised - 2017-01-13
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.ejps.2013.09.003
ER -
TY - JOUR
T1 - 4-(3-Chloro-5-(trifluoromethyl)pyridin-2-yl)-N-(4-methoxypyridin-2 -yl) piperazine-1-carbothioamide (ML267), a Potent Inhibitor of Bacterial Phosphopantetheinyl Transferase That Attenuates Secondary Metabolism and Thwarts Bacterial Growth
AN - 1660395444; PQ0001015742
AB - 4'-Phosphopantetheinyl transferases (PPTases) catalyze a post-translational modification essential to bacterial cell viability and virulence. We present the discovery and medicinal chemistry optimization of 2-pyridinyl-N-(4-aryl)piperazine-1-carbothioamides, which exhibit submicromolar inhibition of bacterial Sfp-PPTase with no activity toward the human orthologue. Moreover, compounds within this class possess antibacterial activity in the absence of a rapid cytotoxic response in human cells. An advanced analogue of this series, ML267 (55), was found to attenuate production of an Sfp-PPTase-dependent metabolite when applied to Bacillus subtilis at sublethal doses. Additional testing revealed antibacterial activity against methicillin-resistant Staphylococcus aureus, and chemical genetic studies implicated efflux as a mechanism for resistance in Escherichia coli. Additionally, we highlight the in vitro absorption, distribution, metabolism, and excretion and in vivo pharmacokinetic profiles of compound 55 to further demonstrate the potential utility of this small-molecule inhibitor.
JF - Journal of Medicinal Chemistry
AU - Foley, Timothy L
AU - Rai, Ganesha
AU - Yasgar, Adam
AU - Daniel, Thomas
AU - Baker, Heather L
AU - Attene-Ramos, Matias
AU - Kosa, Nicolas M
AU - Leister, William
AU - Burkart, Michael D
AU - Jadhav, Ajit
AU - Simeonov, Anton
AU - Maloney, David J
AD - National Center for Advancing Translational Sciences, National Institutes of Health, 9800 Medical Center Drive, Rockville, Maryland 20850, United States
Y1 - 2014/01/22/
PY - 2014
DA - 2014 Jan 22
SP - 1063
EP - 1078
PB - American Chemical Society, P.O. Box 182426 Columbus OH 43218-2426 United States
VL - 57
IS - 3
SN - 0022-2623, 0022-2623
KW - Microbiology Abstracts B: Bacteriology
KW - Bacillus subtilis
KW - Antibacterial activity
KW - Drug resistance
KW - Metabolites
KW - Pharmacokinetics
KW - Virulence
KW - Cytotoxicity
KW - Post-translation
KW - Escherichia coli
KW - Excretion
KW - Staphylococcus aureus
KW - Metabolism
KW - J 02340:Antibiotics & Antimicrobials
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-03-01
N1 - Last updated - 2015-11-16
N1 - SubjectsTermNotLitGenreText - Virulence; Cytotoxicity; Post-translation; Antibacterial activity; Drug resistance; Metabolites; Excretion; Pharmacokinetics; Metabolism; Bacillus subtilis; Escherichia coli; Staphylococcus aureus
DO - http://dx.doi.org/10.1021/jm401752p
ER -
TY - JOUR
T1 - Cytolethal distending toxin B as a cell-killing component of tumor-targeted anthrax toxin fusion proteins.
AN - 1490706502; 24434511
AB - Cytolethal distending toxin (Cdt) is produced by Gram-negative bacteria of several species. It is composed of three subunits, CdtA, CdtB, and CdtC, with CdtB being the catalytic subunit. We fused CdtB from Haemophilus ducreyi to the N-terminal 255 amino acids of Bacillus anthracis toxin lethal factor (LFn) to design a novel, potentially potent antitumor drug. As a result of this fusion, CdtB was transported into the cytosol of targeted cells via the efficient delivery mechanism of anthrax toxin. The fusion protein efficiently killed various human tumor cell lines by first inducing a complete cell cycle arrest in the G2/M phase, followed by induction of apoptosis. The fusion protein showed very low toxicity in mouse experiments and impressive antitumor effects in a Lewis Lung carcinoma model, with a 90% cure rate. This study demonstrates that efficient drug delivery by a modified anthrax toxin system combined with the enzymatic activity of CdtB has great potential as anticancer treatment and should be considered for the development of novel anticancer drugs.
JF - Cell death & disease
AU - Bachran, C
AU - Hasikova, R
AU - Leysath, C E
AU - Sastalla, I
AU - Zhang, Y
AU - Fattah, R J
AU - Liu, S
AU - Leppla, S H
AD - Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Y1 - 2014/01/16/
PY - 2014
DA - 2014 Jan 16
SP - 1
VL - 5
KW - Antigens, Bacterial
KW - 0
KW - Bacterial Toxins
KW - Recombinant Fusion Proteins
KW - anthrax toxin
KW - cytolethal distending toxin
KW - Index Medicus
KW - Recombinant Fusion Proteins -- metabolism
KW - Animals
KW - Humans
KW - Apoptosis -- drug effects
KW - Recombinant Fusion Proteins -- genetics
KW - Mice, Inbred C57BL
KW - Cell Cycle Checkpoints -- drug effects
KW - Recombinant Fusion Proteins -- pharmacology
KW - Mice
KW - Cell Line, Tumor
KW - Male
KW - Female
KW - Bacterial Toxins -- genetics
KW - Neoplasms -- drug therapy
KW - Bacterial Toxins -- metabolism
KW - Antigens, Bacterial -- metabolism
KW - Neoplasms -- physiopathology
KW - Bacterial Toxins -- pharmacology
KW - Antigens, Bacterial -- pharmacology
KW - Antigens, Bacterial -- genetics
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-09-02
N1 - Date created - 2014-01-17
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1038/cddis.2013.540
ER -
TY - JOUR
T1 - Testing multiple biological mediators simultaneously
AN - 1496895174; 19037923
AB - Motivation:Modern biomedical and epidemiological studies often measure hundreds or thousands of biomarkers, such as gene expression or metabolite levels. Although there is an extensive statistical literature on adjusting for 'multiple comparisons' when testing whether these biomarkers are directly associated with a disease, testing whether they are biological mediators between a known risk factor and a disease requires a more complex null hypothesis, thus offering additional methodological challenges.Results:We propose a permutation approach that tests multiple putative mediators and controls the family wise error rate. We demonstrate that, unlike when testing direct associations, replacing the Bonferroni correction with a permutation approach that focuses on the maximum of the test statistics can significantly improve the power to detect mediators even when all biomarkers are independent. Through simulations, we show the power of our method is 2-5 larger than the power achieved by Bonferroni correction. Finally, we apply our permutation test to a case-control study of dietary risk factors and colorectal adenoma to show that, of 149 test metabolites, docosahexaenoate is a possible mediator between fish consumption and decreased colorectal adenoma risk.
JF - Bioinformatics
AU - Boca, Simina M
AU - Sinha, Rashmi
AU - Cross, Amanda J
AU - Moore, Steven C
AU - Sampson, Joshua N
AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, USA
Y1 - 2014/01/15/
PY - 2014
DA - 2014 Jan 15
SP - 214
EP - 220
PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom
VL - 30
IS - 2
SN - 1367-4803, 1367-4803
KW - Biochemistry Abstracts 2: Nucleic Acids; Biotechnology and Bioengineering Abstracts
KW - Gene expression
KW - Statistics
KW - Risk factors
KW - Colorectal cancer
KW - Metabolites
KW - Bioinformatics
KW - biomarkers
KW - Adenoma
KW - Internet
KW - N 14810:Methods
KW - W 30960:Bioinformatics & Computer Applications
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Bioinformatics&rft.atitle=Testing+multiple+biological+mediators+simultaneously&rft.au=Boca%2C+Simina+M%3BSinha%2C+Rashmi%3BCross%2C+Amanda+J%3BMoore%2C+Steven+C%3BSampson%2C+Joshua+N&rft.aulast=Boca&rft.aufirst=Simina&rft.date=2014-01-15&rft.volume=30&rft.issue=2&rft.spage=214&rft.isbn=&rft.btitle=&rft.title=Bioinformatics&rft.issn=13674803&rft_id=info:doi/10.1093%2Fbioinformatics%2Fbtt633
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-02-01
N1 - Last updated - 2016-05-13
N1 - SubjectsTermNotLitGenreText - Gene expression; Statistics; Risk factors; Colorectal cancer; Metabolites; Bioinformatics; Adenoma; biomarkers; Internet
DO - http://dx.doi.org/10.1093/bioinformatics/btt633
ER -
TY - CPAPER
T1 - Microbiome and Intestinal Farnesoid X Receptor in the Control of Obesity
T2 - 2014 Keystone Symposia on Obesity: A Multisystems Perspective
AN - 1518609723; 6280460
JF - 2014 Keystone Symposia on Obesity: A Multisystems Perspective
AU - Gonzalez, Frank
Y1 - 2014/01/12/
PY - 2014
DA - 2014 Jan 12
KW - Obesity
KW - farnesoid X receptors
KW - Intestine
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L2 - http://www.keystonesymposia.org/index.cfm?e=web.Meeting.Program&meetingid=1294
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-04-23
N1 - Last updated - 2014-04-24
ER -
TY - JOUR
T1 - High-Resolution Structures and Orientations of Antimicrobial Peptides Piscidin 1 and Piscidin 3 in Fluid Bilayers Reveal Tilting, Kinking, and Bilayer Immersion
AN - 1660399658; PQ0001052602
AB - While antimicrobial peptides (AMPs) have been widely investigated as potential therapeutics, high-resolution structures obtained under biologically relevant conditions are lacking. Here, the high-resolution structures of the homologous 22-residue long AMPs piscidin 1 (p1) and piscidin 3 (p3) are determined in fluid-phase 3:1 phosphatidylcholine/phosphatidylglycerol (PC/PG) and 1:1 phosphatidylethanolamine/phosphatidylglycerol (PE/PG) bilayers to identify molecular features important for membrane destabilization in bacterial cell membrane mimics. Structural refinement of 1H-15N dipolar couplings and 15N chemical shifts measured by oriented sample solid-state NMR and all-atom molecular dynamics (MD) simulations provide structural and orientational information of high precision and accuracy about these interfacially bound alpha -helical peptides. The tilt of the helical axis, tau , is between 83 degree and 93 degree with respect to the bilayer normal for all systems and analysis methods. The average azimuthal rotation, rho , is 235 degree , which results in burial of hydrophobic residues in the bilayer. The refined NMR and MD structures reveal a slight kink at G13 that delineates two helical segments characterized by a small difference in their tau angles (<10 degree ) and significant difference in their rho angles ( similar to 25 degree ). Remarkably, the kink, at the end of a G(X)4G motif highly conserved among members of the piscidin family, allows p1 and p3 to adopt rho angles that maximize their hydrophobic moments. Two structural features differentiate the more potent p1 from p3: p1 has a larger rho angle and less N-terminal fraying. The peptides have comparable depths of insertion in PC/PG, but p3 is 1.2 Aa more deeply inserted than p1 in PE/PG. In contrast to the ideal alpha -helical structures typically assumed in mechanistic models of AMPs, p1 and p3 adopt disrupted alpha -helical backbones that correct for differences in the amphipathicity of their N- and C-ends, and their centers of mass lie similar to 1.2-3.6 Aa below the plane defined by the C2 atoms of the lipid acyl chains.
JF - Journal of the American Chemical Society
AU - Perrin, BScott
AU - Tian, Ye
AU - Fu, Riqiang
AU - Grant, Christopher V
AU - Chekmenev, Eduard Y
AU - Wieczorek, William E
AU - Dao, Alexander E
AU - Hayden, Robert M
AU - Burzynski, Caitlin M
AU - Venable, Richard M
AU - Sharma, Mukesh
AU - Opella, Stanley J
AU - Pastor, Richard W
AU - Cotten, Myriam L
AD - Laboratory of Computational Biology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, United States
Y1 - 2014/01/10/
PY - 2014
DA - 2014 Jan 10
SP - 3491
EP - 3504
PB - American Chemical Society, P.O. Box 182426 Columbus OH 43218-2426 United States
VL - 136
IS - 9
SN - 0002-7863, 0002-7863
KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Microbiology Abstracts B: Bacteriology
KW - Cell membranes
KW - Lipids
KW - phosphatidylglycerol
KW - Lecithin
KW - Immersion
KW - Hydrophobicity
KW - N.M.R.
KW - phosphatidylethanolamine
KW - Antimicrobial peptides
KW - A 01340:Antibiotics & Antimicrobials
KW - J 02330:Biochemistry
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-03-01
N1 - Last updated - 2016-03-17
N1 - SubjectsTermNotLitGenreText - Cell membranes; Lipids; phosphatidylglycerol; Immersion; Lecithin; N.M.R.; Hydrophobicity; phosphatidylethanolamine; Antimicrobial peptides
DO - http://dx.doi.org/10.1021/ja411119m
ER -
TY - JOUR
T1 - An Insight into the Transcriptome of the Digestive Tract of the Bloodsucking Bug, Rhodnius prolixus
AN - 1496881099; 19022519
AB - The bloodsucking hemipteran Rhodnius prolixus is a vector of Chagas' disease, which affects 7-8 million people today in Latin America. In contrast to other hematophagous insects, the triatomine gut is compartmentalized into three segments that perform different functions during blood digestion. Here we report analysis of transcriptomes for each of the segments using pyrosequencing technology. Comparison of transcript frequency in digestive libraries with a whole-body library was used to evaluate expression levels. All classes of digestive enzymes were highly expressed, with a predominance of cysteine and aspartic proteinases, the latter showing a significant expansion through gene duplication. Although no protein digestion is known to occur in the anterior midgut (AM), protease transcripts were found, suggesting secretion as pro-enzymes, being possibly activated in the posterior midgut (PM). As expected, genes related to cytoskeleton, protein synthesis apparatus, protein traffic, and secretion were abundantly transcribed. Despite the absence of a chitinous peritrophic membrane in hemipterans - which have instead a lipidic perimicrovillar membrane lining over midgut epithelia - several gut-specific peritrophin transcripts were found, suggesting that these proteins perform functions other than being a structural component of the peritrophic membrane. Among immunity-related transcripts, while lysozymes and lectins were the most highly expressed, several genes belonging to the Toll pathway - found at low levels in the gut of most insects - were identified, contrasting with a low abundance of transcripts from IMD and STAT pathways. Analysis of transcripts related to lipid metabolism indicates that lipids play multiple roles, being a major energy source, a substrate for perimicrovillar membrane formation, and a source for hydrocarbons possibly to produce the wax layer of the hindgut. Transcripts related to amino acid metabolism showed an unanticipated priority for degradation of tyrosine, phenylalanine, and tryptophan. Analysis of transcripts related to signaling pathways suggested a role for MAP kinases, GTPases, and LKBP1/AMP kinases related to control of cell shape and polarity, possibly in connection with regulation of cell survival, response of pathogens and nutrients. Together, our findings present a new view of the triatomine digestive apparatus and will help us understand trypanosome interaction and allow insights into hemipteran metabolic adaptations to a blood-based diet. The bloodsucking bug Rhodnius prolixus is a vector of Chagas' disease, which affects 7-8 million people in Latin America. In contrast to other insects, the digestive tract of Rhodnius has three segments that perform different functions during blood digestion. Here we report analysis of transcriptomes for each of these segments using pyrosequencing technology amounting to several million sequences. Comparison of transcript frequency in digestive libraries with a whole-body library was used to evaluate expression levels, leading to the discovery of several families of enzymes associated with the digestion of proteins, carbohydrates, and lipids, as well as proteins involved in immunity, signal transduction, amino-acid metabolism, and detoxification. Together, our findings present a new view of the triatomine digestive apparatus and will help us understand the mechanism of blood digestion by Rhodnius and its interaction with the agent of Chagas' disease, Trypanosoma cruzi, a parasite that grows within the insect's digestive system.
JF - PLoS Neglected Tropical Diseases
AU - Ribeiro, Jose MC
AU - Genta, Fernando A
AU - Sorgine, Marcos HF
AU - Logullo, Raquel
AU - Mesquita, Rafael D
AU - Paiva-Silva, Gabriela O
AU - Majerowicz, David
AU - Medeiros, Marcelo
AU - Koerich, Leonardo
AU - Terra, Walter R
AU - Ferreira, Clelia
AU - Pimentel, Andre C
AU - Bisch, Paulo M
AU - Leite, Daniel C
AU - Diniz, Michelle MP
AU - Junior, Joao Lidio da SGV
AU - Da Silva, Manuela L
AU - Araujo, Ricardo N
AU - Gandara, Ana Caroline P
AU - Brosson, Sebastien
AU - Salmon, Didier
AU - Bousbata, Sabrina
AU - Gonzalez-Caballero, Natalia
AU - Silber, Ariel Mariano
AU - Alves-Bezerra, Michele
AU - Gondim, Katia C
AU - Silva-Neto, Mario Alberto C
AU - Atella, Georgia C
AU - Araujo, Helena
AU - Dias, Felipe A
AU - Polycarpo, Carla
AU - Vionette-Amaral, Raquel J
AU - Fampa, Patricia
AU - Melo, Ana Claudia A
AU - Tanaka, Aparecida S
AU - Balczun, Carsten
AU - Oliveira, Jose Henrique M
AU - Goncalves, Renata LS
AU - Lazoski, Cristiano
AU - Rivera-Pomar, Rolando
AU - Diambra, Luis
AU - Schaub, Guenter A
AU - Garcia, Eloi S
AU - Azambuja, Patricia
AU - Braz, Gloria RC
AU - Oliveira, Pedro L
AD - Section of Vector Biology, Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland, United States of America
Y1 - 2014/01/09/
PY - 2014
DA - 2014 Jan 09
PB - Public Library of Science, 185 Berry Street San Francisco CA 94107 United States
VL - 8
IS - 1
SN - 1935-2727, 1935-2727
KW - ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Entomology Abstracts
KW - Cell survival
KW - Parasites
KW - Secretion
KW - Peritrophic membrane
KW - Hosts
KW - Rhodnius prolixus
KW - gene duplication
KW - Public health
KW - Disease transmission
KW - Gene expression
KW - Digestion
KW - Midgut
KW - Aquatic insects
KW - Trypanosoma cruzi
KW - Protein biosynthesis
KW - Amino acids
KW - Hydrocarbons
KW - Latin America
KW - Transcription
KW - Pest control
KW - Immunity
KW - Lipid metabolism
KW - Blood
KW - Rhodnius
KW - Digestive tract
KW - Aspartic proteinase
KW - Digestive system
KW - Signal transduction
KW - Chagas' disease
KW - Guanosinetriphosphatase
KW - Z 05300:General
KW - Q1 08484:Species interactions: parasites and diseases
KW - Q5 08524:Public health, medicines, dangerous organisms
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PLoS+Neglected+Tropical+Diseases&rft.atitle=An+Insight+into+the+Transcriptome+of+the+Digestive+Tract+of+the+Bloodsucking+Bug%2C+Rhodnius+prolixus&rft.au=Ribeiro%2C+Jose+MC%3BGenta%2C+Fernando+A%3BSorgine%2C+Marcos+HF%3BLogullo%2C+Raquel%3BMesquita%2C+Rafael+D%3BPaiva-Silva%2C+Gabriela+O%3BMajerowicz%2C+David%3BMedeiros%2C+Marcelo%3BKoerich%2C+Leonardo%3BTerra%2C+Walter+R%3BFerreira%2C+Clelia%3BPimentel%2C+Andre+C%3BBisch%2C+Paulo+M%3BLeite%2C+Daniel+C%3BDiniz%2C+Michelle+MP%3BJunior%2C+Joao+Lidio+da+SGV%3BDa+Silva%2C+Manuela+L%3BAraujo%2C+Ricardo+N%3BGandara%2C+Ana+Caroline+P%3BBrosson%2C+Sebastien%3BSalmon%2C+Didier%3BBousbata%2C+Sabrina%3BGonzalez-Caballero%2C+Natalia%3BSilber%2C+Ariel+Mariano%3BAlves-Bezerra%2C+Michele%3BGondim%2C+Katia+C%3BSilva-Neto%2C+Mario+Alberto+C%3BAtella%2C+Georgia+C%3BAraujo%2C+Helena%3BDias%2C+Felipe+A%3BPolycarpo%2C+Carla%3BVionette-Amaral%2C+Raquel+J%3BFampa%2C+Patricia%3BMelo%2C+Ana+Claudia+A%3BTanaka%2C+Aparecida+S%3BBalczun%2C+Carsten%3BOliveira%2C+Jose+Henrique+M%3BGoncalves%2C+Renata+LS%3BLazoski%2C+Cristiano%3BRivera-Pomar%2C+Rolando%3BDiambra%2C+Luis%3BSchaub%2C+Guenter+A%3BGarcia%2C+Eloi+S%3BAzambuja%2C+Patricia%3BBraz%2C+Gloria+RC%3BOliveira%2C+Pedro+L&rft.aulast=Ribeiro&rft.aufirst=Jose&rft.date=2014-01-09&rft.volume=8&rft.issue=1&rft.spage=&rft.isbn=&rft.btitle=&rft.title=PLoS+Neglected+Tropical+Diseases&rft.issn=19352727&rft_id=info:doi/10.1371%2Fjournal.pntd.0002594
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-02-01
N1 - Last updated - 2016-03-17
N1 - SubjectsTermNotLitGenreText - Secretion; Pest control; Hosts; Aquatic insects; Digestive system; Disease transmission; Public health; Cell survival; Parasites; Amino acids; Protein biosynthesis; Hydrocarbons; Transcription; Peritrophic membrane; Immunity; gene duplication; Lipid metabolism; Digestion; Gene expression; Blood; Digestive tract; Aspartic proteinase; Midgut; Guanosinetriphosphatase; Chagas' disease; Signal transduction; Trypanosoma cruzi; Rhodnius; Rhodnius prolixus; Latin America
DO - http://dx.doi.org/10.1371/journal.pntd.0002594
ER -
TY - JOUR
T1 - Cigarette smoking, alcohol intake, and risk of glioma in the NIH-AARP Diet and Health Study
AN - 1496885998; 18984786
AB - Background: Although cigarette smoking and alcohol drinking increase the risk of several cancers and certain components of cigarette smoke and alcohol can penetrate the blood-brain barrier, it remains unclear whether these exposures influence the risk of glioma. Methods: We examined the associations between cigarette smoking, alcohol intake, and risk of glioma in the National Institutes of Health-AARP Diet and Health Study, a prospective study of 477 095 US men and women ages 50-71 years at baseline. Hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated using models with age as the time metric and adjusted for sex, race/ethnicity, education, and marital status. Results: During a median 10.5 person-years of follow-up, 492 men and 212 women were diagnosed with first primary glioma. Among men, current, heavier smoking was associated with a reduced risk of glioma compared with never smoking, but this was based on only nine cases. No associations were observed between smoking behaviours and glioma risk in women. Greater alcohol consumption was associated with a decreased risk of glioma, particularly among men (>2 drinks per day vs <1 drink per week: HR=0.67, 95% CI=0.51-0.90). Conclusion: Smoking and alcohol drinking do not appear to increase the risk of glioma.
JF - British Journal of Cancer
AU - Braganza, M Z
AU - Rajaraman, P
AU - Park, Y
AU - Inskip, P D
AU - Freedman, N D
AU - Hollenbeck, A R
AU - de Gonzalez, A Berrington
AU - Kitahara, C M
AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, 9609 Medical Center Drive, Bethesda, MD 20892, USA
Y1 - 2014/01/07/
PY - 2014
DA - 2014 Jan 07
SP - 242
EP - 248
PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom
VL - 110
IS - 1
SN - 0007-0920, 0007-0920
KW - Toxicology Abstracts; Health & Safety Science Abstracts; Risk Abstracts
KW - Age
KW - Cigarettes
KW - Blood-brain barrier
KW - Cigarette smoke
KW - Risk reduction
KW - Models
KW - Cigarette smoking
KW - Glioma
KW - Ethnic groups
KW - Ethanol
KW - Diets
KW - Alcohol
KW - Alcoholic beverages
KW - Beverages
KW - Marriage
KW - Cancer
KW - Smoke
KW - Brain tumors
KW - Health risks
KW - Education
KW - Drinking behavior
KW - X 24380:Social Poisons & Drug Abuse
KW - H 11000:Diseases/Injuries/Trauma
KW - R2 23060:Medical and environmental health
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1496885998?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+Journal+of+Cancer&rft.atitle=Cigarette+smoking%2C+alcohol+intake%2C+and+risk+of+glioma+in+the+NIH-AARP+Diet+and+Health+Study&rft.au=Braganza%2C+M+Z%3BRajaraman%2C+P%3BPark%2C+Y%3BInskip%2C+P+D%3BFreedman%2C+N+D%3BHollenbeck%2C+A+R%3Bde+Gonzalez%2C+A+Berrington%3BKitahara%2C+C+M&rft.aulast=Braganza&rft.aufirst=M&rft.date=2014-01-07&rft.volume=110&rft.issue=1&rft.spage=242&rft.isbn=&rft.btitle=&rft.title=British+Journal+of+Cancer&rft.issn=00070920&rft_id=info:doi/10.1038%2Fbjc.2013.611
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-02-01
N1 - Last updated - 2014-07-24
N1 - SubjectsTermNotLitGenreText - Diets; Age; Beverages; Alcoholic beverages; Blood-brain barrier; Cigarette smoke; Models; Brain tumors; Cigarette smoking; Drinking behavior; Glioma; Ethnic groups; Ethanol; Smoke; Health risks; Alcohol; Education; Cigarettes; Marriage; Risk reduction; Cancer
DO - http://dx.doi.org/10.1038/bjc.2013.611
ER -
TY - JOUR
T1 - Graves' disease as immune reconstitution disease in HIV-positive patients is associated with naive and primary thymic emigrant CD4 super(+) T-cell recovery
AN - 1768579437; PQ0002676661
AB - Objective: Immune restoration disease (IRD) can develop in HIV-infected patients following antiretroviral therapy (ART) initiation as unmasking or paradoxical worsening of opportunistic infections and, rarely, autoimmune phenomena. Although IRD usually occurs in the first months of ART during memory CD4 super(+) T-cell recovery, Graves' disease occurs as a distinctive late-onset IRD and its pathogenesis is unclear. Design: Seven patients who developed Graves' disease following ART initiation from the primary HIV care clinic at the National Institutes of Health were retrospectively identified and each was matched with two HIV-infected controls based on age, sex, and baseline CD4 super(+) T-cell count. Laboratory evaluations on stored cryopreserved samples were performed. Methods: Immunophenotyping of peripheral blood mononuclear cells (PBMCs), T-cell receptor excision circle (TREC) analysis in PBMCs, measurement of serum cytokines, and luciferase immunoprecipitation systems (LIPS) analysis for autoimmune antibodies were performed on stored samples for cases and controls at baseline and longitudinally following ART initiation. TSH/thyrotropin receptor (TSH-R) antibody testing was performed on serum from cases. Data were analyzed using nonparametric testing. Results: In comparison with controls, the proportion of naive CD4 super(+) T cells increased significantly (P = 0.0027) in the Graves' disease-IRD patients. TREC/10 super(6) PBMCs also increased significantly following ART in Graves' disease-IRD patients compared with controls (P = 0.0071). Similarly, LIPS analysis demonstrated increases in nonthyroid-related autoantibody titers over time following ART in cases compared with controls. Conclusion: Our data suggest that Graves' disease-IRD, in contrast to early-onset IRD, is associated with naive and primary thymic emigrant CD4 super(+) T-cell recovery and inappropriate autoantibody production.
JF - AIDS
AU - Sheikh, Virginia
AU - Dersimonian, Rebecca
AU - Richterman, Aaron G
AU - Porter, Brian O
AU - Natarajan
AU - Burbelo, Peter D
AU - Rupert, Adam
AU - Santich, Brian H
AU - Kardava, Lela
AU - Mican, Joann M
AU - Moir, Susan
AU - Sereti, Irini
AD - National Institute of Allergy and Infectious Diseases (NIAID), sheikhv@niaid.nih.gov
Y1 - 2014/01/02/
PY - 2014
DA - 2014 Jan 02
SP - 31
EP - 39
PB - Lippincott Williams & Wilkins, Inc, 530 Walnut Street Philadelphia PA 19106-3621 United States
VL - 28
IS - 1
SN - 0269-9370, 0269-9370
KW - Health & Safety Science Abstracts; Immunology Abstracts; Virology & AIDS Abstracts
KW - Graves' disease
KW - immune reconstitution inflammatory syndrome
KW - immune restoration disease
KW - naive T cells
KW - T-cell receptor excision circles
KW - Acquired immune deficiency syndrome
KW - T-cell receptor
KW - Age
KW - Data processing
KW - Thymus
KW - antiretroviral therapy
KW - Immunoprecipitation
KW - Immunological memory
KW - Infection
KW - Antiretroviral agents
KW - Cryopreservation
KW - Opportunist infection
KW - Immune reconstitution
KW - CD4 antigen
KW - Peripheral blood mononuclear cells
KW - thyrotropin receptors
KW - Autoantibodies
KW - Human immunodeficiency virus
KW - Lymphocytes T
KW - Cytokines
KW - Sex
KW - V 22360:AIDS and HIV
KW - H 11000:Diseases/Injuries/Trauma
KW - F 06930:Autoimmunity
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1768579437?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS&rft.atitle=Graves%27+disease+as+immune+reconstitution+disease+in+HIV-positive+patients+is+associated+with+naive+and+primary+thymic+emigrant+CD4+super%28%2B%29+T-cell+recovery&rft.au=Sheikh%2C+Virginia%3BDersimonian%2C+Rebecca%3BRichterman%2C+Aaron+G%3BPorter%2C+Brian+O%3BNatarajan%3BBurbelo%2C+Peter+D%3BRupert%2C+Adam%3BSantich%2C+Brian+H%3BKardava%2C+Lela%3BMican%2C+Joann+M%3BMoir%2C+Susan%3BSereti%2C+Irini&rft.aulast=Sheikh&rft.aufirst=Virginia&rft.date=2014-01-02&rft.volume=28&rft.issue=1&rft.spage=31&rft.isbn=&rft.btitle=&rft.title=AIDS&rft.issn=02699370&rft_id=info:doi/10.1097%2FQAD.0000000000000006
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2016-02-01
N1 - Last updated - 2016-03-17
N1 - SubjectsTermNotLitGenreText - Age; T-cell receptor; Data processing; antiretroviral therapy; Thymus; Immunological memory; Immunoprecipitation; Graves' disease; Cryopreservation; Opportunist infection; Immune reconstitution; Peripheral blood mononuclear cells; CD4 antigen; Autoantibodies; thyrotropin receptors; Lymphocytes T; Cytokines; Sex; Acquired immune deficiency syndrome; Human immunodeficiency virus; Infection; Antiretroviral agents
DO - http://dx.doi.org/10.1097/QAD.0000000000000006
ER -
TY - JOUR
T1 - An efficient algorithm coupled with synthetic minority over-sampling technique to classify imbalanced PubChem BioAssay data
AN - 1524412397; 19788022
AB - It is common that imbalanced datasets are often generated from high-throughput screening (HTS). For a given dataset without taking into account the imbalanced nature, most classification methods tend to produce high predictive accuracy for the majority class, but significantly poor performance for the minority class. In this work, an efficient algorithm, GLMBoost. coupled with Synthetic Minority Over-sampling TEchnique (SMOTE) is developed and utilized to overcome the problem for several imbalanced datasets from PubChem BioAssay. By applying the proposed combinatorial method, those data of rare samples (active compounds), for which usually poor results are generated, can be detected apparently with high balanced accuracy (Gmean). As a comparison with GLMBoost, Random Forest (RF) combined with SMOTE is also adopted to classify the same datasets. Our results show that the former (GLMBoost + SMOTE) not only exhibits higher performance as measured by the percentage of correct classification for the rare samples (Sensitivity) and Gmean, but also demonstrates greater computational efficiency than the latter (RF + SMOTE). Therefore, we hope that the proposed combinatorial algorithm based on GLMBoost and SMOTE could be extensively used to tackle the imbalanced classification problem.
JF - Analytica Chimica Acta
AU - Hao, Ming
AU - Wang, Yanli
AU - Bryant, Stephen H
AD - National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Bethesda, MD 20894, USA, ywang@ncbi.nlm.nih.gov
Y1 - 2014/01/02/
PY - 2014
DA - 2014 Jan 02
SP - 117
EP - 127
PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom
VL - 806
SN - 0003-2670, 0003-2670
KW - Environment Abstracts
KW - High-throughput screening
KW - Under-sampling
KW - Over-sampling
KW - PubChem
KW - Imbalanced classification
KW - Sensitivity
KW - Bioassays
KW - Classification
KW - Forests
KW - ENA 07:General
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1524412397?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aenvabstractsmodule&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Analytica+Chimica+Acta&rft.atitle=An+efficient+algorithm+coupled+with+synthetic+minority+over-sampling+technique+to+classify+imbalanced+PubChem+BioAssay+data&rft.au=Hao%2C+Ming%3BWang%2C+Yanli%3BBryant%2C+Stephen+H&rft.aulast=Hao&rft.aufirst=Ming&rft.date=2014-01-02&rft.volume=806&rft.issue=&rft.spage=117&rft.isbn=&rft.btitle=&rft.title=Analytica+Chimica+Acta&rft.issn=00032670&rft_id=info:doi/10.1016%2Fj.aca.2013.10.050
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-05-01
N1 - Number of references - 55
N1 - Last updated - 2015-09-03
N1 - SubjectsTermNotLitGenreText - Sensitivity; Bioassays; Classification; Forests
DO - http://dx.doi.org/10.1016/j.aca.2013.10.050
ER -
TY - JOUR
T1 - From burden-sharing to opportunity-sharing: unlocking the climate negotiations
AN - 1492624428; 18929304
AB - In conventional thinking on climate negotiations, traditional fossil fuel-based economic growth is coupled with carbon emissions, thus mitigation has been regarded as a burden on economic growth. The scarcity within the global emission budget and the interpretation of climate change as 'global public goods' have led climate change negotiations into a burden-sharing deadlock. However, some recent economics studies suggest that mitigation could actually promote local economic growth opportunities; consequently increasing the incentives for unilateral mitigation actions. This article highlights the implications for the strategies of unlocking the climate negotiations deadlock. Following an explanation of how climate change negotiations have led to a burden-sharing game and have become a deadlock, some new ways of thinking (based on the emerging literature) are used to suggest how mitigation could promote local economic growth.Policy relevanceOne policy implication is the need to change the current mindset in global climate change negotiations. The current framing of burden-sharing can be abandoned in favour of opportunity-sharing. This more positive approach will stimulate progress on climate action. Therefore, green growth should be situated at the heart of post-2020 climate change regime. A new two-track architecture is proposed for achieving the transformation as a combined top-down and bottom-up approach. A lower legally binding target based on equity principles of common but differentiated responsibilities (CBDR) could form a more politically realistic and inclusive basis for participation. To complement this, a green growth club would promote a higher voluntary global ambition and accelerate mitigation.
JF - Climate Policy
AU - Zhang, Yongsheng
AU - Shi, He-Ling
AD - Development Research Centre of the State Council, No. 225, Chaoyangmen Nei Dajie, Dongcheng District, Beijing 100010, China
Y1 - 2014/01/02/
PY - 2014
DA - 2014 Jan 02
SP - 63
EP - 81
PB - Taylor & Francis Group Ltd., 2 Park Square Oxford OX14 4RN United Kingdom
VL - 14
IS - 1
SN - 1469-3062, 1469-3062
KW - Sustainability Science Abstracts; Environment Abstracts; Meteorological & Geoastrophysical Abstracts
KW - Mitigation
KW - Responsibility
KW - Climate change
KW - Public policy and climate
KW - Architecture
KW - Economic growth
KW - Incentives
KW - Environmental policy
KW - Carbon emissions
KW - Economics
KW - Emissions
KW - Scarcity
KW - Budgets
KW - ENA 03:Energy
KW - M2 551.583:Variations (551.583)
KW - M3 1010:Issues in Sustainable Development
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492624428?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Assamodule&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Climate+Policy&rft.atitle=From+burden-sharing+to+opportunity-sharing%3A+unlocking+the+climate+negotiations&rft.au=Zhang%2C+Yongsheng%3BShi%2C+He-Ling&rft.aulast=Zhang&rft.aufirst=Yongsheng&rft.date=2014-01-02&rft.volume=14&rft.issue=1&rft.spage=63&rft.isbn=&rft.btitle=&rft.title=Climate+Policy&rft.issn=14693062&rft_id=info:doi/10.1080%2F14693062.2014.857979
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-01-01
N1 - Last updated - 2016-11-09
N1 - SubjectsTermNotLitGenreText - Public policy and climate; Climate change; Architecture; Carbon emissions; Mitigation; Responsibility; Economics; Emissions; Scarcity; Budgets; Incentives; Economic growth; Environmental policy
DO - http://dx.doi.org/10.1080/14693062.2014.857979
ER -
TY - JOUR
T1 - Un-sung Samaritans in the Lives of People with Mental Illness: An Indian Experience
AN - 1752993119; 201600254
AB - Caring is a fundamental issue in the rehabilitation of a person with mental illness and more so for people with severe mental illness. The study examines the load of care giving with reference to the types of care during the symptomatic and recovery phases of mental illness and the various ways in which caregivers adapt their lives to meet the needs of people with mental illness (PWMI). The present research draws its data from the families of 200 persons with mental illness in Andhra Pradesh and Karnataka in India. The data presented in the study was collected from interviews using an interview schedule with open ended questions. The results reveal that people with mental illness require more social care during their recovery phase so as to facilitate their reintegration into mainstream society. Despite their own hardships, families by and large take on the care of their family members with mental illness as a matter of their responsibility. The study records the incredulous gratitude of caregivers at being acknowledged for the work they do. In that regard, the study itself provides a boost to the morale of tired, unacknowledged caregivers. Adapted from the source document.
JF - The Indian Journal of Social Work
AU - Janardhana, N
AU - SHRAVYA,
AU - Naidu, D M
AU - SARASWATHI,
AU - Seshan, Valli
AD - Department of Psychiatric Social Work, National Institute of Mental Health and Neuro Sciences (NIMHANS), Bangalore
Y1 - 2014/01//
PY - 2014
DA - January 2014
SP - 7
EP - 32
PB - Tata Institute of Social Sciences, Mumbai India
VL - 75
IS - 1
SN - 0019-5634, 0019-5634
KW - Caregivers
KW - Rehabilitation
KW - Social Services
KW - Mental Illness
KW - India
KW - article
KW - 6142: mental & emotional health problems
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1752993119?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Asocialservices&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Indian+Journal+of+Social+Work&rft.atitle=Un-sung+Samaritans+in+the+Lives+of+People+with+Mental+Illness%3A+An+Indian+Experience&rft.au=Janardhana%2C+N%3BSHRAVYA%2C%3BNaidu%2C+D+M%3BSARASWATHI%2C%3BSeshan%2C+Valli&rft.aulast=Janardhana&rft.aufirst=N&rft.date=2014-01-01&rft.volume=75&rft.issue=1&rft.spage=7&rft.isbn=&rft.btitle=&rft.title=The+Indian+Journal+of+Social+Work&rft.issn=00195634&rft_id=info:doi/
LA - English
DB - Social Services Abstracts
N1 - Date revised - 2016-01-01
N1 - Number of references - 58
N1 - Last updated - 2016-09-28
N1 - CODEN - IJSWA3
N1 - SubjectsTermNotLitGenreText - Mental Illness; Caregivers; Rehabilitation; India; Social Services
ER -
TY - JOUR
T1 - Guidance for Performing Criticality Analyses of Fuel Storage at Light-Water Reactor Power Plants
AN - 1692315007; PQ0001263023
AB - The Nuclear Energy Institute, through the Spent Fuel Criticality Task Force has developed a guidance document that describes acceptable methods that may be used to perform criticality analyses for the storage of new and spent fuel at light-water reactor (LWR) power plants [1]. The guidance is applicable to new fuel assemblies stored in a new fuel vault, and to new and spent used fuel assemblies stored in spent fuel racks in a spent fuel pool.
JF - Transactions of the American Nuclear Society
AU - Cummings, K W
AD - Nuclear Energy Institute, 1201 F Street, NW, Suite 1100, Washington, DC 20004 kwc@nei.org
Y1 - 2014
PY - 2014
DA - 2014
SP - 342
EP - 345
PB - American Nuclear Society, Inc.
VL - 111
SN - 0003-018X, 0003-018X
KW - Mechanical & Transportation Engineering Abstracts (MT); Environmental Engineering Abstracts (EN); Electronics and Communications Abstracts (EA); CSA / ASCE Civil Engineering Abstracts (CE)
KW - Nuclear power generation
KW - Nuclear reactors
KW - Fuels
KW - Electric power generation
KW - Spent nuclear fuels
KW - Nuclear reactor components
KW - Electric power plants
KW - Nuclear engineering
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1692315007?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aenvironmentalengabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Transactions+of+the+American+Nuclear+Society&rft.atitle=Guidance+for+Performing+Criticality+Analyses+of+Fuel+Storage+at+Light-Water+Reactor+Power+Plants&rft.au=Cummings%2C+K+W&rft.aulast=Cummings&rft.aufirst=K&rft.date=2014-01-01&rft.volume=111&rft.issue=&rft.spage=342&rft.isbn=&rft.btitle=&rft.title=Transactions+of+the+American+Nuclear+Society&rft.issn=0003018X&rft_id=info:doi/
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2015-07-01
N1 - Last updated - 2015-07-01
ER -
TY - JOUR
T1 - Can Substance Use Disorders be Managed Using the Chronic Care Model? Review and Recommendations from a NIDA Consensus Group
AN - 1665163740
AB - Brain imaging and genetic studies over the past two decades suggest that substance use disorders are best considered chronic illnesses. The passing of the Affordable Care Act in the United States has set the occasion for integrating treatment of substance use disorders into mainstream healthcare; and for using the proactive, team-oriented Chronic Care Model (CCM). This paper systematically examines and compares whether and how well the CCM could be applied to the treatment of substance use disorders, using type 2 diabetes as a comparator. The chronic illness management approach is still new in the field of addiction and research is limited. However comparative findings suggest that most proactive, team treatment-oriented clinical management practices now used in diabetes management are applicable to the substance use disorders; capable of being implemented by primary care teams; and should offer comparable potential benefits in the treatment of substance use disorders. Such care should also improve the quality of care for many illnesses now negatively affected by unaddressed substance abuse.
JF - Public Health Reviews
AU - McLellan, A Thomas
AU - Starrels, Joanna L
AU - Tai, Betty
AU - Gordon, Adam J
AU - Brown, Richard
AU - Ghitza, Udi
AU - Gourevitch, Marc
AU - Stein, Jack
AU - Oros, Marla
AU - Horton, Terry
AU - Lindblad, Robert
AU - McNeely, Jennifer
AD - Treatment Research Institute, 600 Public Ledger Building, 150 S. Independence Mall, Philadelphia, PA 19106, USA ; Albert Einstein College of Medicine and Montefiore Medical Center, Bronx, NY, USA ; National Institute of Health, National Institute on Drug Abuse, Bethesda, MD, USA ; University of Pittsburgh School of Medicine, Pittsburgh, PA, USA ; University of Wisconsin, School of Medicine and Public Health, Madison, WI, USA ; New York University School of Medicine, Department of Population Health, New York. NY USA ; The Mosaic Group, Baltimore MD, USA ; Treatment Research Institute, 600 Public Ledger Building, 150 S. Independence Mall, Philadelphia, PA 19106, USA, Christiana Care Health System, Division of Addiction Medicine, Wilmington DE, USA ; Treatment Research Institute, 600 Public Ledger Building, 150 S. Independence Mall, Philadelphia, PA 19106, USA, The EMMES Corporation, Rockville, MD, USA ; Treatment Research Institute, 600 Public Ledger Building, 150 S. Independence Mall, Philadelphia, PA 19106, USA, Albert Einstein College of Medicine and Montefiore Medical Center, Bronx, NY, USA, New York University School of Medicine, Department of Population Health, New York. NY USA ; Treatment Research Institute, 600 Public Ledger Building, 150 S. Independence Mall, Philadelphia, PA 19106, USA
Y1 - 2014
PY - 2014
DA - 2014
SP - 1
EP - 24
CY - Dordrecht
PB - Springer Science & Business Media
VL - 35
IS - 2
SN - 0301-0422
KW - Medical Sciences--Oncology
KW - Substance use disorders
KW - chronic illness
KW - chronic care model
KW - type 2 diabetes management
KW - electronic health records
KW - healthcare reform
KW - Addiction
KW - Teams
KW - Treatment
KW - Type 2 diabetes mellitus
KW - Brain
KW - Brain imaging
KW - Chronic sickness
KW - Clinical guidelines
KW - Clinical management
KW - Diabetes
KW - Disease management
KW - Genetic factors
KW - Health care
KW - Primary health care
KW - Quality of care
KW - Sickness
KW - Substance abuse disorders
KW - United States--US
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665163740?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Public+Health+Reviews&rft.atitle=Can+Substance+Use+Disorders+be+Managed+Using+the+Chronic+Care+Model%3F+Review+and+Recommendations+from+a+NIDA+Consensus+Group&rft.au=McLellan%2C+A+Thomas%3BStarrels%2C+Joanna+L%3BTai%2C+Betty%3BGordon%2C+Adam+J%3BBrown%2C+Richard%3BGhitza%2C+Udi%3BGourevitch%2C+Marc%3BStein%2C+Jack%3BOros%2C+Marla%3BHorton%2C+Terry%3BLindblad%2C+Robert%3BMcNeely%2C+Jennifer&rft.aulast=McLellan&rft.aufirst=A&rft.date=2014-01-01&rft.volume=35&rft.issue=2&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Public+Health+Reviews&rft.issn=03010422&rft_id=info:doi/
LA - English
DB - Applied Social Sciences Index & Abstracts (ASSIA)
N1 - Date revised - 2015-01-09
N1 - Last updated - 2016-06-24
N1 - SubjectsTermNotLitGenreText - United States--US
ER -
TY - JOUR
T1 - carboxypeptidase E-ΔN, a neuroprotein transiently expressed during development protects embryonic neurons against glutamate neurotoxicity.
AN - 1628881739; 25426952
AB - Neuroprotective proteins expressed in the fetus play a critical role during early embryonic neurodevelopment, especially during maternal exposure to alcohol and drugs that cause stress, glutamate neuroexcitotoxicity, and damage to the fetal brain, if prolonged. We have identified a novel protein, carboxypeptidase E-ΔN (CPE-ΔN), which is a splice variant of CPE that has neuroprotective effects on embryonic neurons. CPE-ΔN is transiently expressed in mouse embryos from embryonic day 5.5 to postnatal day 1. It is expressed in embryonic neurons, but not in 3 week or older mouse brains, suggesting a function primarily in utero. CPE-ΔN expression was up-regulated in embryonic hippocampal neurons in response to dexamethasone treatment. CPE-ΔN transduced into rat embryonic cortical and hippocampal neurons protected them from glutamate- and H2O2-induced cell death. When transduced into embryonic cortical neurons, CPE-ΔN was found in the nucleus and enhanced the transcription of FGF2 mRNA. Embryonic cortical neurons challenged with glutamate resulted in attenuated FGF2 levels and cell death, but CPE-ΔN transduced neurons treated in the same manner showed increased FGF2 expression and normal viability. This neuroprotective effect of CPE-ΔN was mediated by secreted FGF2. Through receptor signaling, FGF2 activated the AKT and ERK signaling pathways, which in turn increased BCL-2 expression. This led to inhibition of caspase-3 activity and cell survival.
JF - PloS one
AU - Qin, Xiao-Yan
AU - Cheng, Yong
AU - Murthy, Saravana R K
AU - Selvaraj, Prabhuanand
AU - Loh, Y Peng
AD - Section on Cellular Neurobiology, Program on Developmental Neuroscience, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892, United States of America; College of Life and Environmental Sciences, Minzu University of China, Beijing 100081, China. ; Section on Cellular Neurobiology, Program on Developmental Neuroscience, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892, United States of America.
Y1 - 2014
PY - 2014
DA - 2014
SP - 1
VL - 9
IS - 11
KW - Nerve Tissue Proteins
KW - 0
KW - Neuroprotective Agents
KW - Proto-Oncogene Proteins c-bcl-2
KW - RNA, Messenger
KW - Fibroblast Growth Factor 2
KW - 103107-01-3
KW - Bcl2 protein, mouse
KW - 114100-40-2
KW - Glutamic Acid
KW - 3KX376GY7L
KW - Hydrogen Peroxide
KW - BBX060AN9V
KW - Proto-Oncogene Proteins c-akt
KW - EC 2.7.11.1
KW - Extracellular Signal-Regulated MAP Kinases
KW - EC 2.7.11.24
KW - Carboxypeptidase H
KW - EC 3.4.17.10
KW - Caspase 3
KW - EC 3.4.22.-
KW - Index Medicus
KW - Proto-Oncogene Proteins c-akt -- genetics
KW - Cerebral Cortex -- cytology
KW - Animals
KW - Cerebral Cortex -- drug effects
KW - Cell Nucleus -- metabolism
KW - Transduction, Genetic
KW - Hydrogen Peroxide -- pharmacology
KW - Primary Cell Culture
KW - Cell Nucleus -- drug effects
KW - RNA, Messenger -- genetics
KW - Hippocampus -- drug effects
KW - Rats
KW - Caspase 3 -- genetics
KW - Cell Survival -- drug effects
KW - Hippocampus -- enzymology
KW - Embryo, Mammalian
KW - Signal Transduction
KW - Extracellular Signal-Regulated MAP Kinases -- genetics
KW - Caspase 3 -- metabolism
KW - Proto-Oncogene Proteins c-bcl-2 -- agonists
KW - Proto-Oncogene Proteins c-akt -- metabolism
KW - Cerebral Cortex -- enzymology
KW - Mice
KW - Extracellular Signal-Regulated MAP Kinases -- metabolism
KW - Cell Death -- drug effects
KW - RNA, Messenger -- metabolism
KW - Proto-Oncogene Proteins c-bcl-2 -- metabolism
KW - Hippocampus -- cytology
KW - Proto-Oncogene Proteins c-akt -- agonists
KW - Proto-Oncogene Proteins c-bcl-2 -- genetics
KW - Gene Expression Regulation, Developmental
KW - Carboxypeptidase H -- metabolism
KW - Carboxypeptidase H -- genetics
KW - Fibroblast Growth Factor 2 -- secretion
KW - Neurons -- drug effects
KW - Neurons -- cytology
KW - Fibroblast Growth Factor 2 -- genetics
KW - Neuroprotective Agents -- metabolism
KW - Fibroblast Growth Factor 2 -- agonists
KW - Neurons -- enzymology
KW - Nerve Tissue Proteins -- metabolism
KW - Nerve Tissue Proteins -- genetics
KW - Glutamic Acid -- pharmacology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=carboxypeptidase+E-%CE%94N%2C+a+neuroprotein+transiently+expressed+during+development+protects+embryonic+neurons+against+glutamate+neurotoxicity.&rft.au=Qin%2C+Xiao-Yan%3BCheng%2C+Yong%3BMurthy%2C+Saravana+R+K%3BSelvaraj%2C+Prabhuanand%3BLoh%2C+Y+Peng&rft.aulast=Qin&rft.aufirst=Xiao-Yan&rft.date=2014-01-01&rft.volume=9&rft.issue=11&rft.spage=e112996&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0112996
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-07-13
N1 - Date created - 2014-11-27
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
J Biol Chem. 2000 Apr 14;275(15):10761-6 [10753867]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1371/journal.pone.0112996
ER -
TY - JOUR
T1 - Identification of functionally important residues of the rat P2X4 receptor by alanine scanning mutagenesis of the dorsal fin and left flipper domains.
AN - 1628878480; 25398027
AB - Crystallization of the zebrafish P2X4 receptor in both open and closed states revealed conformational differences in the ectodomain structures, including the dorsal fin and left flipper domains. Here, we focused on the role of these domains in receptor activation, responsiveness to orthosteric ATP analogue agonists, and desensitization. Alanine scanning mutagenesis of the R203-L214 (dorsal fin) and the D280-N293 (left flipper) sequences of the rat P2X4 receptor showed that ATP potency/efficacy was reduced in 15 out of 26 alanine mutants. The R203A, N204A, and N293A mutants were essentially non-functional, but receptor function was restored by ivermectin, an allosteric modulator. The I205A, T210A, L214A, P290A, G291A, and Y292A mutants exhibited significant changes in the responsiveness to orthosteric analog agonists 2-(methylthio)adenosine 5'-triphosphate, adenosine 5'-(γ-thio)triphosphate, 2'(3'-O-(4-benzoylbenzoyl)adenosine 5'-triphosphate, and α,β-methyleneadenosine 5'-triphosphate. In contrast, the responsiveness of L206A, N208A, D280A, T281A, R282A, and H286A mutants to analog agonists was comparable to that of the wild type receptor. Among these mutants, D280A, T281A, R282A, H286A, G291A, and Y292A also exhibited increased time-constant of the desensitizing current response. These experiments, together with homology modeling, indicate that residues located in the upper part of the dorsal fin and left flipper domains, relative to distance from the channel pore, contribute to the organization of the ATP binding pocket and to the initiation of signal transmission towards residues in the lower part of both domains. The R203 and N204 residues, deeply buried in the protein, may integrate the output signal from these two domains towards the gate. In addition, the left flipper residues predominantly account for the control of transition of channels from an open to a desensitized state.
JF - PloS one
AU - Tvrdonova, Vendula
AU - Rokic, Milos B
AU - Stojilkovic, Stanko S
AU - Zemkova, Hana
AD - Department of Cellular and Molecular Neuroendocrinology, Institute of Physiology Academy of Sciences of the Czech Republic, Prague, Czech Republic; Department of Physiology of Animals, Faculty of Science, Charles University, Prague, Czech Republic. ; Department of Cellular and Molecular Neuroendocrinology, Institute of Physiology Academy of Sciences of the Czech Republic, Prague, Czech Republic; Section on Cellular Signaling, Program in Developmental Neuroscience, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, United States of America. ; Section on Cellular Signaling, Program in Developmental Neuroscience, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, United States of America. ; Department of Cellular and Molecular Neuroendocrinology, Institute of Physiology Academy of Sciences of the Czech Republic, Prague, Czech Republic.
Y1 - 2014
PY - 2014
DA - 2014
SP - 1
VL - 9
IS - 11
KW - Purinergic P2X Receptor Agonists
KW - 0
KW - Receptors, Purinergic P2X4
KW - Ivermectin
KW - 70288-86-7
KW - Adenosine Triphosphate
KW - 8L70Q75FXE
KW - Alanine
KW - OF5P57N2ZX
KW - Index Medicus
KW - Animals
KW - Ivermectin -- pharmacology
KW - HEK293 Cells
KW - Humans
KW - Amino Acid Sequence
KW - Molecular Dynamics Simulation
KW - Protein Binding
KW - Purinergic P2X Receptor Agonists -- pharmacology
KW - Mutagenesis
KW - Binding Sites
KW - Ion Channel Gating -- drug effects
KW - Rats
KW - Patch-Clamp Techniques
KW - Sequence Alignment
KW - Alanine -- metabolism
KW - Adenosine Triphosphate -- metabolism
KW - Molecular Sequence Data
KW - Alanine -- genetics
KW - Protein Structure, Tertiary
KW - Receptors, Purinergic P2X4 -- genetics
KW - Receptors, Purinergic P2X4 -- chemistry
KW - Receptors, Purinergic P2X4 -- metabolism
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-12-18
N1 - Date created - 2014-11-15
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Pharmacol Rev. 2011 Sep;63(3):641-83 [21737531]
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Biochemistry. 2011 Oct 4;50(39):8427-36 [21879712]
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Biochemistry. 2014 May 13;53(18):3012-9 [24762105]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1371/journal.pone.0112902
ER -
TY - JOUR
T1 - Photoimmunotherapy of gastric cancer peritoneal carcinomatosis in a mouse model.
AN - 1626162789; 25401794
AB - Photoimmunotherapy (PIT) is a new cancer treatment that combines the specificity of antibodies for targeting tumors with the toxicity induced by photosensitizers after exposure to near infrared (NIR) light. We performed PIT in a model of disseminated gastric cancer peritoneal carcinomatosis and monitored efficacy with in vivo GFP fluorescence imaging. In vitro and in vivo experiments were conducted with a HER2-expressing, GFP-expressing, gastric cancer cell line (N87-GFP). A conjugate comprised of a photosensitizer, IR-700, conjugated to trastuzumab (tra-IR700), followed by NIR light was used for PIT. In vitro PIT was evaluated by measuring cytotoxicity with dead staining and a decrease in GFP fluorescence. In vivo PIT was evaluated in a disseminated peritoneal carcinomatosis model and a flank xenograft using tumor volume measurements and GFP fluorescence intensity. In vivo anti-tumor effects of PIT were confirmed by significant reductions in tumor volume (at day 15, p<0.0001 vs. control) and GFP fluorescence intensity (flank model: at day 3, PIT treated vs. control p<0.01 and peritoneal disseminated model: at day 3 PIT treated vs. control, p<0.05). Cytotoxic effects in vitro were shown to be dependent on the light dose and caused necrotic cell rupture leading to GFP release and a decrease in fluorescence intensity in vitro. Thus, loss of GFP fluorescence served as a useful biomarker of cell necrosis after PIT.
JF - PloS one
AU - Sato, Kazuhide
AU - Choyke, Peter L
AU - Kobayashi, Hisataka
AD - Molecular Imaging Program, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland 20892, United States of America.
Y1 - 2014
PY - 2014
DA - 2014
SP - 1
VL - 9
IS - 11
KW - Antineoplastic Agents
KW - 0
KW - Immunoconjugates
KW - Photosensitizing Agents
KW - Green Fluorescent Proteins
KW - 147336-22-9
KW - Trastuzumab
KW - P188ANX8CK
KW - Index Medicus
KW - Animals
KW - Apoptosis
KW - Combined Modality Therapy
KW - Humans
KW - Tumor Burden
KW - Mice, Nude
KW - Mice
KW - Cell Proliferation
KW - Microscopy, Fluorescence
KW - Tumor Cells, Cultured
KW - Xenograft Model Antitumor Assays
KW - Flow Cytometry
KW - Antineoplastic Agents -- therapeutic use
KW - Fluorescent Antibody Technique
KW - Green Fluorescent Proteins -- metabolism
KW - Female
KW - Immunoenzyme Techniques
KW - Stomach Neoplasms -- pathology
KW - Stomach Neoplasms -- immunology
KW - Peritoneal Neoplasms -- secondary
KW - Peritoneal Neoplasms -- immunology
KW - Immunotherapy
KW - Stomach Neoplasms -- therapy
KW - Photosensitizing Agents -- therapeutic use
KW - Trastuzumab -- therapeutic use
KW - Phototherapy
KW - Peritoneal Neoplasms -- therapy
KW - Immunoconjugates -- therapeutic use
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2016-02-01
N1 - Date created - 2014-11-18
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Bioconjug Chem. 2012 Mar 21;23(3):604-9 [22369484]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1371/journal.pone.0113276
ER -
TY - JOUR
T1 - A murine inhalation model to characterize pulmonary exposure to dry Aspergillus fumigatus conidia.
AN - 1618161981; 25340353
AB - Most murine models of fungal exposure are based on the delivery of uncharacterized extracts or liquid conidia suspensions using aspiration or intranasal approaches. Studies that model exposure to dry fungal aerosols using whole body inhalation have only recently been described. In this study, we aimed to characterize pulmonary immune responses following repeated inhalation of conidia utilizing an acoustical generator to deliver dry fungal aerosols to mice housed in a nose only exposure chamber. Immunocompetent female BALB/cJ mice were exposed to conidia derived from Aspergillus fumigatus wild-type (WT) or a melanin-deficient (Δalb1) strain. Conidia were aerosolized and delivered to mice at an estimated deposition dose of 1×105 twice a week for 4 weeks (8 total). Histopathological and immunological endpoints were assessed 4, 24, 48, and 72 hours after the final exposure. Histopathological analysis showed that conidia derived from both strains induced lung inflammation, especially at 24 and 48 hour time points. Immunological endpoints evaluated in bronchoalveolar lavage fluid (BALF) and the mediastinal lymph nodes showed that exposure to WT conidia led to elevated numbers of macrophages, granulocytes, and lymphocytes. Importantly, CD8+ IL17+ (Tc17) cells were significantly higher in BALF and positively correlated with germination of A. fumigatus WT spores. Germination was associated with specific IgG to intracellular proteins while Δalb1 spores elicited antibodies to cell wall hydrophobin. These data suggest that inhalation exposures may provide a more representative analysis of immune responses following exposures to environmentally and occupationally prevalent fungal contaminants.
JF - PloS one
AU - Buskirk, Amanda D
AU - Green, Brett J
AU - Lemons, Angela R
AU - Nayak, Ajay P
AU - Goldsmith, W Travis
AU - Kashon, Michael L
AU - Anderson, Stacey E
AU - Hettick, Justin M
AU - Templeton, Steven P
AU - Germolec, Dori R
AU - Beezhold, Donald H
AD - Allergy and Clinical Immunology Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, Morgantown, West Virginia, United States of America. ; Pathology and Physiology Research Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, Morgantown, West Virginia, United States of America. ; Biostatistics and Epidemiology Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, Morgantown, West Virginia, United States of America. ; Toxicology Branch, National Toxicology Program Division, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, United States of America.
Y1 - 2014
PY - 2014
DA - 2014
SP - 1
VL - 9
IS - 10
KW - Antibodies, Fungal
KW - 0
KW - Cytokines
KW - Immunoglobulin G
KW - Index Medicus
KW - Animals
KW - Hyphae -- physiology
KW - Cell Count
KW - Acoustics
KW - Lymph Nodes -- pathology
KW - Disease Models, Animal
KW - Antibodies, Fungal -- immunology
KW - Cytokines -- metabolism
KW - Mice, Inbred BALB C
KW - Cell Proliferation
KW - Proteomics
KW - Antibody Formation -- immunology
KW - Flow Cytometry
KW - Immunoglobulin G -- metabolism
KW - Administration, Inhalation
KW - Species Specificity
KW - Bronchoalveolar Lavage Fluid -- cytology
KW - Female
KW - Inhalation Exposure
KW - Aspergillus fumigatus -- physiology
KW - Spores, Fungal -- physiology
KW - Lung -- pathology
KW - Lung -- microbiology
KW - Aspergillus fumigatus -- immunology
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1618161981?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=A+murine+inhalation+model+to+characterize+pulmonary+exposure+to+dry+Aspergillus+fumigatus+conidia.&rft.au=Buskirk%2C+Amanda+D%3BGreen%2C+Brett+J%3BLemons%2C+Angela+R%3BNayak%2C+Ajay+P%3BGoldsmith%2C+W+Travis%3BKashon%2C+Michael+L%3BAnderson%2C+Stacey+E%3BHettick%2C+Justin+M%3BTempleton%2C+Steven+P%3BGermolec%2C+Dori+R%3BBeezhold%2C+Donald+H&rft.aulast=Buskirk&rft.aufirst=Amanda&rft.date=2014-01-01&rft.volume=9&rft.issue=10&rft.spage=e109855&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0109855
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-06-25
N1 - Date created - 2014-10-24
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Med Mycol. 2010 Mar;48(2):217-28 [20055736]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1371/journal.pone.0109855
ER -
TY - JOUR
T1 - Effect of antigen shedding on targeted delivery of immunotoxins in solid tumors from a mathematical model.
AN - 1618151061; 25343405
AB - Most cancer-specific antigens used as targets of antibody-drug conjugates and immunotoxins are shed from the cell surface (Zhang & Pastan (2008) Clin. Cancer Res. 14: 7981-7986), although at widely varying rates and by different mechanisms (Dello Sbarba & Rovida (2002) Biol. Chem. 383: 69-83). Why many cancer-specific antigens are shed and how the shedding affects delivery efficiency of antibody-based protein drugs are poorly understood questions at present. Before a detailed numerical study, it was assumed that antigen shedding would reduce the efficacy of antibody-drug conjugates and immunotoxins. However, our previous study using a comprehensive mathematical model showed that antigen shedding can significantly improve the efficacy of the mesothelin-binding immunotoxin, SS1P (anti-mesothelin-Fv-PE38), and suggested that receptor shedding can be a general mechanism for enhancing the effect of inter-cellular signaling molecules. Here, we improved this model and applied it to both SS1P and another recombinant immunotoxin, LMB-2, which targets CD25. We show that the effect of antigen shedding is influenced by a number of factors including the number of antigen molecules on the cell surface and the endocytosis rate. The high shedding rate of mesothelin is beneficial for SS1P, for which the antigen is large in number and endocytosed rapidly. On the other hand, the slow shedding of CD25 is beneficial for LMB-2, for which the antigen is small in number and endocytosed slowly.
JF - PloS one
AU - Pak, Youngshang
AU - Pastan, Ira
AU - Kreitman, Robert J
AU - Lee, Byungkook
AD - Department of Chemistry and Institute of Functional Materials, Pusan National University, Busan, Republic of Korea; Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America. ; Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
Y1 - 2014
PY - 2014
DA - 2014
SP - 1
VL - 9
IS - 10
KW - Antibodies, Monoclonal
KW - 0
KW - Antigens, Neoplasm
KW - B3(Fv)-PE38KDEL recombinant immunotoxin
KW - Exotoxins
KW - SS1(dsFv)PE38
KW - Index Medicus
KW - Animals
KW - Exotoxins -- pharmacology
KW - Tumor Burden -- drug effects
KW - Kinetics
KW - Humans
KW - Endocytosis -- drug effects
KW - Exotoxins -- therapeutic use
KW - Models, Biological
KW - Neoplasms -- drug therapy
KW - Drug Delivery Systems
KW - Antibodies, Monoclonal -- pharmacology
KW - Antigens, Neoplasm -- immunology
KW - Antibodies, Monoclonal -- therapeutic use
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1618151061?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Effect+of+antigen+shedding+on+targeted+delivery+of+immunotoxins+in+solid+tumors+from+a+mathematical+model.&rft.au=Pak%2C+Youngshang%3BPastan%2C+Ira%3BKreitman%2C+Robert+J%3BLee%2C+Byungkook&rft.aulast=Pak&rft.aufirst=Youngshang&rft.date=2014-01-01&rft.volume=9&rft.issue=10&rft.spage=e110716&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0110716
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-06-26
N1 - Date created - 2014-10-25
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1371/journal.pone.0110716
ER -
TY - JOUR
T1 - The association between selenium and other micronutrients and thyroid cancer incidence in the NIH-AARP Diet and Health Study.
AN - 1615261721; 25329812
AB - Selenium is an essential trace element that is important for thyroid hormone metabolism and has antioxidant properties which protect the thyroid gland from oxidative stress. The association of selenium, as well as intake of other micronutrients, with thyroid cancer is unclear.
We evaluated associations of dietary selenium, beta-carotene, calcium, vitamin D, vitamin C, vitamin E, folate, magnesium, and zinc intake with thyroid cancer risk in the National Institutes of Health - American Association of Retired Persons Diet and Health Study, a large prospective cohort of 566,398 men and women aged 50-71 years in 1995-1996. Multivariable-adjusted Cox proportional hazards regression was used to examine associations between dietary intake of micronutrients, assessed using a food frequency questionnaire, and thyroid cancer cases, ascertained by linkage to state cancer registries and the National Death Index. With the exception of vitamin C, which was associated with an increased risk of thyroid cancer (HR(Q5 vs Q1), 1.34; 95% CI, 1.02-1.76; P(trend), <0.01), we observed no evidence of an association between quintile of selenium (HR(Q5 vs Q1), 1.23; 95% CI, 0.92-1.65; P(trend), 0.26) or other micronutrient intake and thyroid cancer.
Our study does not suggest strong evidence for an association between dietary intake of selenium or other micronutrients and thyroid cancer risk. More studies are needed to clarify the role of selenium and other micronutrients in thyroid carcinogenesis.
JF - PloS one
AU - O'Grady, Thomas J
AU - Kitahara, Cari M
AU - DiRienzo, A Gregory
AU - Gates, Margaret A
AD - University at Albany, School of Public Health, Rensselaer, New York, United States of America. ; Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, Maryland, United States of America.
Y1 - 2014
PY - 2014
DA - 2014
SP - 1
VL - 9
IS - 10
KW - Trace Elements
KW - 0
KW - Selenium
KW - H6241UJ22B
KW - Index Medicus
KW - Prospective Studies
KW - Risk Factors
KW - National Cancer Institute (U.S.)
KW - Humans
KW - Incidence
KW - Aged
KW - Middle Aged
KW - United States -- epidemiology
KW - Male
KW - Female
KW - Thyroid Neoplasms -- epidemiology
KW - Selenium -- adverse effects
KW - Trace Elements -- adverse effects
KW - Surveys and Questionnaires
KW - Selenium -- administration & dosage
KW - Trace Elements -- administration & dosage
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1615261721?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=The+association+between+selenium+and+other+micronutrients+and+thyroid+cancer+incidence+in+the+NIH-AARP+Diet+and+Health+Study.&rft.au=O%27Grady%2C+Thomas+J%3BKitahara%2C+Cari+M%3BDiRienzo%2C+A+Gregory%3BGates%2C+Margaret+A&rft.aulast=O%27Grady&rft.aufirst=Thomas&rft.date=2014-01-01&rft.volume=9&rft.issue=10&rft.spage=e110886&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0110886
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-06-29
N1 - Date created - 2014-10-21
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
J Nutr. 2010 Feb;140(2):317-24 [20032488]
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Eur J Endocrinol. 2010 Sep;163(3):427-34 [20566590]
Surgery. 2010 Dec;148(6):1147-52; discussion 1152-3 [21134545]
Future Oncol. 2010 Nov;6(11):1771-9 [21142662]
Cancer Epidemiol Biomarkers Prev. 2011 Mar;20(3):464-72 [21266520]
Int J Cancer. 2011 Jul 1;129(1):160-72 [20824705]
J Environ Public Health. 2011;2011:850105 [22187575]
Int J Cancer. 2012 Mar 15;130(6):1411-9 [21544808]
Thyroid. 2012 Apr;22(4):422-9 [22280227]
Nutr Cancer. 2012;64(7):929-36 [23061901]
Nutrients. 2012 Nov;4(11):1740-6 [23201844]
Br J Nutr. 2013 Jan 14;109(1):118-28 [22455656]
Clin Endocrinol (Oxf). 2013 Feb;78(2):155-64 [23046013]
Eur J Cancer Prev. 2013 Mar;22(2):158-68 [22926510]
Cochrane Database Syst Rev. 2014;3:CD005195 [24683040]
Cancer Epidemiol Biomarkers Prev. 2014 Jun;23(6):1102-8 [24686895]
J Clin Endocrinol Metab. 2014 Jun;99(6):E1031-4 [24601693]
Am J Clin Nutr. 1999 Nov;70(5):896-903 [10539752]
Am J Epidemiol. 2000 Aug 1;152(3):279-86 [10933275]
Ann Epidemiol. 2002 Aug;12(6):395-401 [12160598]
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Cancer Causes Control. 2002 Oct;13(8):765-75 [12420956]
Eur J Cancer. 2003 Sep;39(13):1912-9 [12932671]
Public Health Nutr. 2004 Feb;7(1A):187-200 [14972060]
Am J Epidemiol. 1986 Jul;124(1):17-27 [3521261]
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Br J Cancer. 1993 Feb;67(2):330-40 [8431362]
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Public Health Nutr. 2008 Feb;11(2):183-95 [17610761]
Cancer Causes Control. 2008 Aug;19(6):585-93 [18240001]
Am J Clin Nutr. 2009 Jan;89(1):347-53 [19056579]
Cancer Causes Control. 2009 Feb;20(1):75-86 [18766448]
Cancer Epidemiol Biomarkers Prev. 2009 Mar;18(3):784-91 [19240234]
Epidemiology. 2010 May;21(3):389-95 [20335813]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1371/journal.pone.0110886
ER -
TY - JOUR
T1 - Cysteine transport through excitatory amino acid transporter 3 (EAAT3).
AN - 1586101928; 25275463
AB - Excitatory amino acid transporters (EAATs) limit glutamatergic signaling and maintain extracellular glutamate concentrations below neurotoxic levels. Of the five known EAAT isoforms (EAATs 1-5), only the neuronal isoform, EAAT3 (EAAC1), can efficiently transport the uncharged amino acid L-cysteine. EAAT3-mediated cysteine transport has been proposed to be a primary mechanism used by neurons to obtain cysteine for the synthesis of glutathione, a key molecule in preventing oxidative stress and neuronal toxicity. The molecular mechanisms underlying the selective transport of cysteine by EAAT3 have not been elucidated. Here we propose that the transport of cysteine through EAAT3 requires formation of the thiolate form of cysteine in the binding site. Using Xenopus oocytes and HEK293 cells expressing EAAT2 and EAAT3, we assessed the transport kinetics of different substrates and measured transporter-associated currents electrophysiologically. Our results show that L-selenocysteine, a cysteine analog that forms a negatively-charged selenolate ion at physiological pH, is efficiently transported by EAATs 1-3 and has a much higher apparent affinity for transport when compared to cysteine. Using a membrane tethered GFP variant to monitor intracellular pH changes associated with transport activity, we observed that transport of either L-glutamate or L-selenocysteine by EAAT3 decreased intracellular pH, whereas transport of cysteine resulted in cytoplasmic alkalinization. No change in pH was observed when cysteine was applied to cells expressing EAAT2, which displays negligible transport of cysteine. Under conditions that favor release of intracellular substrates through EAAT3 we observed release of labeled intracellular glutamate but did not detect cysteine release. Our results support a model whereby cysteine transport through EAAT3 is facilitated through cysteine de-protonation and that once inside, the thiolate is rapidly re-protonated. Moreover, these findings suggest that cysteine transport is predominantly unidirectional and that reverse transport does not contribute to depletion of intracellular cysteine pools.
JF - PloS one
AU - Watts, Spencer D
AU - Torres-Salazar, Delany
AU - Divito, Christopher B
AU - Amara, Susan G
AD - Center for Neuroscience, Department of Neurobiology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America. ; Laboratory of Cellular and Molecular Neurobiology, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland, United States of America. ; Center for Neuroscience, Department of Neurobiology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America; Laboratory of Cellular and Molecular Neurobiology, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland, United States of America.
Y1 - 2014
PY - 2014
DA - 2014
SP - 1
VL - 9
IS - 10
KW - Excitatory Amino Acid Transporter 2
KW - 0
KW - Excitatory Amino Acid Transporter 3
KW - Selenocysteine
KW - 0CH9049VIS
KW - Glutamic Acid
KW - 3KX376GY7L
KW - Cysteine
KW - K848JZ4886
KW - Index Medicus
KW - Excitatory Amino Acid Transporter 2 -- metabolism
KW - Animals
KW - Glutamic Acid -- metabolism
KW - Oocytes -- metabolism
KW - Selenocysteine -- metabolism
KW - Hydrogen-Ion Concentration
KW - Humans
KW - HEK293 Cells
KW - Xenopus
KW - Cysteine -- metabolism
KW - Excitatory Amino Acid Transporter 3 -- metabolism
KW - Cysteine -- analogs & derivatives
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1586101928?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Cysteine+transport+through+excitatory+amino+acid+transporter+3+%28EAAT3%29.&rft.au=Watts%2C+Spencer+D%3BTorres-Salazar%2C+Delany%3BDivito%2C+Christopher+B%3BAmara%2C+Susan+G&rft.aulast=Watts&rft.aufirst=Spencer&rft.date=2014-01-01&rft.volume=9&rft.issue=10&rft.spage=e109245&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0109245
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-12-22
N1 - Date created - 2014-10-03
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1371/journal.pone.0109245
ER -
TY - JOUR
T1 - Examination of the ligand-binding and enzymatic properties of a bilin-binding protein from the poisonous caterpillar Lonomia obliqua.
AN - 1542004600; 24972000
AB - The bilin-binding proteins (BBP) from lepidopteran insects are members of the lipocalin family of proteins and play a special role in pigmentation through the binding of biliverdin IXγ. Lopap, a BBP-like protein from the venom of the toxic caterpillar Lonomia obliqua has been reported to act as a serine protease that activates the coagulation proenzyme prothrombin. Here we show that BBPLo, a variant of lopap from the same organism binds biliverdin IXγ, forming a complex that is spectrally identical with previously described BBP proteins. Although BBPLo is nearly identical in sequence to lopap, no prothrombinase activity was detected in our recombinant preparations using reconstituted systems containing coagulation factors Xa and Va, as well as anionic phospholipids. In addition to biliverdin, BBPLo was found to form a 1:1 complex with heme prompting us to examine whether the unusual biliverdin IXγ ligand of BBPs forms as a result of oxidation of bound heme in situ rather than by a conventional heme oxygenase. Using ascorbate or a NADPH(+)-ferredoxin reductase-ferredoxin system as a source of reducing equivalents, spectral changes are seen that suggest an initial reduction of heme to the Fe(II) state and formation of an oxyferrous complex. The complex then disappears and a product identified as a 5-coordinate carbonyl complex of verdoheme, an intermediate in the biosynthesis of biliverdin, is formed. However, further reaction to form biliverdin was not observed, making it unlikely that biliverdin IXγ is formed by this pathway.
JF - PloS one
AU - Veiga, Ana B G
AU - Ribeiro, José M C
AU - Francischetti, Ivo M B
AU - Xu, Xueqing
AU - Guimarães, Jorge A
AU - Andersen, John F
AD - Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Disease, National Institutes of Health, Rockville, Maryland, United States of America; Center of Biotechnology, Universidade Federal do Rio Grande do Sul, Porto Alegre RS, Brazil. ; Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Disease, National Institutes of Health, Rockville, Maryland, United States of America. ; Center of Biotechnology, Universidade Federal do Rio Grande do Sul, Porto Alegre RS, Brazil.
Y1 - 2014
PY - 2014
DA - 2014
SP - 1
VL - 9
IS - 6
KW - Bile Pigments
KW - 0
KW - Insect Proteins
KW - Ligands
KW - Heme
KW - 42VZT0U6YR
KW - Ferredoxin-NADP Reductase
KW - EC 1.18.1.2
KW - Endopeptidases
KW - EC 3.4.-
KW - Index Medicus
KW - Oxidation-Reduction
KW - Animals
KW - Heme -- chemistry
KW - Molecular Sequence Data
KW - Heme -- pharmacology
KW - Ferredoxin-NADP Reductase -- chemistry
KW - Heme -- analogs & derivatives
KW - Amino Acid Sequence
KW - Substrate Specificity
KW - Protein Binding
KW - Lepidoptera -- enzymology
KW - Insect Proteins -- chemistry
KW - Bile Pigments -- pharmacology
KW - Endopeptidases -- metabolism
KW - Bile Pigments -- chemistry
KW - Endopeptidases -- chemistry
KW - Insect Proteins -- metabolism
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Examination+of+the+ligand-binding+and+enzymatic+properties+of+a+bilin-binding+protein+from+the+poisonous+caterpillar+Lonomia+obliqua.&rft.au=Veiga%2C+Ana+B+G%3BRibeiro%2C+Jos%C3%A9+M+C%3BFrancischetti%2C+Ivo+M+B%3BXu%2C+Xueqing%3BGuimar%C3%A3es%2C+Jorge+A%3BAndersen%2C+John+F&rft.aulast=Veiga&rft.aufirst=Ana+B&rft.date=2014-01-01&rft.volume=9&rft.issue=6&rft.spage=e95424&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0095424
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-10-26
N1 - Date created - 2014-06-28
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
Biochemistry. 1999 Dec 14;38(50):16678-85 [10600131]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1371/journal.pone.0095424
ER -
TY - JOUR
T1 - Profiling animal toxicants by automatically mining public bioassay data: a big data approach for computational toxicology.
AN - 1539713293; 24950175
AB - In vitro bioassays have been developed and are currently being evaluated as potential alternatives to traditional animal toxicity models. Already, the progress of high throughput screening techniques has resulted in an enormous amount of publicly available bioassay data having been generated for a large collection of compounds. When a compound is tested using a collection of various bioassays, all the testing results can be considered as providing a unique bio-profile for this compound, which records the responses induced when the compound interacts with different cellular systems or biological targets. Profiling compounds of environmental or pharmaceutical interest using useful toxicity bioassay data is a promising method to study complex animal toxicity. In this study, we developed an automatic virtual profiling tool to evaluate potential animal toxicants. First, we automatically acquired all PubChem bioassay data for a set of 4,841 compounds with publicly available rat acute toxicity results. Next, we developed a scoring system to evaluate the relevance between these extracted bioassays and animal acute toxicity. Finally, the top ranked bioassays were selected to profile the compounds of interest. The resulting response profiles proved to be useful to prioritize untested compounds for their animal toxicity potentials and form a potential in vitro toxicity testing panel. The protocol developed in this study could be combined with structure-activity approaches and used to explore additional publicly available bioassay datasets for modeling a broader range of animal toxicities.
JF - PloS one
AU - Zhang, Jun
AU - Hsieh, Jui-Hua
AU - Zhu, Hao
AD - Department of Chemistry, Rutgers University, Camden, New Jersey, United States of America; The Rutgers Center for Computational and Integrative Biology, Camden, New Jersey, United States of America. ; Biomolecular Screening Branch, Division of National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, United States of America.
Y1 - 2014
PY - 2014
DA - 2014
SP - 1
VL - 9
IS - 6
KW - Anti-Bacterial Agents
KW - 0
KW - Hazardous Substances
KW - Index Medicus
KW - Rats
KW - Animals
KW - Data Mining
KW - Humans
KW - Toxicity Tests
KW - Anti-Bacterial Agents -- toxicity
KW - Drug Evaluation, Preclinical
KW - Structure-Activity Relationship
KW - Computational Biology -- methods
KW - High-Throughput Screening Assays -- methods
KW - Toxicology -- methods
KW - Hazardous Substances -- toxicity
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1539713293?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Profiling+animal+toxicants+by+automatically+mining+public+bioassay+data%3A+a+big+data+approach+for+computational+toxicology.&rft.au=Zhang%2C+Jun%3BHsieh%2C+Jui-Hua%3BZhu%2C+Hao&rft.aulast=Zhang&rft.aufirst=Jun&rft.date=2014-01-01&rft.volume=9&rft.issue=6&rft.spage=e99863&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0099863
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-10-13
N1 - Date created - 2014-06-21
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
JAMA. 1993 Mar 24-31;269(12):1532-6 [8445816]
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Nucleic Acids Res. 2012 Jan;40(Database issue):D400-12 [22140110]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1371/journal.pone.0099863
ER -
TY - JOUR
T1 - Genome-wide binding of MBD2 reveals strong preference for highly methylated loci.
AN - 1536682141; 24927503
AB - MBD2 is a subunit of the NuRD complex that is postulated to mediate gene repression via recruitment of the complex to methylated DNA. In this study we adopted an MBD2 tagging-approach to study its genome wide binding characteristics. We show that in vivo MBD2 is mainly recruited to CpG island promoters that are highly methylated. Interestingly, MBD2 binds around 1 kb downstream of the transcription start site of a subset of ∼ 400 CpG island promoters that are characterized by the presence of active histone marks, RNA polymerase II (Pol2) and low to medium gene expression levels and H3K36me3 deposition. These tagged-MBD2 binding sites in MCF-7 show increased methylation in a cohort of primary breast cancers but not in normal breast samples, suggesting a putative role for MBD2 in breast cancer.
JF - PloS one
AU - Menafra, Roberta
AU - Brinkman, Arie B
AU - Matarese, Filomena
AU - Franci, Gianluigi
AU - Bartels, Stefanie J J
AU - Nguyen, Luan
AU - Shimbo, Takashi
AU - Wade, Paul A
AU - Hubner, Nina C
AU - Stunnenberg, Hendrik G
AD - Department of Molecular Biology, Nijmegen Centre for Molecular Life Sciences, Radboud University Nijmegen, Nijmegen, The Netherlands. ; Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, United States of America.
Y1 - 2014
PY - 2014
DA - 2014
SP - 1
VL - 9
IS - 6
KW - DNA-Binding Proteins
KW - 0
KW - MBD2 protein, human
KW - RNA Polymerase II
KW - EC 2.7.7.-
KW - Index Medicus
KW - Gene Expression Regulation, Neoplastic
KW - Promoter Regions, Genetic
KW - Humans
KW - CpG Islands
KW - Molecular Sequence Data
KW - MCF-7 Cells
KW - Sequence Analysis, RNA
KW - Female
KW - Binding Sites
KW - Breast Neoplasms -- genetics
KW - RNA Polymerase II -- metabolism
KW - DNA-Binding Proteins -- chemistry
KW - DNA Methylation
KW - Breast Neoplasms -- metabolism
KW - DNA-Binding Proteins -- metabolism
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1536682141?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Genome-wide+binding+of+MBD2+reveals+strong+preference+for+highly+methylated+loci.&rft.au=Menafra%2C+Roberta%3BBrinkman%2C+Arie+B%3BMatarese%2C+Filomena%3BFranci%2C+Gianluigi%3BBartels%2C+Stefanie+J+J%3BNguyen%2C+Luan%3BShimbo%2C+Takashi%3BWade%2C+Paul+A%3BHubner%2C+Nina+C%3BStunnenberg%2C+Hendrik+G&rft.aulast=Menafra&rft.aufirst=Roberta&rft.date=2014-01-01&rft.volume=9&rft.issue=6&rft.spage=e99603&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0099603
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-10-26
N1 - Date created - 2014-06-14
N1 - Date revised - 2017-01-14
N1 - Genetic sequence - GSE54693; GEO
N1 - SuppNotes - Cited By:
Carcinogenesis. 2000 Mar;21(3):461-7 [10688866]
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Mol Cell. 2005 Aug 5;19(3):381-91 [16061184]
Mol Cell Biol. 2006 Feb;26(3):843-51 [16428440]
Trends Biochem Sci. 2006 Feb;31(2):89-97 [16403636]
EMBO Rep. 2006 Jun;7(6):628-34 [16648823]
Science. 2007 Feb 23;315(5815):1141-3 [17322062]
Mol Cell Biol. 2007 May;27(10):3750-7 [17353271]
Mol Cell. 2008 Jun 20;30(6):755-66 [18514006]
Pathobiology. 2008;75(5):281-7 [18931530]
Nat Biotechnol. 2008 Dec;26(12):1367-72 [19029910]
Elife. 2014;3:e02407 [24843027]
Genome Res. 2014 Jun;24(6):896-905 [24714810]
Nat Biotechnol. 2009 Apr;27(4):361-8 [19329998]
BMC Genomics. 2010;11:137 [20181289]
J Cell Biol. 2010 May 17;189(4):739-54 [20479470]
PLoS One. 2010;5(8):e11982 [20700456]
Methods. 2011 Apr;53(4):453-9 [21184827]
Genes Dev. 2011 May 15;25(10):1010-22 [21576262]
Cancer Res. 2011 Sep 1;71(17):5859-70 [21724586]
EMBO J. 2011 Sep 14;30(18):3786-98 [21822215]
Methods Mol Biol. 2012;809:105-20 [22113271]
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Brief Funct Genomics. 2012 May;11(3):251-64 [22184333]
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Nucleic Acids Res. 2013 Jan 7;41(1):e28 [23066101]
Nucleic Acids Res. 2013 Mar 1;41(5):3010-21 [23361464]
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Genes Dev. 2000 Oct 1;14(19):2452-60 [11018013]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1371/journal.pone.0099603
ER -
TY - JOUR
T1 - Coordinated regulation of nuclear receptor CAR by CCRP/DNAJC7, HSP70 and the ubiquitin-proteasome system.
AN - 1521327612; 24789201
AB - The constitutive active/androstane receptor (CAR) plays an important role as a coordinate transcription factor in the regulation of various hepatic metabolic pathways for chemicals such as drugs, glucose, fatty acids, bilirubin, and bile acids. Currently, it is known that in its inactive state, CAR is retained in the cytoplasm in a protein complex with HSP90 and the tetratricopeptide repeat protein cytosoplasmic CAR retention protein (CCRP). Upon activation by phenobarbital (PB) or the PB-like inducer 1,4-bis[2-(3,5-dichloropyridyloxy)]-benzene (TCPOBOP), CAR translocates into the nucleus. We have identified two new components to the cytoplasmic regulation of CAR: ubiquitin-dependent degradation of CCRP and protein-protein interaction with HSP70. Treatment with the proteasome inhibitor MG132 (5 µM) causes CAR to accumulate in the cytoplasm of transfected HepG2 cells. In the presence of MG132, TCPOBOP increases CCRP ubiquitination in HepG2 cells co-expressing CAR, while CAR ubiquitination was not detected. MG132 treatment of HepG2 also attenuated of TCPOBOP-induced CAR transcriptional activation on reporter constructs which contain CAR-binding DNA elements derived from the human CYP2B6 gene. The elevation of cytoplasmic CAR protein with MG132 correlated with an increase of HSP70, and to a lesser extent HSP60. Both CCRP and CAR were found to interact with endogenous HSP70 in HepG2 cells by immunoprecipitation analysis. Induction of HSP70 levels by heat shock also increased cytoplasmic CAR levels, similar to the effect of MG132. Lastly, heat shock attenuated TCPOBOP-induced CAR transcriptional activation, also similar to the effect of MG132. Collectively, these data suggest that ubiquitin-proteasomal regulation of CCRP and HSP70 are important contributors to the regulation of cytoplasmic CAR levels, and hence the ability of CAR to respond to PB or PB-like inducers.
JF - PloS one
AU - Timsit, Yoav E
AU - Negishi, Masahiko
AD - The Pharmacogenetics Section, Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, United States of America.
Y1 - 2014
PY - 2014
DA - 2014
SP - 1
VL - 9
IS - 5
KW - Dnajc7 protein, mouse
KW - 0
KW - HSP70 Heat-Shock Proteins
KW - Leupeptins
KW - Ligands
KW - Proteasome Inhibitors
KW - Pyridines
KW - Receptors, Cytoplasmic and Nuclear
KW - Ubiquitin
KW - constitutive androstane receptor
KW - 1,4-bis(2-(3,5-dichloropyridyloxy))benzene
KW - 76150-91-9
KW - Proteasome Endopeptidase Complex
KW - EC 3.4.25.1
KW - benzyloxycarbonylleucyl-leucyl-leucine aldehyde
KW - RF1P63GW3K
KW - Phenobarbital
KW - YQE403BP4D
KW - Index Medicus
KW - Animals
KW - Proteasome Inhibitors -- pharmacology
KW - Dose-Response Relationship, Drug
KW - Humans
KW - Transcriptional Activation -- drug effects
KW - Mice
KW - Cytoplasm -- drug effects
KW - Leupeptins -- pharmacology
KW - Phenobarbital -- pharmacology
KW - Hep G2 Cells
KW - Ubiquitination -- drug effects
KW - Cytoplasm -- metabolism
KW - Heat-Shock Response -- drug effects
KW - Pyridines -- pharmacology
KW - HSP70 Heat-Shock Proteins -- metabolism
KW - Ubiquitin -- metabolism
KW - Proteasome Endopeptidase Complex -- metabolism
KW - Receptors, Cytoplasmic and Nuclear -- metabolism
KW - Receptors, Cytoplasmic and Nuclear -- genetics
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Coordinated+regulation+of+nuclear+receptor+CAR+by+CCRP%2FDNAJC7%2C+HSP70+and+the+ubiquitin-proteasome+system.&rft.au=Timsit%2C+Yoav+E%3BNegishi%2C+Masahiko&rft.aulast=Timsit&rft.aufirst=Yoav&rft.date=2014-01-01&rft.volume=9&rft.issue=5&rft.spage=e96092&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0096092
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-12-22
N1 - Date created - 2014-05-05
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1371/journal.pone.0096092
ER -
TY - JOUR
T1 - Effects of calorie restriction and diet-induced obesity on murine colon carcinogenesis, growth and inflammatory factors, and microRNA expression.
AN - 1516722074; 24732966
AB - Obesity is an established colon cancer risk factor, while preventing or reversing obesity via a calorie restriction (CR) diet regimen decreases colon cancer risk. Unfortunately, the biological mechanisms underlying these associations are poorly understood, hampering development of mechanism-based approaches for preventing obesity-related colon cancer. We tested the hypotheses that diet-induced obesity (DIO) would increase (and CR would decrease) colon tumorigenesis in the mouse azoxymethane (AOM) model. In addition, we established that changes in inflammatory cytokines, growth factors, and microRNAs are associated with these energy balance-colon cancer links, and thus represent mechanism-based targets for colon cancer prevention. Mice were injected with AOM once a week for 5 weeks and randomized to: 1) control diet; 2) 30% CR diet; or 3) DIO diet. Mice were euthanized at week 5 (n = 12/group), 10 (n = 12/group), and 20 (n = 20/group) after the last AOM injection. Colon tumors were counted, and cytokines, insulin-like growth factor 1 (IGF-1), IGF binding protein 3 (IGFBP-3), adipokines, proliferation, apoptosis, and expression of microRNAs (miRs) were measured. The DIO diet regimen induced an obese phenotype (∼36% body fat), while CR induced a lean phenotype (∼14% body fat); controls were intermediate (∼26% body fat). Relative to controls, DIO increased (and CR decreased) the number of colon tumors (p = 0.01), cytokines (p<0.001), IGF-1 (p = 0.01), and proliferation (p<0.001). DIO decreased (and CR increased) IGFBP-3 and apoptosis (p<0.001). miRs including mir-425, mir-196, mir-155, mir-150, mir-351, mir-16, let-7, mir34, and mir-138 were differentially expressed between the dietary groups. We conclude that the enhancing effects of DIO and suppressive effects of CR on colon carcinogenesis are associated with alterations in several biological pathways, including inflammation, IGF-1, and microRNAs.
JF - PloS one
AU - Olivo-Marston, Susan E
AU - Hursting, Stephen D
AU - Perkins, Susan N
AU - Schetter, Aaron
AU - Khan, Mohammed
AU - Croce, Carlo
AU - Harris, Curtis C
AU - Lavigne, Jackie
AD - Laboratory of Human Carcinogenesis, National Cancer Institute, Center for Cancer Research, National Institutes of Health, Bethesda, Maryland, United States of America; Division of Epidemioogy, The Ohio State University College of Public Health, Columbus, Ohio, United States of America. ; Department of Nutritional Sciences, University of Texas-Austin, Austin, Texas, United States of America; Department of Molecular Carcinogenesis, University of Texas-MD Anderson Cancer Center, Smithville, Texas, United States of America. ; Center for Cancer Training, The National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America. ; Laboratory of Human Carcinogenesis, National Cancer Institute, Center for Cancer Research, National Institutes of Health, Bethesda, Maryland, United States of America. ; Department of Molecular Virology, Immunology and Medical Genetics, The Ohio State University College of Medicine, Columbus, Ohio, United States of America. ; Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, Maryland, United States of America.
Y1 - 2014
PY - 2014
DA - 2014
SP - 1
VL - 9
IS - 4
KW - Adipokines
KW - 0
KW - Cytokines
KW - Insulin-Like Growth Factor Binding Protein 3
KW - MicroRNAs
KW - Insulin-Like Growth Factor I
KW - 67763-96-6
KW - Index Medicus
KW - Animals
KW - Glucose Tolerance Test
KW - Apoptosis
KW - Random Allocation
KW - Insulin-Like Growth Factor I -- metabolism
KW - Mice
KW - Body Composition
KW - Cytokines -- metabolism
KW - Cell Proliferation
KW - Body Weight
KW - Risk Factors
KW - Carcinogenesis
KW - Inflammation -- metabolism
KW - Adipokines -- metabolism
KW - Insulin-Like Growth Factor Binding Protein 3 -- metabolism
KW - Male
KW - Gene Expression Regulation, Neoplastic
KW - MicroRNAs -- metabolism
KW - Colonic Neoplasms -- complications
KW - Caloric Restriction
KW - Diet
KW - Colonic Neoplasms -- pathology
KW - Obesity -- complications
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Effects+of+calorie+restriction+and+diet-induced+obesity+on+murine+colon+carcinogenesis%2C+growth+and+inflammatory+factors%2C+and+microRNA+expression.&rft.au=Olivo-Marston%2C+Susan+E%3BHursting%2C+Stephen+D%3BPerkins%2C+Susan+N%3BSchetter%2C+Aaron%3BKhan%2C+Mohammed%3BCroce%2C+Carlo%3BHarris%2C+Curtis+C%3BLavigne%2C+Jackie&rft.aulast=Olivo-Marston&rft.aufirst=Susan&rft.date=2014-01-01&rft.volume=9&rft.issue=4&rft.spage=e94765&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0094765
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-01-19
N1 - Date created - 2014-04-15
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1371/journal.pone.0094765
ER -
TY - JOUR
T1 - Cytocidal activities of topoisomerase 1 inhibitors and 5-azacytidine against pheochromocytoma/paraganglioma cells in primary human tumor cultures and mouse cell lines.
AN - 1499137534; 24516563
AB - There is currently no effective treatment for metastatic pheochromocytomas and paragangliomas. A deficiency in current chemotherapy regimens is that the metastases usually grow very slowly. Drugs that target dividing tumor cells have therefore had limited success. To improve treatment, new strategies and valid experimental models are required for pre-clinical testing. However, development of models has itself been hampered by the absence of human pheochromocytoma/paraganglioma cell lines for cultures or xenografts. Topoisomerase 1 (TOP1) inhibitors are drugs that interfere with mechanisms that maintain DNA integrity during transcription in both quiescent and dividing cells. We used primary cultures of representative human tumors to establish the cytotoxicity of camptothecin, a prototypical TOP1 inhibitor, against non-dividing pheochromocytoma/paraganglioma cells, and then employed a mouse pheochromocytoma model (MPC) to show that efficacy of low concentrations of camptothecin and other TOP1 inhibitors is increased by intermittent coadministration of sub-toxic concentrations of 5-azacytidine, a DNA methylation inhibitor that modulates transcription. We then tested the same drugs against a clonal MPC derivative that expresses CMV reporter-driven luciferase and GFP, intended for in vivo drug testing. Unexpectedly, luciferase expression, bioluminescence and GFP expression were paradoxically increased by both camptothecin and SN38, the active metabolite of irinotecan, thereby masking cell death. Expression of chromogranin A, a marker for neuroendocrine secretory granules, was not increased, indicating that the drug effects on levels of luciferase and GFP are specific to the GFP-luciferase construct rather than generalized cellular responses. Our findings provide proof of principle for use of TOP1 inhibitors against pheochromocytoma/paraganglioma and suggest novel strategies for enhancing efficacy and reducing toxicity by optimizing the combination and timing of their use in conjunction with other drugs. The paradoxical effects of TOP1 inhibitors on luciferase and GFP dictate a need for caution in the use of CMV promoter-regulated constructs for cancer-related imaging studies.
JF - PloS one
AU - Powers, James F
AU - Korgaonkar, Parimal G
AU - Fliedner, Stephanie
AU - Giubellino, Alessio
AU - Pacak, Karel
AU - Sahagian, G Gary
AU - Tischler, Arthur S
AD - Department of Pathology, Tufts Medical Center, Boston, Massachusetts, United States of America. ; Small Animal Imaging/Preclinical Testing Facility, Tufts University School of Medicine, Boston, Massachusetts, United States of America. ; Program in Reproductive and Adult Endocrinology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, United States of America ; 1st Department of Medicine, University Medical Center Schleswig-Holstein Lübeck, Lübeck, Germany. ; Program in Reproductive and Adult Endocrinology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, United States of America.
Y1 - 2014
PY - 2014
DA - 2014
SP - 1
VL - 9
IS - 2
KW - Topoisomerase I Inhibitors
KW - 0
KW - Azacitidine
KW - M801H13NRU
KW - Index Medicus
KW - Animals
KW - Humans
KW - Mice
KW - Cell Line, Tumor
KW - Topoisomerase I Inhibitors -- pharmacology
KW - Azacitidine -- therapeutic use
KW - Azacitidine -- pharmacology
KW - Paraganglioma -- pathology
KW - Topoisomerase I Inhibitors -- therapeutic use
KW - Paraganglioma -- drug therapy
KW - Pheochromocytoma -- drug therapy
KW - Adrenal Gland Neoplasms -- pathology
KW - Pheochromocytoma -- pathology
KW - Cell Death -- drug effects
KW - Adrenal Gland Neoplasms -- drug therapy
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Cytocidal+activities+of+topoisomerase+1+inhibitors+and+5-azacytidine+against+pheochromocytoma%2Fparaganglioma+cells+in+primary+human+tumor+cultures+and+mouse+cell+lines.&rft.au=Powers%2C+James+F%3BKorgaonkar%2C+Parimal+G%3BFliedner%2C+Stephanie%3BGiubellino%2C+Alessio%3BPacak%2C+Karel%3BSahagian%2C+G+Gary%3BTischler%2C+Arthur+S&rft.aulast=Powers&rft.aufirst=James&rft.date=2014-01-01&rft.volume=9&rft.issue=2&rft.spage=e87807&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0087807
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2015-05-22
N1 - Date created - 2014-02-11
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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Erratum In:
PLoS One. 2014;9(3):e92492
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1371/journal.pone.0087807
ER -
TY - JOUR
T1 - Overview of Exocrine Pancreatic Pathobiology
AN - 1496897455; 19022983
AB - Exocrine pancreas is a source of several enzymes that are essential for the digestive process. The exocrine pancreatic secretion is tightly regulated by the neuroendocrine system. The endocrine pancreas is tightly integrated anatomically and physiologically with the exocrine pancreas and modulates its function. Compound-induced pancreatitis is not a common event in toxicology or drug development, but it becomes a significant liability when encountered. Understanding the species-specific differences in physiology is essential to understand the underlying pathobiology of pancreatic disease in animal models and its relevance to human disease. This review will mainly focus on understanding the morphology and physiology of the pancreas, unique islet-exocrine interactions, and pancreatitis.
JF - Toxicologic Pathology
AU - Pandiri, Arun R
AD - Experimental Pathology Laboratories, Inc., Research Triangle Park, North Carolina, USA, pandiriak@niehs.nih.govapandiri@epl-inc.com
Y1 - 2014/01//
PY - 2014
DA - January 2014
SP - 207
EP - 216
PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom
VL - 42
IS - 1
SN - 0192-6233, 0192-6233
KW - Toxicology Abstracts
KW - animal models
KW - digestive system
KW - endocrine system.
KW - Pancreatic diseases
KW - Pancreas
KW - Reviews
KW - Secretion
KW - Animal models
KW - Enzymes
KW - Drug development
KW - Neuroendocrine system
KW - Pancreatitis
KW - X 24300:Methods
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1496897455?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+Pathology&rft.atitle=Overview+of+Exocrine+Pancreatic+Pathobiology&rft.au=Pandiri%2C+Arun+R&rft.aulast=Pandiri&rft.aufirst=Arun&rft.date=2014-01-01&rft.volume=42&rft.issue=1&rft.spage=207&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F0192623313509907
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-02-01
N1 - Number of references - 96
N1 - Last updated - 2016-02-04
N1 - SubjectsTermNotLitGenreText - Pancreatic diseases; Secretion; Reviews; Pancreas; Animal models; Enzymes; Drug development; Neuroendocrine system; Pancreatitis
DO - http://dx.doi.org/10.1177/0192623313509907
ER -
TY - JOUR
T1 - Overview of the Pancreatic Toxicity and Carcinogenesis Session
AN - 1496880899; 19022962
AB - The theme of the Society of Toxicologic Pathology Annual Symposium 2013 was "Toxicologic Pathology of the Digestive Tract and Pancreas." The last session focused on pancreatic toxicity and carcinogenesis. This overview highlights the various presentations in this session, focusing on pancreatic Toxicologic Pathology, responses of the pancreas to xenobiotics, and current understanding on pancreatic carcinogenesis. The objective of this symposium overview and the subsequent articles from this session is to enable the audience to develop a better appreciation for the pancreas as a target organ in toxicological studies.
JF - Toxicologic Pathology
AU - Pandiri, Arun R
AU - Schultze, AEric
AD - Experimental Pathology Laboratories, Inc., Research Triangle Park, North Carolina, USA, pandiriak@niehs.nih.govapandiri@epl-inc.com
Y1 - 2014/01//
PY - 2014
DA - January 2014
SP - 204
EP - 206
PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom
VL - 42
IS - 1
SN - 0192-6233, 0192-6233
KW - Toxicology Abstracts
KW - exocrine pancreas
KW - islet-acinar axis
KW - pancreatitis
KW - cholecystokinin
KW - CCK agonist
KW - pancreatic cancer.
KW - Digestive tract
KW - Pancreas
KW - Reviews
KW - Carcinogenesis
KW - Toxicity
KW - Xenobiotics
KW - Toxicity testing
KW - X 24300:Methods
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1496880899?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+Pathology&rft.atitle=Overview+of+the+Pancreatic+Toxicity+and+Carcinogenesis+Session&rft.au=Pandiri%2C+Arun+R%3BSchultze%2C+AEric&rft.aulast=Pandiri&rft.aufirst=Arun&rft.date=2014-01-01&rft.volume=42&rft.issue=1&rft.spage=204&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F0192623313505931
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date revised - 2014-02-01
N1 - Number of references - 17
N1 - Last updated - 2016-02-04
N1 - SubjectsTermNotLitGenreText - Digestive tract; Reviews; Pancreas; Carcinogenesis; Xenobiotics; Toxicity; Toxicity testing
DO - http://dx.doi.org/10.1177/0192623313505931
ER -
TY - JOUR
T1 - Histone deacetylase inhibitors selectively target homology dependent DNA repair defective cells and elevate non-homologous endjoining activity.
AN - 1492707586; 24466340
AB - We have previously used the ATAD5-luciferase high-throughput screening assay to identify genotoxic compounds with potential chemotherapeutic capabilities. The successful identification of known genotoxic agents, including the histone deacetylase inhibitor (HDACi) trichostatin A (TSA), confirmed the specificity of the screen since TSA has been widely studied for its ability to cause apoptosis in cancer cells. Because many cancers have acquired mutations in DNA damage checkpoints or repair pathways, we hypothesized that these cancers may be susceptible to treatments that target compensatory pathways. Here, we used a panel of isogenic chicken DT40 B lymphocyte mutant and human cell lines to investigate the ability of TSA to define selective pathways that promote HDACi toxicity.
HDACi induced a DNA damage response and reduced viability in all repair deficient DT40 mutants although ATM-nulls were least affected. The most dramatic sensitivity was observed in mutants lacking the homology dependent repair (HDR) factor BLM or the non-homologous end-joining (NHEJ) and HDR factors, KU/RAD54, suggesting an involvement of either HDR or NHEJ in HDACi-induced cell death. To extend these findings, we measured the frequencies of HDR and NHEJ after HDACi treatment and monitored viability in human cell lines comparably deficient in HDR or NHEJ. Although no difference in HDR frequency was observed between HDACi treated and untreated cells, HDR-defective human cell lines were clearly more sensitive than wild type. Unexpectedly, cells treated with HDACis showed a significantly elevated NHEJ frequency. HDACi targeting drugs induced significant increases in NHEJ activity in human cell lines but did not alter HDR frequency. Moreover, HDR is required for cellular resistance to HDACi therapy; therefore, NHEJ does not appear to be a critical axis for HDACi resistance. Rather, HDACi compounds induced DNA damage, most likely double strand breaks (DSBs), and HDR proficiency is correlated with cell survival.
JF - PloS one
AU - Smith, Stephanie
AU - Fox, Jennifer
AU - Mejia, Marco
AU - Ruangpradit, Wanvipa
AU - Saberi, Alihossein
AU - Kim, Sunmi
AU - Choi, Yongjun
AU - Oh, Sehyun
AU - Wang, Yucai
AU - Choi, Kyungho
AU - Li, Lei
AU - Hendrickson, Eric A
AU - Takeda, Shunichi
AU - Muller, Mark
AU - Myung, Kyungjae
AD - Genome Instability Section, Genetics and Molecular Biology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland, United States of America. ; Department of Molecular Biology and Microbiology, College of Medicine, University of Central Florida, Orlando, Florida, United States of America. ; Department of Radiation Genetics Kyoto University, Medical School, Kyoto, 606-8501 Japan. ; Genome Instability Section, Genetics and Molecular Biology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland, United States of America ; Department of Radiation Genetics Kyoto University, Medical School, Kyoto, 606-8501 Japan ; Department of Environmental Health School of Public Hearth, Seoul National University, Seoul, Korea. ; Department of Biochemistry, Molecular Biology and Biophysics, University of Minnesota Medical School, Minneapolis, Minnesota, United States of America. ; Department of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America ; The University of Texas Graduate School of Biomedical Sciences at Houston, Houston Texas, United States of America. ; Department of Environmental Health School of Public Hearth, Seoul National University, Seoul, Korea. ; Department of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America ; Department of Genetics, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America.
Y1 - 2014
PY - 2014
DA - 2014
SP - 1
VL - 9
IS - 1
KW - Antigens, Nuclear
KW - 0
KW - DNA-Binding Proteins
KW - Histone Deacetylase Inhibitors
KW - Hydroxamic Acids
KW - RNA, Small Interfering
KW - trichostatin A
KW - 3X2S926L3Z
KW - vorinostat
KW - 58IFB293JI
KW - Luciferases
KW - EC 1.13.12.-
KW - RAD51 protein, human
KW - EC 2.7.7.-
KW - Rad51 Recombinase
KW - Bloom syndrome protein
KW - EC 3.6.1.-
KW - RecQ Helicases
KW - EC 3.6.4.12
KW - Xrcc6 protein, human
KW - Ku Autoantigen
KW - EC 4.2.99.-
KW - Index Medicus
KW - Rad51 Recombinase -- antagonists & inhibitors
KW - Animals
KW - Humans
KW - RecQ Helicases -- metabolism
KW - Luciferases -- metabolism
KW - DNA-Binding Proteins -- genetics
KW - RNA, Small Interfering -- genetics
KW - Antigens, Nuclear -- genetics
KW - DNA Damage -- genetics
KW - DNA Damage -- drug effects
KW - Rad51 Recombinase -- metabolism
KW - Blotting, Western
KW - Chickens
KW - Antigens, Nuclear -- metabolism
KW - Cell Survival -- drug effects
KW - Cells, Cultured
KW - Electrophoresis, Gel, Pulsed-Field
KW - RecQ Helicases -- genetics
KW - DNA-Binding Proteins -- antagonists & inhibitors
KW - Rad51 Recombinase -- genetics
KW - Hydroxamic Acids -- pharmacology
KW - Fluorescent Antibody Technique
KW - DNA-Binding Proteins -- metabolism
KW - DNA Repair -- genetics
KW - Neoplasms -- drug therapy
KW - B-Lymphocytes -- drug effects
KW - Neoplasms -- pathology
KW - Histone Deacetylase Inhibitors -- pharmacology
KW - B-Lymphocytes -- cytology
KW - Mutation -- genetics
KW - DNA End-Joining Repair -- genetics
KW - B-Lymphocytes -- metabolism
KW - Neoplasms -- genetics
KW - DNA Repair -- drug effects
KW - DNA End-Joining Repair -- drug effects
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492707586?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Histone+deacetylase+inhibitors+selectively+target+homology+dependent+DNA+repair+defective+cells+and+elevate+non-homologous+endjoining+activity.&rft.au=Smith%2C+Stephanie%3BFox%2C+Jennifer%3BMejia%2C+Marco%3BRuangpradit%2C+Wanvipa%3BSaberi%2C+Alihossein%3BKim%2C+Sunmi%3BChoi%2C+Yongjun%3BOh%2C+Sehyun%3BWang%2C+Yucai%3BChoi%2C+Kyungho%3BLi%2C+Lei%3BHendrickson%2C+Eric+A%3BTakeda%2C+Shunichi%3BMuller%2C+Mark%3BMyung%2C+Kyungjae&rft.aulast=Smith&rft.aufirst=Stephanie&rft.date=2014-01-01&rft.volume=9&rft.issue=1&rft.spage=e87203&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0087203
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-09-29
N1 - Date created - 2014-01-27
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1371/journal.pone.0087203
ER -
TY - JOUR
T1 - Bisphenol A exposure alters developmental gene expression in the fetal rhesus macaque uterus.
AN - 1492705012; 24465770
AB - Bisphenol A (BPA) exposure results in numerous developmental and functional abnormalities in reproductive organs in rodent models, but limited data are available regarding BPA effects in the primate uterus. To determine if maternal oral BPA exposure affects fetal uterine development in a non-human primate model, pregnant rhesus macaques carrying female fetuses were exposed orally to 400 µg/kg BPA or vehicle control daily from gestation day (GD) 50-100 or GD100-165. Fetal uteri were collected at the completion of treatment (GD100 or GD165); tissue histology, cell proliferation, and expression of estrogen receptor alpha (ERα) and progesterone receptor (PR) were compared to that of controls. Gene expression analysis was conducted using rhesus macaque microarrays. There were no significant differences in histology or in the percentage of cells expressing the proliferation marker Ki-67, ERα, or PR in BPA-exposed uteri compared to controls at GD100 or GD165. Minimal differences in gene expression were observed between BPA-exposed and control GD100 uteri. However, at GD165, BPA-exposed uteri had significant differences in gene expression compared to controls. Several of the altered genes, including HOXA13, WNT4, and WNT5A, are critical for reproductive organ development and/or adult function. We conclude that second or third trimester BPA exposure does not significantly affect fetal uterus development based on morphological, proliferation, and steroid hormone receptor assessments. However, differences in expression of key developmental genes after third trimester exposure suggest that BPA could alter transcriptional signals influencing uterine function later in life.
JF - PloS one
AU - Calhoun, Kathryn C
AU - Padilla-Banks, Elizabeth
AU - Jefferson, Wendy N
AU - Liu, Liwen
AU - Gerrish, Kevin E
AU - Young, Steven L
AU - Wood, Charles E
AU - Hunt, Patricia A
AU - Vandevoort, Catherine A
AU - Williams, Carmen J
AD - Reproductive Medicine Group, Laboratory of Reproductive & Developmental Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, United States of America ; Department of Obstetrics and Gynecology, Division of Reproductive Endocrinology and Infertility, University of North Carolina-Chapel Hill, Chapel Hill, North Carolina, United States of America. ; Reproductive Medicine Group, Laboratory of Reproductive & Developmental Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, United States of America. ; Microarray Group, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, United States of America. ; Department of Obstetrics and Gynecology, Division of Reproductive Endocrinology and Infertility, University of North Carolina-Chapel Hill, Chapel Hill, North Carolina, United States of America. ; National Health and Environmental Effects Research Laboratory, Office of Research and Development, US Environmental Protection Agency, Research Triangle Park, North Carolina, United States of America. ; School of Molecular Biosciences, Washington State University, Pullman, Washington, United States of America. ; Department of Obstetrics and Gynecology and California National Primate Research Center, University of California Davis, Davis, California, United States of America.
Y1 - 2014
PY - 2014
DA - 2014
SP - 1
VL - 9
IS - 1
KW - Benzhydryl Compounds
KW - 0
KW - Endocrine Disruptors
KW - Estrogen Receptor alpha
KW - Phenols
KW - Receptors, Progesterone
KW - beta Catenin
KW - bisphenol A
KW - MLT3645I99
KW - Index Medicus
KW - Animals
KW - Oligonucleotide Array Sequence Analysis
KW - Gene Regulatory Networks
KW - Fetal Development -- drug effects
KW - Estrogen Receptor alpha -- metabolism
KW - Maternal Exposure
KW - Pregnancy
KW - Receptors, Progesterone -- genetics
KW - Maternal-Fetal Exchange
KW - Receptors, Progesterone -- metabolism
KW - Estrogen Receptor alpha -- genetics
KW - beta Catenin -- metabolism
KW - Environmental Exposure
KW - Macaca mulatta
KW - Female
KW - Transcriptome -- drug effects
KW - Uterus -- metabolism
KW - Endocrine Disruptors -- toxicity
KW - Benzhydryl Compounds -- toxicity
KW - Phenols -- toxicity
KW - Uterus -- pathology
KW - Uterus -- embryology
KW - Uterus -- drug effects
KW - Gene Expression Regulation, Developmental -- drug effects
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492705012?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Bisphenol+A+exposure+alters+developmental+gene+expression+in+the+fetal+rhesus+macaque+uterus.&rft.au=Calhoun%2C+Kathryn+C%3BPadilla-Banks%2C+Elizabeth%3BJefferson%2C+Wendy+N%3BLiu%2C+Liwen%3BGerrish%2C+Kevin+E%3BYoung%2C+Steven+L%3BWood%2C+Charles+E%3BHunt%2C+Patricia+A%3BVandevoort%2C+Catherine+A%3BWilliams%2C+Carmen+J&rft.aulast=Calhoun&rft.aufirst=Kathryn&rft.date=2014-01-01&rft.volume=9&rft.issue=1&rft.spage=e85894&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0085894
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-11-11
N1 - Date created - 2014-01-27
N1 - Date revised - 2017-01-14
N1 - SuppNotes - Cited By:
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1371/journal.pone.0085894
ER -
TY - JOUR
T1 - Genetic polymorphisms in NQO1 and SOD2: interactions with smoking, schistosoma infection, and bladder cancer risk in Egypt.
AN - 1490762841; 24035474
AB - Bladder cancer is the most prevalent form of cancer in men among Egyptians, for whom tobacco smoke exposure and Schistosoma haematobium (SH) infection are the major risk factors. We hypothesized that functional polymorphisms in
quinone oxidoreductase 1 (NQO1) and superoxide dismutase 2 (SOD2), modulators of the effects of reactive oxidative species, can influence an individual's susceptibility to these carcinogenic exposures and hence the risk of bladder cancer. We assessed the effects of potential interactions between functional polymorphisms in the NQO1 and SOD2 genes and exposure to smoking and SH infection on bladder cancer risk among 902 cases and 804 population-based controls in Egypt. We used unconditional logistic regression to estimate the odds ratios (OR) and confidence intervals (CI) 95%.
Water pipe and cigarette smoking were more strongly associated with cancer risk among individuals with the TT genotype for SOD2 (OR [CI 95%] = 4.41 [1.86-10.42]) as compared with those with the CC genotype (OR [CI 95%] = 2.26 [0.97-6.74]). Conversely, the risk associated with SH infection was higher among the latter (OR [CI 95%] = 3.59 [2.21-5.84]) than among the former (OR [CI 95%] = 1.86 [1.33-2.60]). Polymorphisms in NQO1 genotype showed a similar pattern, but to a much lesser extent. The highest odds for having bladder cancer following SH infection were observed among individuals with the CC genotypes for both NQO1 and SOD2 (OR [CI 95%] = 4.41 [2.32-8.38]). Our findings suggest that genetic polymorphisms in NQO1 and SOD2 play important roles in the etiology of bladder cancer by modulating the effects of known contributing factors such as smoking and SH infection.
Copyright © 2014 Elsevier Inc. All rights reserved.
JF - Urologic oncology
AU - Goerlitz, David
AU - Amr, Sania
AU - Dash, Chiranjeev
AU - Saleh, Doa'a A
AU - El Daly, Mai
AU - Abdel-Hamid, Mohamed
AU - El Kafrawy, Sherif
AU - Hifnawy, Tamer
AU - Ezzat, Sameera
AU - Abdel-Aziz, Mohamed A
AU - Khaled, Hussein
AU - Zheng, Yun-Ling
AU - Mikhail, Nabiel
AU - Loffredo, Christopher A
AD - Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC. ; Department of Epidemiology and Public Health, University of Maryland School of Medicine, Baltimore, MD. ; Department of Public Health, Cairo University, Cairo, Egypt. ; Department of Microbiology, National Hepatology and Tropical Medicine Research Institute, Cairo, Egypt; National Liver Institute, Menoufiya University, Shibin El Kom, Egypt. ; Department of Microbiology, National Hepatology and Tropical Medicine Research Institute, Cairo, Egypt; Department of Microbiology, Minia University, Minia, Egypt. ; Department of Microbiology, National Hepatology and Tropical Medicine Research Institute, Cairo, Egypt; National Liver Institute, Menoufiya University, Shibin El Kom, Egypt; King Fahd Medical Research Center, King Abdulaziz University, Jeddah, Saudi Arabia. ; Public Health Department, Beni Suif University, Beni Suif, Egypt. ; National Liver Institute, Menoufiya University, Shibin El Kom, Egypt. ; Department of Urology, Assiut University, Assiut, Egypt. ; Department of Medical Oncology, National Cancer Institute, Cairo, Egypt. ; Department of Microbiology, National Hepatology and Tropical Medicine Research Institute, Cairo, Egypt; Department of Urology, Assiut University, Assiut, Egypt. ; Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC. Electronic address: cal9@georgetown.edu.
Y1 - 2014/01//
PY - 2014
DA - January 2014
SP - 47.e15
EP - 20
VL - 32
IS - 1
KW - Superoxide Dismutase
KW - EC 1.15.1.1
KW - superoxide dismutase 2
KW - NAD(P)H Dehydrogenase (Quinone)
KW - EC 1.6.5.2
KW - NQO1 protein, human
KW - Index Medicus
KW - Bladder cancer
KW - Smoking
KW - Epidemiology
KW - Schistosomiasis
KW - NQO1
KW - SOD2
KW - Animals
KW - Odds Ratio
KW - Gene Frequency
KW - Humans
KW - Smoking -- adverse effects
KW - Aged
KW - Egypt
KW - Genotype
KW - Logistic Models
KW - Risk Factors
KW - Host-Parasite Interactions
KW - Middle Aged
KW - Schistosomiasis haematobia -- parasitology
KW - Female
KW - Male
KW - Schistosoma haematobium -- physiology
KW - NAD(P)H Dehydrogenase (Quinone) -- genetics
KW - Polymorphism, Single Nucleotide
KW - Urinary Bladder Neoplasms -- etiology
KW - Genetic Predisposition to Disease -- genetics
KW - Urinary Bladder Neoplasms -- genetics
KW - Superoxide Dismutase -- genetics
KW - Urinary Bladder Neoplasms -- parasitology
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L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Urologic+oncology&rft.atitle=Genetic+polymorphisms+in+NQO1+and+SOD2%3A+interactions+with+smoking%2C+schistosoma+infection%2C+and+bladder+cancer+risk+in+Egypt.&rft.au=Goerlitz%2C+David%3BAmr%2C+Sania%3BDash%2C+Chiranjeev%3BSaleh%2C+Doa%27a+A%3BEl+Daly%2C+Mai%3BAbdel-Hamid%2C+Mohamed%3BEl+Kafrawy%2C+Sherif%3BHifnawy%2C+Tamer%3BEzzat%2C+Sameera%3BAbdel-Aziz%2C+Mohamed+A%3BKhaled%2C+Hussein%3BZheng%2C+Yun-Ling%3BMikhail%2C+Nabiel%3BLoffredo%2C+Christopher+A&rft.aulast=Goerlitz&rft.aufirst=David&rft.date=2014-01-01&rft.volume=32&rft.issue=1&rft.spage=47.e15&rft.isbn=&rft.btitle=&rft.title=Urologic+oncology&rft.issn=1873-2496&rft_id=info:doi/10.1016%2Fj.urolonc.2013.06.016
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-09-26
N1 - Date created - 2013-12-23
N1 - Date revised - 2017-01-13
N1 - SuppNotes - Cited By:
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Jpn J Cancer Res. 2002 Jul;93(7):736-43 [12149138]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.urolonc.2013.06.016
ER -
TY - JOUR
T1 - Cytotoxicity of synthetic cannabinoids on primary neuronal cells of the forebrain: the involvement of cannabinoid CB1 receptors and apoptotic cell death.
AN - 1490743906; 24211273
AB - The abuse of herbal products containing synthetic cannabinoids has become an issue of public concern. The purpose of this paper was to evaluate the acute cytotoxicity of synthetic cannabinoids on mouse brain neuronal cells. Cytotoxicity induced by synthetic cannabinoid (CP-55,940, CP-47,497, CP-47,497-C8, HU-210, JWH-018, JWH-210, AM-2201, and MAM-2201) was examined using forebrain neuronal cultures. These synthetic cannabinoids induced cytotoxicity in the forebrain cultures in a concentration-dependent manner. The cytotoxicity was suppressed by preincubation with the selective CB1 receptor antagonist AM251, but not with the selective CB2 receptor antagonist AM630. Furthermore, annexin-V-positive cells were found among the treated forebrain cells. Synthetic cannabinoid treatment induced the activation of caspase-3, and preincubation with a caspase-3 inhibitor significantly suppressed the cytotoxicity. These synthetic cannabinoids induced apoptosis through a caspase-3-dependent mechanism in the forebrain cultures. Our results indicate that the cytotoxicity of synthetic cannabinoids towards primary neuronal cells is mediated by the CB1 receptor, but not by the CB2 receptor, and further suggest that caspase cascades may play an important role in the apoptosis induced by these synthetic cannabinoids. In conclusion, excessive synthetic cannabinoid abuse may present a serious acute health concern due to neuronal damage or deficits in the brain. Copyright © 2013 Elsevier Inc. All rights reserved.
JF - Toxicology and applied pharmacology
AU - Tomiyama, Ken-ichi
AU - Funada, Masahiko
AD - Department of Drug Dependence Research, National Institute of Mental Health, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan. ; Department of Drug Dependence Research, National Institute of Mental Health, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan. Electronic address: mfunada@ncnp.go.jp.
Y1 - 2014/01/01/
PY - 2014
DA - 2014 Jan 01
SP - 17
EP - 23
VL - 274
IS - 1
KW - Cannabinoids
KW - 0
KW - Cytotoxins
KW - Receptor, Cannabinoid, CB1
KW - Index Medicus
KW - Apoptosis
KW - ∆(9)-tetrahydrocannabinol
KW - Δ(9)-THC
KW - Z-DEVD-FMK
KW - CB
KW - phosphate-buffered saline
KW - Designer drug
KW - PBS
KW - Cannabinoid receptor
KW - Z-Asp(OMe)-Glu(OMe)-Val-Asp(OMe)-fluoromethylketone
KW - cannabinoid
KW - DMEM
KW - DMSO
KW - fetal bovine serum
KW - Dulbecco's modified Eagle's medium
KW - FBS
KW - room temperature
KW - MAP-2
KW - RT
KW - Cytotoxicity
KW - microtubule-associated protein-2
KW - Primary neuronal cells
KW - dimethyl sulfoxide
KW - Synthetic cannabinoid
KW - Animals
KW - Mice, Inbred ICR
KW - Dose-Response Relationship, Drug
KW - Cells, Cultured
KW - Mice
KW - Female
KW - Pregnancy
KW - Neurons -- metabolism
KW - Prosencephalon -- metabolism
KW - Cytotoxins -- toxicity
KW - Cannabinoids -- toxicity
KW - Neurons -- drug effects
KW - Apoptosis -- physiology
KW - Apoptosis -- drug effects
KW - Prosencephalon -- drug effects
KW - Receptor, Cannabinoid, CB1 -- biosynthesis
KW - Cannabinoids -- chemical synthesis
KW - Cytotoxins -- chemical synthesis
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-02-24
N1 - Date created - 2013-12-20
N1 - Date revised - 2017-01-13
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.taap.2013.10.028
ER -
TY - JOUR
T1 - Phase II trial of bevacizumab and satraplatin in docetaxel-pretreated metastatic castrate-resistant prostate cancer.
AN - 1490735993; 23433892
AB - Satraplatin is an oral platinum compound that has demonstrated efficacy and tolerability in prostate cancer. Preclinical synergy between bevacizumab and platinum has been noted.
Docetaxel-pretreated metastatic castrate-resistant prostate cancer patients with disease progression were eligible. Satraplatin 80 mg/m(2) orally on days 1 to 5, prednisone 5mg twice daily, and bevacizumab 10mg/kg on day 1, and 15 mg/kg on day 15 were administered in 35-day cycles. Thirty one patients were enrolled. Grade 3 or 4 toxicities were pulmonary embolism in 2 patients and thrombocytopenia in 1 patient. 31% of the patients had a ≥ 30% decline in prostate-specific antigen. Median time to progression was 7.0 months (90% confidence interval [CI] 4.7-8.5mo) and median overall survival was 11.2 months (90% CI 9.1-16.4 mo). Polymorphism in the excision repair cross-complementation-1 (ERCC-1) gene was associated with time to progression (hazard ratio = 1.91). A circulating tumor cell count ≥ 5 was moderately prognostic of overall survival (hazard ratio = 1.49) as compared with CTC <5.
The combination was tolerable, and revealed promising efficacy in metastatic castrate-resistant prostate cancer. ERCC1 genotype maybe predictive of clinical benefit with platinum-based therapy in metastatic prostate cancer. Copyright © 2014 Elsevier Inc. All rights reserved.
JF - Urologic oncology
AU - Vaishampayan, Ulka N
AU - Fontana, Joseph
AU - Heilbrun, Lance K
AU - Smith, Daryn
AU - Heath, Elisabeth
AU - Dickow, Brenda
AU - Figg, William D
AD - Department of Oncology, Department of Medicine, Barbara Ann Karmanos Cancer Institute, Wayne State University, Detroit, MI. Electronic address: vaishamu@karmanos.org. ; Department of Oncology, Department of Medicine, Barbara Ann Karmanos Cancer Institute, Wayne State University, Detroit, MI. ; Biostatistics Core, Barbara Ann Karmanos Cancer Institute, Detroit, MI. ; Clinical Trials Office, Barbara Ann Karmanos Cancer Institute, Detroit, MI. ; Medical Oncology Branch, National Cancer Institute, Bethesda, MD.
Y1 - 2014/01//
PY - 2014
DA - January 2014
SP - 31.e25
EP - 33
VL - 32
IS - 1
KW - Antibodies, Monoclonal, Humanized
KW - 0
KW - DNA-Binding Proteins
KW - Organoplatinum Compounds
KW - Bevacizumab
KW - 2S9ZZM9Q9V
KW - satraplatin
KW - 8D7B37T28G
KW - ERCC1 protein, human
KW - EC 3.1.-
KW - Endonucleases
KW - Prostate-Specific Antigen
KW - EC 3.4.21.77
KW - Index Medicus
KW - Prostate cancer
KW - Excision repair polymorphism
KW - Phase II clinical trial
KW - Chemotherapy
KW - Humans
KW - DNA-Binding Proteins -- genetics
KW - Disease Progression
KW - Aged
KW - Endonucleases -- genetics
KW - Genotype
KW - Aged, 80 and over
KW - Prostate-Specific Antigen -- blood
KW - Treatment Outcome
KW - Neoplasm Metastasis
KW - Middle Aged
KW - Male
KW - Neoplastic Cells, Circulating
KW - Proportional Hazards Models
KW - Organoplatinum Compounds -- administration & dosage
KW - Antibodies, Monoclonal, Humanized -- administration & dosage
KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use
KW - Prostatic Neoplasms, Castration-Resistant -- drug therapy
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-12-29
N1 - Date created - 2013-12-23
N1 - Date revised - 2017-01-13
N1 - SuppNotes - Cited By:
BJU Int. 2005 Nov;96(7):990-4 [16225514]
Oncology. 2005;68(1):2-9 [15741753]
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J Clin Oncol. 2007 Apr 20;25(12):1539-44 [17442997]
Curr Treat Options Oncol. 2007 Feb;8(1):89-95 [17634836]
Oncology. 2007;72(5-6):364-70 [18204222]
Clin Cancer Res. 2008 Oct 1;14(19):6302-9 [18829513]
Pharmacogenet Genomics. 2009 Aug;19(8):613-25 [19620936]
Expert Opin Investig Drugs. 2009 Nov;18(11):1787-97 [19888874]
J Clin Oncol. 2009 Nov 10;27(32):5431-8 [19805692]
N Engl J Med. 2011 May 26;364(21):1995-2005 [21612468]
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N1 - Last updated - 2017-01-18
DO - http://dx.doi.org/10.1016/j.urolonc.2012.11.017
ER -
TY - JOUR
T1 - CYP2E1-dependent and leptin-mediated hepatic CD57 expression on CD8+ T cells aid progression of environment-linked nonalcoholic steatohepatitis.
AN - 1490730983; 24211274
AB - Environmental toxins induce a novel CYP2E1/leptin signaling axis in liver. This in turn activates a poorly characterized innate immune response that contributes to nonalcoholic steatohepatitis (NASH) progression. To identify the relevant subsets of T-lymphocytes in CYP2E1-dependent, environment-linked NASH, we utilized a model of diet induced obese (DIO) mice that are chronically exposed to bromodichloromethane. Mice deficient in CYP2E1, leptin (ob/ob mice), or both T and B cells (Pfp/Rag2 double knockout (KO) mice) were used to delineate the role of each of these factors in metabolic oxidative stress-induced T cell activation. Results revealed that elevated levels of lipid peroxidation, tyrosyl radical formation, mitochondrial tyrosine nitration and hepatic leptin as a consequence of metabolic oxidative stress caused increased levels of hepatic CD57, a marker of peripheral blood lymphocytes including NKT cells. CD8+CD57+ cytotoxic T cells but not CD4+CD57+ cells were significantly decreased in mice lacking CYP2E1 and leptin. There was a significant increase in the levels of T cell cytokines IL-2, IL-1β, and IFN-γ in bromodichloromethane exposed DIO mice but not in mice that lacked CYP2E1, leptin or T and B cells. Apoptosis as evidenced by TUNEL assay and levels of cleaved caspase-3 was significantly lower in leptin and Pfp/Rag2 KO mice and highly correlated with protection from NASH. The results described above suggest that higher levels of oxidative stress-induced leptin mediated CD8+CD57+ T cells play an important role in the development of NASH. It also provides a novel insight of immune dysregulation and may be a key biomarker in NASH.
© 2013.
JF - Toxicology and applied pharmacology
AU - Seth, Ratanesh Kumar
AU - Das, Suvarthi
AU - Kumar, Ashutosh
AU - Chanda, Anindya
AU - Kadiiska, Maria B
AU - Michelotti, Gregory
AU - Manautou, Jose
AU - Diehl, Anna Mae
AU - Chatterjee, Saurabh
AD - Environmental Health and Disease Laboratory, Department of Environmental Health Sciences, Arnold School of Public Health, University of South Carolina, Columbia, SC 29208, USA. ; Free Radical Metabolism Group, Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA. ; Division of Gastroenterology, Duke University, Durham, NC 27707, USA. ; Dept. of Pharmaceutical Sciences, University of Connecticut, Storrs, CT 06269-3092, USA. ; Environmental Health and Disease Laboratory, Department of Environmental Health Sciences, Arnold School of Public Health, University of South Carolina, Columbia, SC 29208, USA. Electronic address: schatt@mailbox.sc.edu.
Y1 - 2014/01/01/
PY - 2014
DA - 2014 Jan 01
SP - 42
EP - 54
VL - 274
IS - 1
KW - Antigens, CD57
KW - 0
KW - Cytokines
KW - Inflammation Mediators
KW - Leptin
KW - Trihalomethanes
KW - bromodichloromethane
KW - 7LN464CH2O
KW - Cytochrome P-450 CYP2E1
KW - EC 1.14.13.-
KW - Index Medicus
KW - Apoptosis
KW - CD3
KW - IL-2
KW - Bromodichloromethane
KW - Lipid peroxidation
KW - Animals
KW - Cytokines -- biosynthesis
KW - Mice
KW - Non-alcoholic Fatty Liver Disease
KW - Inflammation Mediators -- metabolism
KW - Mice, Knockout
KW - Mice, 129 Strain
KW - Oxidative Stress -- physiology
KW - Obesity -- metabolism
KW - Oxidative Stress -- drug effects
KW - Mice, Inbred C57BL
KW - Trihalomethanes -- toxicity
KW - Gene Expression Regulation
KW - Obesity -- chemically induced
KW - Male
KW - CD8-Positive T-Lymphocytes -- drug effects
KW - Fatty Liver -- chemically induced
KW - Fatty Liver -- metabolism
KW - CD8-Positive T-Lymphocytes -- metabolism
KW - Cytochrome P-450 CYP2E1 -- deficiency
KW - Antigens, CD57 -- biosynthesis
KW - Leptin -- deficiency
KW - Environmental Exposure -- adverse effects
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LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-02-24
N1 - Date created - 2013-12-20
N1 - Date revised - 2017-01-13
N1 - SuppNotes - Cited By:
Gastroenterology. 2002 May;122(5):1399-410 [11984526]
Hepatogastroenterology. 2003 Jan-Feb;50(49):178-82 [12630018]
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Clin Immunol. 2006 Dec;121(3):314-23 [17035093]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.taap.2013.10.029
ER -
TY - CONF
T1 - Cumulative risk: toxicity and interactions of physical and chemical stressors.
AN - 1490725836; 24154487
AB - Recent efforts to update cumulative risk assessment procedures to incorporate nonchemical stressors ranging from physical to psychosocial reflect increased interest in consideration of the totality of variables affecting human health and the growing desire to develop community-based risk assessment methods. A key roadblock is the uncertainty as to how nonchemical stressors behave in relationship to chemical stressors. Physical stressors offer a reasonable starting place for measuring the effects of nonchemical stressors and their modulation of chemical effects (and vice versa), as they clearly differ from chemical stressors; and "doses" of many physical stressors are more easily quantifiable than those of psychosocial stressors. There is a commonly held belief that virtually nothing is known about the impact of nonchemical stressors on chemically mediated toxicity or the joint impact of coexposure to chemical and nonchemical stressors. Although this is generally true, there are several instances where a substantial body of evidence exists. A workshop titled "Cumulative Risk: Toxicity and Interactions of Physical and Chemical Stressors" held at the 2013 Society of Toxicology Annual Meeting provided a forum for discussion of research addressing the toxicity of physical stressors and what is known about their interactions with chemical stressors, both in terms of exposure and effects. Physical stressors including sunlight, heat, radiation, infectious disease, and noise were discussed in reference to identifying pathways of interaction with chemical stressors, data gaps, and suggestions for future incorporation into cumulative risk assessments.
JF - Toxicological sciences : an official journal of the Society of Toxicology
AU - Rider, Cynthia V
AU - Boekelheide, Kim
AU - Catlin, Natasha
AU - Gordon, Christopher J
AU - Morata, Thais
AU - Selgrade, Maryjane K
AU - Sexton, Kenneth
AU - Simmons, Jane Ellen
Y1 - 2014/01//
PY - 2014
DA - January 2014
SP - 3
EP - 11
VL - 137
IS - 1
KW - Environmental Pollutants
KW - 0
KW - Index Medicus
KW - radiation
KW - infectious disease
KW - cumulative risk
KW - joint action
KW - noise.
KW - sunlight
KW - nonchemical stressors
KW - temperature
KW - Animals
KW - Sunlight -- adverse effects
KW - Risk Factors
KW - Humans
KW - Hot Temperature -- adverse effects
KW - X-Rays -- adverse effects
KW - Communicable Diseases -- complications
KW - Noise -- adverse effects
KW - Risk Assessment
KW - Toxicology -- methods
KW - Environmental Exposure -- adverse effects
KW - Environmental Pollutants -- adverse effects
KW - Stress, Physiological
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1490725836?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=Toxicological+sciences+%3A+an+official+journal+of+the+Society+of+Toxicology&rft.atitle=Cumulative+risk%3A+toxicity+and+interactions+of+physical+and+chemical+stressors.&rft.au=Rider%2C+Cynthia+V%3BBoekelheide%2C+Kim%3BCatlin%2C+Natasha%3BGordon%2C+Christopher+J%3BMorata%2C+Thais%3BSelgrade%2C+Maryjane+K%3BSexton%2C+Kenneth%3BSimmons%2C+Jane+Ellen&rft.aulast=Rider&rft.aufirst=Cynthia&rft.date=2014-01-01&rft.volume=137&rft.issue=1&rft.spage=3&rft.isbn=&rft.btitle=&rft.title=Toxicological+sciences+%3A+an+official+journal+of+the+Society+of+Toxicology&rft.issn=1096-0929&rft_id=info:doi/10.1093%2Ftoxsci%2Fkft228
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-08-28
N1 - Date created - 2013-12-25
N1 - Date revised - 2017-01-13
N1 - SuppNotes - Cited By:
Hear Res. 2000 Dec;150(1-2):206-14 [11077204]
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Toxicol Sci. 2010 Oct;117(2):457-65 [20616210]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1093/toxsci/kft228
ER -
TY - JOUR
T1 - Purification of a serine protease and evidence for a protein C activator from the saliva of the tick, Ixodes scapularis.
AN - 1490712270; 24184517
AB - The saliva of ticks is critical to their survival as parasites and hematophagous animals. In this study, we have purified an enzyme with trypsin-like activity from the saliva of the tick vector of Lyme Disease, Ixodes scapularis. This enzyme, named as IXOSP (I. scapularis salivary serine protease), is a 29.9 kDa molecule with N-terminus FPxMVxLRIKxR. A BLAST search identified IXOSP as a secreted serine protease (AAY66740) with a conserved catalytic triad His, Asp, and Ser. In vitro studies demonstrated that IXOSP cleaves chromogenic substrates with arginine in the P1 position, by a mechanism inhibited by PMSF or aprotinin. Gene expression studies revealed that IXOSP is expressed at different tick developmental stages, including eggs, and unfed or fed adult tick salivary glands, but not in nymphs or in the midgut. While the physiological substrate for IXOSP remains to be identified, we demonstrated that I. scapularis saliva activate protein C (PC) resulting in the production of activated PC, a potent anticoagulant that also regulates a myriad of inflammatory responses through protease activated receptors. In contrast, the salivary glands of Anopheles gambiae, Anopheles stephensi, Anopheles albimanus, Aedes aegypti, Lutzomyia longipalpis, and Phlebotomus ariasi did not activate protein C. These discoveries are discussed in the context of blood coagulation, inflammation and vector-host interactions. Published by Elsevier Ltd.
JF - Toxicon : official journal of the International Society on Toxinology
AU - Pichu, Sivakamasundari
AU - Ribeiro, José M C
AU - Mather, Thomas N
AU - Francischetti, Ivo M B
AD - Center for Vector-Borne Disease, University of Rhode Island, Kingston, RI 02881, USA. Electronic address: au_sudha@yahoo.com. ; Section of Vector Biology, Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. ; Center for Vector-Borne Disease, University of Rhode Island, Kingston, RI 02881, USA. ; Section of Vector Biology, Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: ifrancischetti@niaid.nih.gov.
Y1 - 2014/01//
PY - 2014
DA - January 2014
SP - 32
EP - 39
VL - 77
KW - DNA Primers
KW - 0
KW - Oligopeptides
KW - protein C activator peptide
KW - Serine Proteases
KW - EC 3.4.-
KW - Index Medicus
KW - Serine protease
KW - Activated protein C (APC)
KW - Saliva
KW - Ixodes scapularis
KW - Protease activated receptors (PAR)
KW - Sequence Analysis, Protein
KW - Mass Spectrometry
KW - Gene Expression Regulation, Developmental -- physiology
KW - Animals
KW - Rhode Island
KW - DNA Primers -- genetics
KW - Gene Expression Regulation, Enzymologic -- physiology
KW - Molecular Sequence Data
KW - Amino Acid Sequence
KW - Computational Biology
KW - Species Specificity
KW - Serine Proteases -- toxicity
KW - Serine Proteases -- isolation & purification
KW - Serine Proteases -- genetics
KW - Hemostasis -- drug effects
KW - Oligopeptides -- genetics
KW - Oligopeptides -- isolation & purification
KW - Saliva -- enzymology
KW - Ixodes -- enzymology
KW - Oligopeptides -- toxicity
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1490712270?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicon+%3A+official+journal+of+the+International+Society+on+Toxinology&rft.atitle=Purification+of+a+serine+protease+and+evidence+for+a+protein+C+activator+from+the+saliva+of+the+tick%2C+Ixodes+scapularis.&rft.au=Pichu%2C+Sivakamasundari%3BRibeiro%2C+Jos%C3%A9+M+C%3BMather%2C+Thomas+N%3BFrancischetti%2C+Ivo+M+B&rft.aulast=Pichu&rft.aufirst=Sivakamasundari&rft.date=2014-01-01&rft.volume=77&rft.issue=&rft.spage=32&rft.isbn=&rft.btitle=&rft.title=Toxicon+%3A+official+journal+of+the+International+Society+on+Toxinology&rft.issn=1879-3150&rft_id=info:doi/10.1016%2Fj.toxicon.2013.10.025
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-08-19
N1 - Date created - 2013-12-30
N1 - Date revised - 2017-01-13
N1 - SuppNotes - Cited By:
Insect Biochem Mol Biol. 2000 Feb;30(2):95-105 [10696585]
Front Cell Infect Microbiol. 2013;3:43 [23971008]
J Biol Chem. 2001 Apr 6;276(14):11199-203 [11278252]
Clin Microbiol Infect. 2001 Feb;7(2):80-3 [11298147]
Insect Biochem Mol Biol. 2001 Jun 22;31(8):817-25 [11378417]
Prep Biochem Biotechnol. 2001 May;31(2):201-7 [11426706]
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J Exp Med. 2002 Sep 2;196(5):561-4 [12208872]
Annu Rev Entomol. 2003;48:73-88 [12194906]
Insect Biochem Mol Biol. 2003 Apr;33(4):407-15 [12650689]
Biochem Biophys Res Commun. 2003 Jun 13;305(4):869-75 [12767911]
Insect Biochem Mol Biol. 2004 Jan;34(1):1-17 [14723893]
Insect Mol Biol. 2004 Feb;13(1):9-18 [14728662]
Med Vet Entomol. 2004 Mar;18(1):20-4 [15009442]
Infect Immun. 2004 May;72(5):2989-94 [15102811]
J Mol Biol. 2004 Jul 16;340(4):783-95 [15223320]
Anal Biochem. 1983 Jul 15;132(2):288-93 [6353999]
Int J Parasitol. 1983 Oct;13(5):447-54 [6642860]
Eur J Biochem. 1990 Mar 30;188(3):507-15 [2110057]
J Med Entomol. 1990 Jul;27(4):646-50 [2388239]
Nucleic Acids Res. 1997 Sep 1;25(17):3389-402 [9254694]
Nucleic Acids Res. 1997 Dec 15;25(24):4876-82 [9396791]
Thromb Haemost. 2005 Jul;94(1):167-74 [16113800]
Toxicon. 2006 Jan;47(1):1-20 [16364387]
Insect Biochem Mol Biol. 2006 Feb;36(2):111-29 [16431279]
Trends Parasitol. 2007 Sep;23(9):397-407 [17656153]
Exp Appl Acarol. 2007;42(4):291-300 [17710557]
Eukaryot Cell. 2007 Oct;6(10):1745-57 [17715367]
Annu Rev Entomol. 2008;53:323-43 [17877457]
Parasitol Int. 2008 Dec;57(4):499-505 [18775510]
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Thromb Haemost. 2009 Sep;102(3):437-53 [19718463]
J Biol Chem. 2011 Apr 1;286(13):10960-9 [21270122]
BMC Biochem. 2011;12:32 [21708020]
Ticks Tick Borne Dis. 2012 Feb;3(1):18-26 [22309855]
Arterioscler Thromb Vasc Biol. 2012 Sep;32(9):2185-98 [22796577]
Ticks Tick Borne Dis. 2013 Feb;4(1-2):160-3 [23141105]
Insect Biochem Mol Biol. 2001 Mar 15;31(4-5):465-72 [11222956]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1016/j.toxicon.2013.10.025
ER -
TY - JOUR
T1 - Serum- and glucocorticoid-regulated kinase 2 determines drug-activated pregnane X receptor to induce gluconeogenesis in human liver cells.
AN - 1469217474; 24204015
AB - Drug activation of the human nuclear pregnane X receptor (PXR) induced gluconeogenic genes and increased glucose production. In this study, we have determined that serum- and glucocorticoid-regulated kinase 2 (SGK2) is an essential factor that mediates this PXR-regulated glucose 6-phosphatase (G6Pase) induction and glucose production. Both SGK2 and G6Pase mRNAs were increased in rifampicin-treated HepG2 cells stably expressing human PXR. Reporter and chromatin immunoprecipitation assays delineated PXR activation of the SGK2 gene to a distal and proximal DNA sequence within its promoter: distal PXR response element (-2587/-2209) and proximal PXR response element (-115/-75), respectively. Small interfering RNA (siRNA) knockdown of SGK2 severely attenuated PXR-regulated induction of G6Pase as well as glucose production. SGK2 constitutes an insulin-independent signal pathway to regulate gluconeogenesis because siRNA knockdown of the insulin-responsive transcription factor forkhead box protein O1 did not affect rifampicin induction of G6Pase. Rifampicin treatment of two different samples of human primary hepatocytes revealed that PXR induces G6Pase in the presence of high levels of SGK2, whereas PXR represses G6Pase in its absence. Mediating PXR activation of the G6Pase gene is the first biological role found for hepatic SGK2 and might have therapeutic implications for side effects, such as diabetes, caused by drugs that activate PXR.
JF - The Journal of pharmacology and experimental therapeutics
AU - Gotoh, Saki
AU - Negishi, Masahiko
AD - Pharmacogenetics Section, Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina.
Y1 - 2014/01//
PY - 2014
DA - January 2014
SP - 131
EP - 140
VL - 348
IS - 1
KW - Enzyme Inhibitors
KW - 0
KW - Immediate-Early Proteins
KW - Receptors, Steroid
KW - pregnane X receptor
KW - Protein-Serine-Threonine Kinases
KW - EC 2.7.11.1
KW - serum-glucocorticoid regulated kinase
KW - Rifampin
KW - VJT6J7R4TR
KW - Index Medicus
KW - Animals
KW - Hep G2 Cells
KW - Liver -- drug effects
KW - Cells, Cultured
KW - Humans
KW - Mice, Inbred C3H
KW - Liver -- metabolism
KW - Enzyme Inhibitors -- pharmacology
KW - Mice
KW - Rifampin -- pharmacology
KW - Male
KW - Gluconeogenesis -- drug effects
KW - Hepatocytes -- drug effects
KW - Protein-Serine-Threonine Kinases -- metabolism
KW - Gluconeogenesis -- physiology
KW - Immediate-Early Proteins -- metabolism
KW - Receptors, Steroid -- metabolism
KW - Immediate-Early Proteins -- antagonists & inhibitors
KW - Protein-Serine-Threonine Kinases -- antagonists & inhibitors
KW - Receptors, Steroid -- agonists
KW - Hepatocytes -- metabolism
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1469217474?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.atitle=Serum-+and+glucocorticoid-regulated+kinase+2+determines+drug-activated+pregnane+X+receptor+to+induce+gluconeogenesis+in+human+liver+cells.&rft.au=Gotoh%2C+Saki%3BNegishi%2C+Masahiko&rft.aulast=Gotoh&rft.aufirst=Saki&rft.date=2014-01-01&rft.volume=348&rft.issue=1&rft.spage=131&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.issn=1521-0103&rft_id=info:doi/10.1124%2Fjpet.113.209379
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-02-10
N1 - Date created - 2013-12-16
N1 - Date revised - 2017-01-13
N1 - SuppNotes - Cited By:
Biochem J. 1999 Nov 15;344 Pt 1:189-97 [10548550]
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Clin Pharmacol Ther. 2001 Jun;69(6):400-6 [11406737]
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Clin Pharmacol Ther. 2003 Oct;74(4):334-40 [14534520]
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Am Rev Respir Dis. 1982 Jan;125(1):23-7 [7039435]
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Clin Pharmacol Ther. 2013 Jun;93(6):556-63 [23588309]
Pflugers Arch. 2007 Mar;453(6):863-70 [17051390]
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J Biol Chem. 2011 Feb 4;286(5):3570-8 [21127053]
Environ Health Perspect. 2012 Jun;120(6):779-89 [22296744]
Atheroscler Suppl. 2012 Aug;13(1):1-10 [22818818]
Clin Pharmacol Ther. 2000 Nov;68(5):495-500 [11103752]
N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1124/jpet.113.209379
ER -
TY - JOUR
T1 - Chemopreventive effects of an HDAC2-selective inhibitor on rat colon carcinogenesis and APCmin/+ mouse intestinal tumorigenesis.
AN - 1467635900; 24218540
AB - Epigenetic modulators, particularly histone deacetylases (HDACs), are valid targets for cancer prevention and therapy. Recent studies report that HDAC2 overexpression is associated with colon tumor progression and is a potential target for colon cancer prevention. This study tested chemopreventive and dose-response effects of Ohio State University HDAC42 (OSU-HDAC42), a selective HDAC2 inhibitor, using a rat colon carcinogenesis model to assess aberrant crypt foci inhibition and a familial adenomatous polyposis model to assess intestinal tumor inhibition. Colonic aberrant crypt foci were induced by azoxymethane (AOM) (15 mg/kg body weight, once-weekly subcutaneous injections at 8 and 9 weeks age). One week after AOM treatment, groups of rats were fed an AIN-76A diet containing 0, 75, 150, and 300 ppm OSU-HDAC42 for 8 weeks, and colonic aberrant crypt foci were evaluated. To assess the inhibitory effect of OSU-HDAC42 on small-intestinal polyps and colon tumor growth, 6-week-old male C57Bl/6J-APC(min/+)mice were fed an AIN-76A diet containing 150 ppm OSU-HADC42 or 300 ppm pan-HDAC inhibitor suberoylanilide hydroxyamic acid (SAHA) for 80 days. Our results demonstrate that dietary OSU-HDAC42 produced dose-dependent inhibition of AOM-induced colonic aberrant crypt foci formation (13-50%; P 46%; P 1 mm (P 26%) in APC(min/+)mice, whereas 300 ppm SAHA showed nonsignificant inhibition. Mice fed 150 ppm OSU-HDAC42 had significantly decreased HDAC2, proliferating cell nuclear antigen, B cell lymphoma 2, cyclin-dependent kinase 2, and cell division cycle homolog 25C expression levels and increased p53 expression levels. These observations demonstrate the chemopreventive efficacy of OSU-HDAC42 against chemically induced and polyposis models of intestinal tumorigenesis.
JF - The Journal of pharmacology and experimental therapeutics
AU - Ravillah, Durgadevi
AU - Mohammed, Altaf
AU - Qian, Li
AU - Brewer, Misty
AU - Zhang, Yuting
AU - Biddick, Laura
AU - Steele, Vernon E
AU - Rao, Chinthalapally V
AD - Hematology-Oncology Section, Department of Medicine, Center for Cancer Prevention and Drug Development, PCS Oklahoma Cancer Center, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma (D.R., A.M., L.Q., M.B., Y.Z., L.B., C.V.R.); and Division of Cancer Prevention, Chemoprevention Agent Development Research Group, National Institutes of Health National Cancer Institute, Bethesda, Maryland (V.E.S.).
Y1 - 2014/01//
PY - 2014
DA - January 2014
SP - 59
EP - 68
VL - 348
IS - 1
KW - APC protein, human
KW - 0
KW - Adenomatous Polyposis Coli Protein
KW - Histone Deacetylase Inhibitors
KW - OSU-HDAC42 compound
KW - Phenylbutyrates
KW - Hdac2 protein, mouse
KW - EC 3.5.1.98
KW - Histone Deacetylase 2
KW - Index Medicus
KW - Rats
KW - Animals
KW - Rats, Inbred F344
KW - Humans
KW - Mice, Inbred C57BL
KW - Mice
KW - HCT116 Cells
KW - Mice, Transgenic
KW - Male
KW - Female
KW - Histone Deacetylase 2 -- antagonists & inhibitors
KW - Phenylbutyrates -- therapeutic use
KW - Colonic Neoplasms -- genetics
KW - Adenomatous Polyposis Coli Protein -- biosynthesis
KW - Phenylbutyrates -- pharmacology
KW - Disease Models, Animal
KW - Carcinogenesis -- pathology
KW - Intestinal Neoplasms -- prevention & control
KW - Histone Deacetylase 2 -- metabolism
KW - Carcinogenesis -- genetics
KW - Carcinogenesis -- drug effects
KW - Histone Deacetylase Inhibitors -- therapeutic use
KW - Intestinal Neoplasms -- genetics
KW - Intestinal Neoplasms -- enzymology
KW - Colonic Neoplasms -- pathology
KW - Colonic Neoplasms -- prevention & control
KW - Adenomatous Polyposis Coli Protein -- genetics
UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1467635900?accountid=14244
L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.atitle=Chemopreventive+effects+of+an+HDAC2-selective+inhibitor+on+rat+colon+carcinogenesis+and+APCmin%2F%2B+mouse+intestinal+tumorigenesis.&rft.au=Ravillah%2C+Durgadevi%3BMohammed%2C+Altaf%3BQian%2C+Li%3BBrewer%2C+Misty%3BZhang%2C+Yuting%3BBiddick%2C+Laura%3BSteele%2C+Vernon+E%3BRao%2C+Chinthalapally+V&rft.aulast=Ravillah&rft.aufirst=Durgadevi&rft.date=2014-01-01&rft.volume=348&rft.issue=1&rft.spage=59&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.issn=1521-0103&rft_id=info:doi/10.1124%2Fjpet.113.208645
LA - English
DB - ProQuest Environmental Science Collection
N1 - Date completed - 2014-02-10
N1 - Date created - 2013-12-11
N1 - Date revised - 2017-01-13
N1 - SuppNotes - Cited By:
Cell Death Differ. 2005 Apr;12(4):395-404 [15665816]
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N1 - Last updated - 2017-01-19
DO - http://dx.doi.org/10.1124/jpet.113.208645
ER -